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J Biol Chem, Vol. 273, Issue 44, 28545-28548, October 30, 1998
From the Clinical Gene Therapy Branch, National Human Genome
Research Institute, National Institutes of Health,
Bethesda, Maryland 20892-1851
CCAAT/enhancer-binding proteins (C/EBPs) comprise
a family of transcription factors that are critical for normal cellular differentiation and function in a variety of tissues. The prototypic C/EBP is a modular protein, consisting of an activation domain, a
dimerization bZIP region, and a DNA-binding domain. All family members
share the highly conserved dimerization domain, required for DNA
binding, by which they form homo- and heterodimers with other family
members. C/EBPs are least conserved in their activation domains and
vary from strong activators to dominant negative repressors. The
pleiotropic effects of C/EBPs are in part because of tissue- and
stage-specific expression. Dimerization of different C/EBP proteins
precisely modulates transcriptional activity of target genes. Recent
work with mice deficient in specific C/EBPs underscores the effects of
these factors in tissue development, function, and response to
injury.
The CCAAT/enhancer-binding proteins
(C/EBPs)1 encompass a family
of transcription factors with structural as well as functional homologies. Similarities between C/EBP family members suggest an
evolutionary history of genetic duplications with subsequent pressure
to diversify. The resulting family of proteins varies in tissue
specificity and transactivating ability. Since the cloning of the
family's original member, C/EBP The prototypic C/EBP, like many transcription factors, is a modular
protein, consisting of an activation domain, a DNA-binding basic
region, and a leucine-rich dimerization domain. The dimerization domain, aptly termed the "leucine zipper," is a heptad of leucine repeats that intercalate with repeats of the dimer partner, forming a
coiled coil of In this review, C/EBP genes are designated C/EBP Two isoforms of C/EBP A fraction of ribosomes ignore the first two AUG codons and initiate
translation at the third AUG, 351 nucleotides downstream of the first
AUG (14, 15). This shorter 30-kDa protein retains its dimerization and
DNA-binding domains; however, it possesses an altered transactivation
potential compared with the 42-kDa isoform (14, 15).
The human, mouse, and rat genes for C/EBP Like C/EBP C/EBP C/EBP C/EBP C/EBP C/EBP Hepatic Phenotypes--
Coordinate expression of specific C/EBP
isoforms is essential for normal hepatic synthetic activity and
response to injury; however, C/EBP
Hepatocyte proliferation following partial hepatectomy is accompanied
by profound changes in C/EBP expression patterns. C/EBP
The duality of C/EBP Adipose Phenotype--
Adipocytes grown in tissue culture and in
animal models lacking C/EBP
Mice deficient for both C/EBP
Preadipocyte differentiation into functional adipocytes results from a
highly regulated cascade of C/EBP isoform expression. Dexamethasone-
and methylisobutylxanthine-stimulated 3T3-L1 preadipocytes express high
levels of C/EBP
C/EBP
Transient modulation of C/EBP levels in response to insulin and
dexamethasone suggests a dynamic role in adipocyte metabolism (65).
Induction of C/EBP
CHOP regulates stress-inducible growth arrest in adipose tissue. Late
in adipogenesis and during conditions of nutrient deprivation CHOP
mRNA transcription is enhanced (45, 70, 71). CHOP attenuates C/EBP
The oncogenic variant of CHOP is found exclusively in myxoid
liposarcomas (73). Chromosomal translocation of t(12;16)(q13;p11) fuses
CHOP to an RNA-binding protein, which possesses strong homology to
protein expressed in Ewing's sarcoma (74). TLS-CHOP (translocated in
liposarcoma-CHOP) fails to cause cell grow arrest and interferes with
normal CHOP activity (72).
Hematopoietic Phenotypes--
Profound abnormalities of the
hematopoietic system are seen in C/EBP
C/EBP
In B cells, C/EBP
Mice nullizygous for C/EBP Other Systems--
C/EBPs role in the function of other organ
systems is only beginning to be elucidated. A significant percentage of
C/EBP
Normal ovarian physiology is dependent upon both C/EBP C/EBPs act as pivotal regulators of cellular differentiation,
terminal function, and response to inflammatory insult. Their extensive
involvement in hepatic, adipose, and hematopoietic systems suggests the
certainty of C/EBPs role in other tissues and systems. As potent
mediators of gene expression, C/EBPs may be the future of some gene
therapies or offer a deeper understanding of the forces driving
oncogenesis. We are only beginning to understand the intricate pathways
that transduce cell surface receptor signaling to gene transcription
and subsequent protein activation. Future work with animal models
deficient in multiple C/EBP isoforms will further elucidate these
complex pathways.
We are grateful to L. Garrett and T. Hernandez for excellent technical assistance and devoted animal care,
to Drs. T. Decker, T. Fredrickson, D. G. Tenen, M. Eckhaus, P. P.
Liu, L. H. Castilla, and D. Horn for expert advice and reagents, and
to D. Bodine, S. Holland, and P. Murphy for critical input. We thank
Dr. R. M. Blaese for creating an inspiring environment and providing
constant support. We also wish to apologize to many colleagues whose
excellent work may not have been quoted in this review because of space restrictions.
*
This minireview will be reprinted
in the 1998 Minireview Compendium, which
will be available in December, 1998. This is the first article of five in the
"Biological Role of the Isoforms of C/EBP Minireview Series."
The abbreviations used are:
C/EBP, CCAAT/enhancer-binding protein; LPS, lipopolysaccharide; IL, interleukin; TNF, tumor necrosis factor; G-CSF, granulocyte
colony-stimulating factor; GM-CSF, granulocyte-macrophage
colony-stimulating factor; CHOP, C/EBP homologous protein; PPAR, peroxisome proliferator-activated receptor.
MINIREVIEW
Biological Role of the CCAAT/Enhancer-binding Protein Family of
Transcription Factors*
ABSTRACT
Top
Abstract
Introduction
References
INTRODUCTION
Top
Abstract
Introduction
References
, nearly a decade ago, five other
C/EBPs have been identified that interact with each other and
transcription factors in other protein families to regulate mRNA
transcription. The pleiotropic effects of C/EBPs are in part because of
tissue- and stage-specific expression, leaky ribosomal reading,
post-transcriptional modifications, and variable DNA binding
specificities. These mechanisms result in variable amounts of the C/EBP
isoforms, available to dimerize and bind to cognate sites in different
tissues. Recent work with mice genetically altered to abolish
expression of C/EBPs underscores the role these factors play in normal
tissue development and cellular function, cellular proliferation, and
functional differentiation.
