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From the Department of Biological Chemistry, Johns Hopkins
University School of Medicine, Baltimore, Maryland 21205
INTRODUCTION The raison d'etre of the adipocyte
is to store energy (in the form of triacylglycerol) for use during
periods of caloric insufficiency. Adipocytes first appear late in fetal
development preparatory to postnatal life when a substantial energy
reserve is needed to survive periods of fasting. Considerable