-helices in parallel orientation (1-3).
Electrostatic interactions between amino acids along the dimerization
interface determine the specificity of dimer formation among C/EBP
family members as well as with transcription factors of the NF-
B and Fos/Jun families (2). C/EBP dimerization is a prerequisite to DNA
binding (4). DNA binding specificity, however, is determined by the DNA
contact surface, the "basic" region of approximately 20 amino
acids, upstream of the leucine zipper, specifically by three amino
acids lying along the protein-DNA interface (1, 5). Domains responsible
for transcriptional activation and/or repression are located in the
N-terminal end of the protein.
, -
,
-
, -
, -
, and -
as proposed by Cao et al. (6);
however, Table I lists alternative
nomenclature. C/EBP was the first member cloned (7-12).
Expression patterns of C/EBP mRNA are similar in the mouse and
human with measurable levels in liver, adipose, intestine, lung,
adrenal gland, peripheral blood mononuclear cells, and placenta (8,
12). In liver and adipose, highest levels of C/EBP mRNA are
detected only in differentiated tissue (8, 12). Autoregulation of
C/EBP mRNA occurs by different mechanisms in the mouse and in
humans. The murine C/EBP promoter directly binds C/EBP within 200 base pairs of the transcriptional start resulting in 3-fold activation
(9). Autoregulation of the human C/EBP promoter occurs by
C/EBP-induced binding of USF, a ubiquitously expressed transcription
factor, to its upstream site within the C/EBP promoter (13).
Cloned C/EBP genes and phenotypic characterization of knockout models
are generated from its mRNA by a ribosomal
scanning mechanism (14, 15). The full-length protein is 42 kDa and
contains three transactivation domains (TEI-III) (16-18). TEI and
TEII mediate cooperative binding of C/EBP to TBP (TATA box-binding
protein) and TFIIB, two components of the RNA polymerase II basal
transcriptional apparatus (17). TEIII contains a negative regulatory
subdomain (16).
have been
cloned (6, 19-23). Constitutive expression of C/EBP is highest in liver, intestine, lung, and adipose; however, in the mouse, it is also
detectable in kidney, heart, and spleen by Northern analysis (6).
Stimulation with lipopolysaccharide (LPS), IL-6, IL-1, dexamethasone,
and glucagon strongly induces C/EBP expression, suggesting a role in
the mediation of the inflammatory response (20, 24-26).
, two C/EBP isoforms are generated from a single
mRNA by a leaky ribosomal scanning mechanism. The full-length 32-kDa protein, also termed LAP, encodes for the conserved activation domains found in other C/EBP proteins, as well as two regulatory domains, RD1 and RD2, which confer DNA binding inhibition in a cell
type-specific manner (27). The truncated protein, LIP, translated from
the third, in-frame AUG, possesses only the DNA-binding and leucine
zipper domains (22, 28). Heterodimerization of the truncated isoform
with the full-length C/EBP (LAP) attenuates transcriptional activity
in substoichiometric amounts, suggesting a dominant negative mechanism
of transcriptional regulation (28).
was originally identified as a mediator of IL-6 signaling,
binding to IL-6-responsive elements in the promoters of acute phase
response genes TNF, IL-8, and G-CSF (20, 22). Signal transduction of
the acute phase response by IL-1 and LPS also induces C/EBP
transcription (20, 25). TNF promotes nuclear localization of
C/EBP and C/EBP in response to inflammatory stress (29). Cytokine
stimulation further increases C/EBP transcriptional activity by
enhanced DNA binding (22). Post-transcriptional modifications of
C/EBP by protein kinases in the signal transduction pathway of
C/EBP appear to activate transcription (30, 31).
is a short, intronless gene, whose mRNA is
ubiquitously expressed with highest levels found in non-differentiated, progenitor cells (19, 32, 33). The 16.4-kDa encoded protein possesses a
leucine zipper dimerization domain and DNA-binding region; however, it
lacks transcriptional transactivating elements (33). Heterodimerization
with C/EBP and C/EBP attenuates transcriptional activation of
target genes, suggesting dominant negative regulation of C/EBP
transactivation in undifferentiated, non-induced cells (33).
is an intronless gene (6, 34-38). Constitutive
expression of C/EBP is detected in intestines, adipose, and lung, with high levels of expression in all tissues following LPS stimulation (6, 25, 36). The 269-amino acid protein encodes a leucine zipper
dimerization domain and DNA-binding region, readily forming heterodimers with C/EBP and C/EBP (6). Transactivating efficiency of C/EBP is comparable with that of C/EBP and C/EBP (6). The
DNA-binding region of C/EBP differs from C/EBP in that it contains 2 proline and 4 glycine residues, which may interrupt the
predicted -helical structure (6). Diminished DNA binding affinity of
the C/EBP basic domain compared with C/EBP and C/EBP is likely
the result of sequence divergence (6).
was originally identified from a rat genomic
library, but the start site could not be determined and no expression was detected (38). Subsequently, the full-length C/EBP
gene was cloned (39, 40). Human C/EBP contains two
intronic sequences and five in-frame AUG initiation sites, three of
which satisfy the Kozak context (41). Four mRNA isoforms, expressed
primarily in myeloid and lymphoid cells, are generated by the use of
alternative promoters combined with differential splicing (41). The
highest level of expression is detected in promyelocyte and late
myeloblast-like cell lines (39, 42). Further, induction of C/EBP
mRNA with retinoids promotes granulocytic differentiation of
promyelocyte line NB4 (42, 43). The four C/EBP mRNA isoforms
translate into three proteins possessing identical leucine zipper
domains and variably truncated activation domains, with differing
transcriptional activities (40, 41).
, which is induced by DNA damage, was
originally cloned in hamster and named growth arrest and DNA
damage-inducible gene (gadd153) (44). Spanning 5 kilobases,
it consists of four exons and is expressed ubiquitously (45). Like
other C/EBP proteins, C/EBP possesses a leucine zipper dimerization
domain and DNA-binding region (45). C/EBP readily heterodimerizes
with other C/EBPs; however, the presence of two prolines in the
DNA-binding region disrupts its helical structure and prevents dimer
binding to the cognate DNA enhancer element (45). C/EBP functions as
a dominant negative inhibitor of C/EBP transcriptional activation by
preventing heterodimer binding of C/EBP and C/EBP to classic
C/EBP enhancer sequences (45).
C/EBP-deficient Animal Models
is the predominant nuclear signal
regulating terminal hepatocyte differentiation and function.
Elimination of C/EBP in targeted mouse knockout models
results in profound derangement of liver structure and function (Table
I). C/EBP 
/ mice have disturbed hepatic architecture with acinar
formation, resembling proliferative or pseudoglandular hepatocellular
carcinoma (46, 47). c-Myc and c-Jun RNAs are induced consistent with a
proliferative liver (46). Metabolic derangements are pronounced with an
impairment of hepatic glycogen storage, and the majority of mice die
soon after birth because of hypoglycemia (46, 47). Known target genes
of C/EBP have decreased expression at birth, including albumin,
glycogen synthase, phosphoenolpyruvate carboxykinase, and glucose
6-phosphatase (47). Low level expression of phosphoenolpyruvate carboxykinase and perinatal lethality is also seen in a subset of
C/EBP / mice, suggesting involvement of the C/EBP isoform in
gluconeogenic pathways (48).
mRNA
decreases following partial hepatectomy whereas C/EBP mRNA increases (49-51). C/EBP mRNA levels rise following partial
hepatectomy, as well as sham surgery, in keeping with its role as an
inflammatory/injury response mediator (50). C/EBP:C/EBP
heterodimers are replaced by increased amounts of C/EBP homodimers
during the early G1 period after partial hepatectomy (52,
53). The necessary down-regulation of C/EBP expression during liver
regeneration may be mediated by the increased binding of C/EBP
homodimers to the C/EBP promoter, normally transactivated by a:b
heterodimers in the non-proliferative state (53).
function in mediating cell cycle arrest and
hepatic metabolism is clearly demonstrated in the C/EBP knockout
mouse. C/EBP functions similarly in adipose tissue, inducing
adipocyte differentiation and mediating transcription of
adipose-specific genes.
fail to accumulate lipids. Uncoupling
protein is responsible for uncoupled mitochondrial respiration and heat
generation and is a marker for differentiation of brown adipose tissue.
C/EBP-deficient mice have minimal levels of uncoupling protein
expression at 2 h postpartum, which increases to 60% that of
control mice by 32 h postpartum (47). Gene transcription of fatty
acid synthase, GLUT4, and 422/aP2 is unaltered in white adipose tissue
of the C/EBP-deficient mouse, which is inconsistent with
transcriptional data from 3T3-L1 cell lines (47, 54-56). Redundant
transcriptional elements operating in the animal model may regulate the
fatty acid synthesis pathway, compensating for the lack of
C/EBP.
and C/EBP expire perinatally,
similar to C/EBP knockout mice (57). C/EBP:C/EBP double knockout mice did not accumulate lipid droplets in brown adipose tissue
and had significantly reduced epidydimal fat pads in surviving adults
(57). Despite these defects, C/EBP and PPAR expression was
normal, suggesting that C/EBP and PPAR are not sufficient for
adipocyte differentiation in the absence of C/EBP and C/EBP (57).
and C/EBP. These factors diminish during the late
phase of differentiation concordant with the appearance of high levels
of C/EBP (6, 58). Ectopic expression of C/EBP in 3T3-L1 cells
arrests mitotic growth (59). Likewise, abrogation of C/EBP
expression, either by antisense interactions or hydrocortisone administration, prevents terminal adipocyte differentiation (14, 60).
interacts with known regulators of cell cycle progression; it
activates transcription and induces post-transcriptional stabilization
of p21(WAT-1/CIP-1/SDI-1) protein, an inhibitor of
cyclin-dependent kinase (61, 62). Additionally, c-Myc and C/EBP share a reciprocal relationship, balancing proliferation versus growth arrest via C/EBP-transactivated expression
of gadd45 (growth arrest-associated gene), a target of p53
tumor suppressor protein at G1 (63, 64).
and C/EBP occurs within 1 h of insulin stimulation, resulting in a 20-fold increase of transcription factor
levels by 4 h (65). Insulin treatment also decreased DNA binding
of C/EBP while increasing nuclear C/EBP and C/EBP binding
(65). Insulin also induces rapid dephosphorylation of C/EBP and
represses C/EBP expression, modulating adipocyte gene transcription
(e.g. GLUT4) (65, 66). Another gene target of C/EBP, the
obese gene (67, 68), may be similarly regulated. Likewise,
dexamethasone rapidly induces C/EBP levels, reciprocally repressing C/EBP expression (69).
and C/EBP activity by forming non-DNA binding heterodimers, and if expressed early in the adipogenesis program, will inhibit differentiation (45, 70). Induction of CHOP in adipocytes by cellular
stress blocks G1 to S phase progression resulting in growth
arrest (72).
-, C/EBP-, and
C/EBP-deficient mice. Mice deficient in C/EBP display an early
block in the maturation of granulocytes (75). Peripheral blood and bone
marrow smears show only myeloblastic cells of the myeloid lineage (75).
The G-CSF receptor message is undetectable in these cells, suggesting a
loss of G-CSF signal-directed maturation (75). In transient assays,
C/EBP contributes to tissue-specific expression of G-CSF and GM-CSF
receptors (76-78) and neutrophil elastase (79, 80). Evidence suggests
that C/EBP plays an early, pivotal role in the granulocyte
lineage.
-deficient mice are highly susceptible to Candida
albicans, Listeria monocytogenes, and Salmonella typhi
(81, 82). Lethality from these pathogens may be in part because of
macrophage defects and escape of phagocytosed bacteria from the
phagosome to the cytoplasm (82). Low IL-12 levels and depressed
delayed-type hypersensitivity, consistent with an impaired Th1 immune
response, are seen in these mice (81). Elevated IL-6 levels, reported by one group, in C/EBP-deficient mice coincide with splenomegaly, peripheral lymphadenopathy, plasmacytosis, and extramedullary hematopoiesis, as seen in Castleman's disease in humans (81).
is the predominant isoform in early cells,
decreasing with cellular maturity (83). C/EBP becomes highly expressed in mature B cells and with LPS stimulation (83). Consistent with this observation, C/EBP sites are activators in mature B cells but
not in early cells, suggesting that C/EBP and C/EBP play
reciprocal roles (83).
survive only 2-5 months after birth
(84). Frequently, these mice succumb to tissue effacement by immature
granulocytes; however, 60% of mice typed have a systemic infection
with Pseudomonas aeruginosa at time of death (84). C/EBP-deficient mice generate atypical hyposegmented granulocytes that are functionally defective, lacking an oxidative burst (84). Additionally, derangements in cytokine signaling are evidenced by low
levels of mRNAs for interferon-, IL-2, IL-4, IL-12p40, and
TNF- (84). These results suggest that C/EBP acts temporally downstream of C/EBP in granulopoiesis, blocking the last steps in
terminal differentiation of mature segmented granulocytes.
-deficient mice succumb to respiratory defects soon after birth
(46). Histologic examination of C/EBP-deficient lungs shows
hyperproliferation of type 2 pneumocytes (46). C/EBP expression is
temporally correlated with the appearance of surfactant A protein and
is not present in A549 cells, a cell line that does not express
surfactant proteins (85).
and C/EBP.
Rat ovarian follicles express C/EBP in a cell-, time-, and
hormonally specific manner (86). Attenuation of C/EBP expression results in decreased responsiveness to exogenous gonadotropins and
decreased ovulation rate (86). Additionally, attenuation of C/EBP
expression is associated with elevated expression of proto-oncogene
c-myc (86). C/EBP mediates signal transduction of
luteinizing hormone and is essential for the formation of corpora lutea
(87). C/EBP-deficient mice fail to down-regulate expression of
prostaglandin endoperoxidase synthase 2 and p450 aromatase in response
to luteinizing hormone and are sterile (87).
Conclusions
ACKNOWLEDGEMENTS
FOOTNOTES
To whom correspondence should be addressed: Aurora Biosciences,
Inc., 11010 Torreyana Rd., San Diego, CA 92121. Tel.: 619-452-5000; E-mail: xanthopoulosk{at}aurorabio.com.
REFERENCES
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Abstract
Introduction
References
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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 C. Resende, G. Regalo, C. Duraes, F. Carneiro, and J. C. Machado Genetic Changes of CEBPA in Cancer: Mutations or Polymorphisms? J. Clin. Oncol., June 10, 2007; 25(17): 2493 - 2494. [Full Text] [PDF]
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A. Khanna-Gupta, H. Sun, T. Zibello, H. M. Lee, R. Dahl, L. A. Boxer, and N. Berliner Growth factor independence-1 (Gfi-1) plays a role in mediating specific granule deficiency (SGD) in a patient lacking a gene-inactivating mutation in the C/EBP{epsilon} gene Blood, May 15, 2007; 109(10): 4181 - 4190. [Abstract] [Full Text] [PDF]
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T. Akasaka, T. Balasas, L. J. Russell, K.-j. Sugimoto, A. Majid, R. Walewska, E. L. Karran, D. G. Brown, K. Cain, L. Harder, et al. Five members of the CEBP transcription factor family are targeted by recurrent IGH translocations in B-cell precursor acute lymphoblastic leukemia (BCP-ALL) Blood, April 15, 2007; 109(8): 3451 - 3461. [Abstract] [Full Text] [PDF]
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 H. Liao, M. C. Hyman, D. A. Lawrence, and D. J. Pinsky Molecular regulation of the PAI-1 gene by hypoxia: contributions of Egr-1, HIF-1{alpha}, and C/EBP{alpha} FASEB J, March 1, 2007; 21(3): 935 - 949. [Abstract] [Full Text] [PDF]
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W. J. Oh, V. Rishi, A. Orosz, M. J. Gerdes, and C. Vinson Inhibition of CCAAT/Enhancer Binding Protein Family DNA Binding in Mouse Epidermis Prevents and Regresses Papillomas Cancer Res., February 15, 2007; 67(4): 1867 - 1876. [Abstract] [Full Text] [PDF]
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 G. Mameli, S. L. Deshmane, M. Ghafouri, J. Cui, K. Simbiri, K. Khalili, R. Mukerjee, A. Dolei, S. Amini, and B. E. Sawaya C/EBPbeta regulates human immunodeficiency virus 1 gene expression through its association with cdk9 J. Gen. Virol., February 1, 2007; 88(2): 631 - 640. [Abstract] [Full Text] [PDF]
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T. I. Cesena, J.-R. Cardinaux, R. Kwok, and J. Schwartz CCAAT/Enhancer-binding Protein (C/EBP) beta Is Acetylated at Multiple Lysines: ACETYLATION OF C/EBPbeta AT LYSINE 39 MODULATES ITS ABILITY TO ACTIVATE TRANSCRIPTION J. Biol. Chem., January 12, 2007; 282(2): 956 - 967. [Abstract] [Full Text] [PDF]
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 F. Meyer, S. Perez, V. Geiser, M. Sintek, M. Inman, and C. Jones A Protein Encoded by the Bovine Herpesvirus 1 Latency-Related Gene Interacts with Specific Cellular Regulatory Proteins, Including CCAAT Enhancer Binding Protein Alpha J. Virol., January 1, 2007; 81(1): 59 - 67. [Abstract] [Full Text] [PDF]
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J. Dong, S. Fujii, S. Imagawa, S. Matsumoto, M. Matsushita, S. Todo, H. Tsutsui, and B. E. Sobel IL-1 and IL-6 induce hepatocyte plasminogen activator inhibitor-1 expression through independent signaling pathways converging on C/EBP{delta} Am J Physiol Cell Physiol, January 1, 2007; 292(1): C209 - C215. [Abstract] [Full Text] [PDF]
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W. Wei, H. Yang, M. Menconi, P. Cao, C. E. Chamberlain, and P.-O. Hasselgren Treatment of cultured myotubes with the proteasome inhibitor beta-lactone increases the expression of the transcription factor C/EBPbeta Am J Physiol Cell Physiol, January 1, 2007; 292(1): C216 - C226. [Abstract] [Full Text] [PDF]
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P. J. McFie, G.-L. Wang, N. A. Timchenko, H. L. Wilson, X. Hu, and W. J. Roesler Identification of a Co-repressor That Inhibits the Transcriptional and Growth-Arrest Activities of CCAAT/Enhancer-binding Protein {alpha} J. Biol. Chem., June 30, 2006; 281(26): 18069 - 18080. [Abstract] [Full Text] [PDF]
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 C. S. Shin, M. J. Jeon, J.-Y. Yang, S.-J. Her, D. Kim, S. W. Kim, and S. Y. Kim CCAAT/enhancer-binding protein {delta} activates the Runx2-mediated transcription of mouse osteocalcin II promoter. J. Mol. Endocrinol., June 1, 2006; 36(3): 531 - 546. [Abstract] [Full Text] [PDF]
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H. Nakajima, N. Watanabe, F. Shibata, T. Kitamura, Y. Ikeda, and M. Handa N-terminal Region of CCAAT/Enhancer-binding Protein {epsilon} Is Critical for Cell Cycle Arrest, Apoptosis, and Functional Maturation during Myeloid Differentiation J. Biol. Chem., May 19, 2006; 281(20): 14494 - 14502. [Abstract] [Full Text] [PDF]
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T. T. C. Yang, P. M. U. Ung, M. Rincon, and C.-W. Chow Role of the CCAAT/Enhancer-binding Protein NFATc2 Transcription Factor Cascade in the Induction of Secretory Phospholipase A2 J. Biol. Chem., April 28, 2006; 281(17): 11541 - 11552. [Abstract] [Full Text] [PDF]
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F. Berberich-Siebelt, I. Berberich, M. Andrulis, B. Santner-Nanan, M. K. Jha, S. Klein-Hessling, A. Schimpl, and E. Serfling SUMOylation Interferes with CCAAT/Enhancer-Binding Protein beta-Mediated c-myc Repression, but Not IL-4 Activation in T Cells. J. Immunol., April 15, 2006; 176(8): 4843 - 4851. [Abstract] [Full Text] [PDF]
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 P. C. Martis, J. A. Whitsett, Y. Xu, A.-K. T. Perl, H. Wan, and M. Ikegami C/EBP{alpha} is required for lung maturation at birth Development, March 15, 2006; 133(6): 1155 - 1164. [Abstract] [Full Text] [PDF]
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H. Ikeda, K. Omoteyama, K. Yoshida, S. Nishi, and M. Sakai CCAAT Enhancer-binding Protein {alpha} Suppresses the Rat Placental Glutathione S-Transferase Gene in Normal Liver J. Biol. Chem., March 10, 2006; 281(10): 6734 - 6741. [Abstract] [Full Text] [PDF]
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N Salma, H Xiao, and A N Imbalzano Temporal recruitment of CCAAT/enhancer-binding proteins to early and late adipogenic promoters in vivo J. Mol. Endocrinol., February 1, 2006; 36(1): 139 - 151. [Abstract] [Full Text] [PDF]
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 S. Kawai, T. Kato, M. Sato, and A. Amano Odd-Skipped Related 2 gene transcription is regulated by CCAAT enhancer-binding protein {delta} in mesenchymal C3H10T1/2 cells Genes Cells, February 1, 2006; 11(2): 163 - 175. [Abstract] [Full Text] [PDF]
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T. Schneider-Merck, Y. Pohnke, R. Kempf, M. Christian, J. J. Brosens, and B. Gellersen Physical Interaction and Mutual Transrepression between CCAAT/Enhancer-binding Protein {beta} and the p53 Tumor Suppressor J. Biol. Chem., January 6, 2006; 281(1): 269 - 278. [Abstract] [Full Text] [PDF]
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 A. Paquin, F. Barnabe-Heider, R. Kageyama, and F. D. Miller CCAAT/Enhancer-Binding Protein Phosphorylation Biases Cortical Precursors to Generate Neurons Rather Than Astrocytes In Vivo J. Neurosci., November 16, 2005; 25(46): 10747 - 10758. [Abstract] [Full Text] [PDF]
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M. E. Tome, D. B. F. Johnson, L. M. Rimsza, R. A. Roberts, T. M. Grogan, T. P. Miller, L. W. Oberley, and M. M. Briehl A redox signature score identifies diffuse large B-cell lymphoma patients with a poor prognosis Blood, November 15, 2005; 106(10): 3594 - 3601. [Abstract] [Full Text] [PDF]
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S. Gery, A. F. Gombart, W. S. Yi, C. Koeffler, W.-K. Hofmann, and H. P. Koeffler Transcription profiling of C/EBP targets identifies Per2 as a gene implicated in myeloid leukemia Blood, October 15, 2005; 106(8): 2827 - 2836. [Abstract] [Full Text] [PDF]
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 V. Waters, S. Sokol, B. Reddy, G. Soong, J. Chun, and A. Prince The Effect of Cyclosporin A on Airway Cell Proinflammatory Signaling and Pneumonia Am. J. Respir. Cell Mol. Biol., August 1, 2005; 33(2): 138 - 144. [Abstract] [Full Text] [PDF]
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 K. Vouk, P. Hudler, L. Strmsnik, M. Fink, G. Majdic, B. Zorn, E. Lalli, P. Sassone-Corsi, N. Debeljak, R. Komel, et al. Combinations of genetic changes in the human cAMP-responsive element modulator gene: a clue towards understanding some forms of male infertility? Mol. Hum. Reprod., August 1, 2005; 11(8): 567 - 574. [Abstract] [Full Text] [PDF]
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S. K. Roy, J. D. Shuman, L. C. Platanias, P. S. Shapiro, S. P. M. Reddy, P. F. Johnson, and D. V. Kalvakolanu A Role for Mixed Lineage Kinases in Regulating Transcription Factor CCAAT/Enhancer-binding Protein-{beta}-dependent Gene Expression in Response to Interferon-{gamma} J. Biol. Chem., July 1, 2005; 280(26): 24462 - 24471. [Abstract] [Full Text] [PDF]
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 J.-M. Wang, J. T. Tseng, and W.-C. Chang Induction of Human NF-IL6{beta} by Epidermal Growth Factor Is Mediated through the p38 Signaling Pathway and cAMP Response Element-binding Protein Activation in A431 Cells Mol. Biol. Cell, July 1, 2005; 16(7): 3365 - 3376. [Abstract] [Full Text] [PDF]
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T. Ikezoe, S. Gery, D. Yin, J. O'Kelly, L. Binderup, N. Lemp, H. Taguchi, and H. P. Koeffler CCAAT/Enhancer-Binding Protein {delta}: A Molecular Target of 1,25-Dihydroxyvitamin D3 in Androgen-Responsive Prostate Cancer LNCaP Cells Cancer Res., June 1, 2005; 65(11): 4762 - 4768. [Abstract] [Full Text] [PDF]
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 C. P. Martinez-Jimenez, M. J. Gomez-Lechon, J. V. Castell, and R. Jover Transcriptional Regulation of the Human Hepatic CYP3A4: Identification of a New Distal Enhancer Region Responsive to CCAAT/Enhancer-Binding Protein {beta} Isoforms (Liver Activating Protein and Liver Inhibitory Protein) Mol. Pharmacol., June 1, 2005; 67(6): 2088 - 2101. [Abstract] [Full Text] [PDF]
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N. A. Timchenko, G.-L. Wang, and L. T. Timchenko RNA CUG-binding Protein 1 Increases Translation of 20-kDa Isoform of CCAAT/Enhancer-binding Protein {beta} by Interacting with the {alpha} and {beta} Subunits of Eukaryotic Initiation Translation Factor 2 J. Biol. Chem., May 27, 2005; 280(21): 20549 - 20557. [Abstract] [Full Text] [PDF]
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 P.-Z. Zheng, K.-K. Wang, Q.-Y. Zhang, Q.-H. Huang, Y.-Z. Du, Q.-H. Zhang, D.-K. Xiao, S.-H. Shen, S. Imbeaud, E. Eveno, et al. Systems analysis of transcriptome and proteome in retinoic acid/arsenic trioxide-induced cell differentiation/apoptosis of promyelocytic leukemia PNAS, May 24, 2005; 102(21): 7653 - 7658. [Abstract] [Full Text] [PDF]
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Q. Meng, A. Raha, S. Roy, J. Hu, and D. V. Kalvakolanu IFN-{gamma}-Stimulated Transcriptional Activation by IFN-{gamma}-Activated Transcriptional Element-Binding Factor 1 Occurs via an Inducible Interaction with CAAAT/Enhancer-Binding Protein-{beta} J. Immunol., May 15, 2005; 174(10): 6203 - 6211. [Abstract] [Full Text] [PDF]
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 S. Nikolajewa, A. Beyer, M. Friedel, J. Hollunder, and T. Wilhelm Common patterns in type II restriction enzyme binding sites Nucleic Acids Res., May 11, 2005; 33(8): 2726 - 2733. [Abstract] [Full Text] [PDF]
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 N. Takai, N. Kawamata, C. S. Walsh, S. Gery, J. C. Desmond, S. Whittaker, J. W. Said, L. M. Popoviciu, P. A. Jones, I. Miyakawa, et al. Discovery of Epigenetically Masked Tumor Suppressor Genes in Endometrial Cancer Mol. Cancer Res., May 1, 2005; 3(5): 261 - 269. [Abstract] [Full Text] [PDF]
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 S. Gery, S. Tanosaki, S. Bose, N. Bose, J. Vadgama, and H. P. Koeffler Down-Regulation and Growth Inhibitory Role of C/EBP{alpha} in Breast Cancer Clin. Cancer Res., May 1, 2005; 11(9): 3184 - 3190. [Abstract] [Full Text] [PDF]
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 J. Dong, S. Fujii, H. Li, H. Nakabayashi, M. Sakai, S. Nishi, D. Goto, T. Furumoto, S. Imagawa, T. A.K.M. Zaman, et al. Interleukin-6 and Mevastatin Regulate Plasminogen Activator Inhibitor-1 Through CCAAT/Enhancer-Binding Protein-{delta} Arterioscler. Thromb. Vasc. Biol., May 1, 2005; 25(5): 1078 - 1084. [Abstract] [Full Text] [PDF]
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K. J. Serio, K. V. Reddy, and T. D. Bigby Lipopolysaccharide induces 5-lipoxygenase-activating protein gene expression in THP-1 cells via a NF-{kappa}B and C/EBP-mediated mechanism Am J Physiol Cell Physiol, May 1, 2005; 288(5): C1125 - C1133. [Abstract] [Full Text] [PDF]
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K. Karaya, S. Mori, H. Kimoto, Y. Shima, Y. Tsuji, H. Kurooka, S. Akira, and Y. Yokota Regulation of Id2 expression by CCAAT/enhancer binding protein {beta} Nucleic Acids Res., April 4, 2005; 33(6): 1924 - 1934. [Abstract] [Full Text] [PDF]
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J. Kim, S. Sharma, Y. Li, E. Cobos, J. J. Palvimo, and S. C. Williams Repression and Coactivation of CCAAT/Enhancer-binding Protein {epsilon} by Sumoylation and Protein Inhibitor of Activated STATx Proteins J. Biol. Chem., April 1, 2005; 280(13): 12246 - 12254. [Abstract] [Full Text] [PDF]
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 H.-L. Fang, M. Abdolalipour, Z. Duanmu, J. R. Smigelski, A. Weckle, T. A. Kocarek, and M. Runge-Morris REGULATION OF GLUCOCORTICOID-INDUCIBLE HYDROXYSTEROID SULFOTRANSFERASE (SULT2A-40/41) GENE TRANSCRIPTION IN PRIMARY CULTURED RAT HEPATOCYTES: ROLE OF CCAAT/ENHANCER-BINDING PROTEIN LIVER-ENRICHED TRANSCRIPTION FACTORS Drug Metab. Dispos., January 1, 2005; 33(1): 147 - 156. [Abstract] [Full Text] [PDF]
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S. Gery, D. J. Park, P. T. Vuong, D. Y. Chih, N. Lemp, and H. P. Koeffler Retinoic acid regulates C/EBP homologous protein expression (CHOP), which negatively regulates myeloid target genes Blood, December 15, 2004; 104(13): 3911 - 3917. [Abstract] [Full Text] [PDF]
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S. Gerlo, P. Verdood, B. Gellersen, E. L. Hooghe-Peters, and R. Kooijman Mechanism of Prostaglandin (PG)E2-Induced Prolactin Expression in Human T Cells: Cooperation of Two PGE2 Receptor Subtypes, E-Prostanoid (EP) 3 and EP4, Via Calcium- and Cyclic Adenosine 5'-Monophosphate-Mediated Signaling Pathways J. Immunol., November 15, 2004; 173(10): 5952 - 5962. [Abstract] [Full Text] [PDF]
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J. T. Chun, V. Di Dato, B. D'Andrea, M. Zannini, and R. Di Lauro The CRE-Like Element Inside the 5'-Upstream Region of the Rat Sodium/Iodide Symporter Gene Interacts with Diverse Classes of b-Zip Molecules that Regulate Transcriptional Activities through Strong Synergy with Pax-8 Mol. Endocrinol., November 1, 2004; 18(11): 2817 - 2829. [Abstract] [Full Text] [PDF]
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K. Matsusue, O. Gavrilova, G. Lambert, H. B. Brewer Jr., J. M. Ward, Y. Inoue, D. LeRoith, and F. J. Gonzalez Hepatic CCAAT/Enhancer Binding Protein {alpha} Mediates Induction of Lipogenesis and Regulation of Glucose Homeostasis in Leptin-Deficient Mice Mol. Endocrinol., November 1, 2004; 18(11): 2751 - 2764. [Abstract] [Full Text] [PDF]
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Y. Inoue, J. Inoue, G. Lambert, S. H. Yim, and F. J. Gonzalez Disruption of Hepatic C/EBP{alpha} Results in Impaired Glucose Tolerance and Age-dependent Hepatosteatosis J. Biol. Chem., October 22, 2004; 279(43): 44740 - 44748. [Abstract] [Full Text] [PDF]
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J. R. Friedman, B. Larris, P. P. Le, T. H. Peiris, A. Arsenlis, J. Schug, J. W. Tobias, K. H. Kaestner, and L. E. Greenbaum Orthogonal analysis of C/EBP{beta} targets in vivo during liver proliferation PNAS, August 31, 2004; 101(35): 12986 - 12991. [Abstract] [Full Text] [PDF]
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F. Yang and D. Bleich Transcriptional Regulation of Cyclooxygenase-2 Gene in Pancreatic {beta}-Cells J. Biol. Chem., August 20, 2004; 279(34): 35403 - 35411. [Abstract] [Full Text] [PDF]
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Q.-S. Zhu, B. Qian, and D. Levy CCAAT/Enhancer-binding Protein {alpha} (C/EBP{alpha}) Activates Transcription of the Human Microsomal Epoxide Hydrolase Gene (EPHX1) through the Interaction with DNA-bound NF-Y J. Biol. Chem., July 16, 2004; 279(29): 29902 - 29910. [Abstract] [Full Text] [PDF]
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C. Chen, E. E. Dudenhausen, Y.-X. Pan, C. Zhong, and M. S. Kilberg Human CCAAT/Enhancer-binding Protein {beta} Gene Expression Is Activated by Endoplasmic Reticulum Stress through an Unfolded Protein Response Element Downstream of the Protein Coding Sequence J. Biol. Chem., July 2, 2004; 279(27): 27948 - 27956. [Abstract] [Full Text] [PDF]
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P. Gervois, R. Kleemann, A. Pilon, F. Percevault, W. Koenig, B. Staels, and T. Kooistra Global Suppression of IL-6-induced Acute Phase Response Gene Expression after Chronic in Vivo Treatment with the Peroxisome Proliferator-activated Receptor-{alpha} Activator Fenofibrate J. Biol. Chem., April 16, 2004; 279(16): 16154 - 16160. [Abstract] [Full Text] [PDF]
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M. W. Feinberg, M. Watanabe, M. A. Lebedeva, A. S. Depina, J.-i. Hanai, T. Mammoto, J. P. Frederick, X.-F. Wang, V. P. Sukhatme, and M. K. Jain Transforming Growth Factor-{beta}1 Inhibition of Vascular Smooth Muscle Cell Activation Is Mediated via Smad3 J. Biol. Chem., April 16, 2004; 279(16): 16388 - 16393. [Abstract] [Full Text] [PDF]
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C. F. A. Vogel, E. Sciullo, S. Park, C. Liedtke, C. Trautwein, and F. Matsumura Dioxin Increases C/EBP{beta} Transcription by Activating cAMP/Protein Kinase A J. Biol. Chem., March 5, 2004; 279(10): 8886 - 8894. [Abstract] [Full Text] [PDF]
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P. Klausen, M. D. Bjerregaard, N. Borregaard, and J. B. Cowland End-stage differentiation of neutrophil granulocytes in vivo is accompanied by up-regulation of p27kip1 and down-regulation of CDK2, CDK4, and CDK6 J. Leukoc. Biol., March 1, 2004; 75(3): 569 - 578. [Abstract] [Full Text] [PDF]
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S. Frohling, R. F. Schlenk, I. Stolze, J. Bihlmayr, A. Benner, S. Kreitmeier, K. Tobis, H. Dohner, and K. Dohner CEBPA Mutations in Younger Adults With Acute Myeloid Leukemia and Normal Cytogenetics: Prognostic Relevance and Analysis of Cooperating Mutations J. Clin. Oncol., February 15, 2004; 22(4): 624 - 633. [Abstract] [Full Text] [PDF]
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C. R. Walkley, L. E. Purton, H. J. Snelling, Y.-D. Yuan, H. Nakajima, P. Chambon, R. A. S. Chandraratna, and G. A. McArthur Identification of the molecular requirements for an RAR{alpha}-mediated cell cycle arrest during granulocytic differentiation Blood, February 15, 2004; 103(4): 1286 - 1295. [Abstract] [Full Text] [PDF]
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C.-H. Shen and L. A. Steiner Genome Structure and Thymic Expression of an Endogenous Retrovirus in Zebrafish J. Virol., January 15, 2004; 78(2): 899 - 911. [Abstract] [Full Text] [PDF]
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S. E. Ross, H. S. Radomska, B. Wu, P. Zhang, J. N. Winnay, L. Bajnok, W. S. Wright, F. Schaufele, D. G. Tenen, and O. A. MacDougald Phosphorylation of C/EBP{alpha} Inhibits Granulopoiesis Mol. Cell. Biol., January 15, 2004; 24(2): 675 - 686. [Abstract] [Full Text] [PDF]
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C. Fux, B. Mitta, B. P. Kramer, and M. Fussenegger Dual-regulated expression of C/EBP-{alpha} and BMP-2 enables differential differentiation of C2C12 cells into adipocytes and osteoblasts Nucleic Acids Res., January 2, 2004; 32(1): e1 - e1. [Abstract] [Full Text] [PDF]
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Y. Ji and G. P. Studzinski Retinoblastoma Protein and CCAAT/Enhancer-Binding Protein {beta} Are Required for 1,25-Dihydroxyvitamin D3-Induced Monocytic Differentiation of HL60 Cells Cancer Res., January 1, 2004; 64(1): 370 - 377. [Abstract] [Full Text] [PDF]
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W.-C. Su, H.-Y. Chou, C.-J. Chang, Y.-M. Lee, W.-H. Chen, K.-H. Huang, M.-Y. Lee, and S.-C. Lee Differential Activation of a C/EBP{beta} Isoform by a Novel Redox Switch May Confer the Lipopolysaccharide-inducible Expression of Interleukin-6 Gene J. Biol. Chem., December 19, 2003; 278(51): 51150 - 51158. [Abstract] [Full Text] [PDF]
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P.-P. Kuang and R. H. Goldstein Regulation of elastin gene transcription by interleukin-1{beta}-induced C/EBP{beta} isoforms Am J Physiol Cell Physiol, December 1, 2003; 285(6): C1349 - C1355. [Abstract] [Full Text] [PDF]
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A.-M. Barlier-Mur, B. Chailley-Heu, C. Pinteur, A. Henrion-Caude, C. Delacourt, and J. R. Bourbon Maturational Factors Modulate Transcription Factors CCAAT/Enhancer-Binding Proteins {alpha}, {beta}, {delta}, and Peroxisome Proliferator-Activated Receptor-{gamma} in Fetal Rat Lung Epithelial Cells Am. J. Respir. Cell Mol. Biol., November 1, 2003; 29(5): 620 - 626. [Abstract] [Full Text]
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A. Puig-Kroger, T. Sanchez-Elsner, N. Ruiz, E. J. Andreu, F. Prosper, U. B. Jensen, J. Gil, P. Erickson, H. Drabkin, Y. Groner, et al. RUNX/AML and C/EBP factors regulate CD11a integrin expression in myeloid cells through overlapping regulatory elements Blood, November 1, 2003; 102(9): 3252 - 3261. [Abstract] [Full Text] [PDF]
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K. A. Kovacs, M. Steinmann, P. J. Magistretti, O. Halfon, and J.-R. Cardinaux CCAAT/Enhancer-binding Protein Family Members Recruit the Coactivator CREB-binding Protein and Trigger Its Phosphorylation J. Biol. Chem., September 19, 2003; 278(38): 36959 - 36965. [Abstract] [Full Text] [PDF]
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G. P. Pilipuk, M. D. Galigniana, and J. Schwartz Subnuclear Localization of C/EBP{beta} Is Regulated by Growth Hormone and Dependent on MAPK J. Biol. Chem., September 12, 2003; 278(37): 35668 - 35677. [Abstract] [Full Text] [PDF]
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C. Ji, W. Chang, M. Centrella, and T. L. McCarthy Activation Domains of CCAAT Enhancer Binding Protein {delta}: Regions Required for Native Activity and Prostaglandin E2-Dependent Transactivation of Insulin-Like Growth Factor I Gene Expression in Rat Osteoblasts Mol. Endocrinol., September 1, 2003; 17(9): 1834 - 1843. [Abstract] [Full Text] [PDF]
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V. V. Kravchenko, J. C. Mathison, K. Schwamborn, F. Mercurio, and R. J. Ulevitch IKKi/IKK{epsilon} Plays a Key Role in Integrating Signals Induced by Pro-inflammatory Stimuli J. Biol. Chem., July 11, 2003; 278(29): 26612 - 26619. [Abstract] [Full Text] [PDF]
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 J. R. S. Newman and A. E. Keating Comprehensive Identification of Human bZIP Interactions with Coiled-Coil Arrays Science, June 27, 2003; 300(5628): 2097 - 2101. [Abstract] [Full Text] [PDF]
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Y. Chen, S. Zhuang, S. Cassenaer, D. E. Casteel, T. Gudi, G. R. Boss, and R. B. Pilz Synergism between Calcium and Cyclic GMP in Cyclic AMP Response Element-Dependent Transcriptional Regulation Requires Cooperation between CREB and C/EBP-{beta} Mol. Cell. Biol., June 15, 2003; 23(12): 4066 - 4082. [Abstract] [Full Text] [PDF]
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 A. Rigotti, H. E. Miettinen, and M. Krieger The Role of the High-Density Lipoprotein Receptor SR-BI in the Lipid Metabolism of Endocrine and Other Tissues Endocr. Rev., June 1, 2003; 24(3): 357 - 387. [Abstract] [Full Text] [PDF]
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A. Suzuki, A. Iwama, H. Miyashita, H. Nakauchi, and H. Taniguchi Role for growth factors and extracellular matrix in controlling differentiation of prospectively isolated hepatic stem cells Development, June 1, 2003; 130(11): 2513 - 2524. [Abstract] [Full Text] [PDF]
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M. D. Bjerregaard, J. Jurlander, P. Klausen, N. Borregaard, and J. B. Cowland The in vivo profile of transcription factors during neutrophil differentiation in human bone marrow Blood, June 1, 2003; 101(11): 4322 - 4332. [Abstract] [Full Text] [PDF]
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A. Khanna-Gupta, T. Zibello, H. Sun, P. Gaines, and N. Berliner Chromatin immunoprecipitation (ChIP) studies indicate a role for CCAAT enhancer binding proteins alpha and epsilon (C/EBPalpha and C/EBPepsilon ) and CDP/cut in myeloid maturation-induced lactoferrin gene expression Blood, May 1, 2003; 101(9): 3460 - 3468. [Abstract] [Full Text] [PDF]
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T. T. C. Yang and C.-W. Chow Transcription Cooperation by NFAT{middle dot}C/EBP Composite Enhancer Complex J. Biol. Chem., April 25, 2003; 278(18): 15874 - 15885. [Abstract] [Full Text] [PDF]
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K. V. Reddy, K. J. Serio, C. R. Hodulik, and T. D. Bigby 5-Lipoxygenase-activating Protein Gene Expression. KEY ROLE OF CCAAT/ENHANCER-BINDING PROTEINS (C/EBP) IN CONSTITUTIVE AND TUMOR NECROSIS FACTOR (TNF) alpha -INDUCED EXPRESSION IN THP-1 CELLS J. Biol. Chem., April 11, 2003; 278(16): 13810 - 13818. [Abstract] [Full Text] [PDF]
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B. L. Kagan, R. T. Henke, R. Cabal-Manzano, G. E. Stoica, Q. Nguyen, A. Wellstein, and A. T. Riegel Complex Regulation of the Fibroblast Growth Factor-binding Protein in MDA- MB-468 Breast Cancer Cells by CCAAT/Enhancer-binding Protein {beta} Cancer Res., April 1, 2003; 63(7): 1696 - 1705. [Abstract] [Full Text] [PDF]
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M. Trauner and J. L. Boyer Bile Salt Transporters: Molecular Characterization, Function, and Regulation Physiol Rev, April 1, 2003; 83(2): 633 - 671. [Abstract] [Full Text] [PDF]
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L. R. Dearth and J. DeWille Posttranscriptional and Posttranslational Regulation of C/EBPdelta in G0 Growth-arrested Mammary Epithelial Cells J. Biol. Chem., March 21, 2003; 278(13): 11246 - 11255. [Abstract] [Full Text] [PDF]
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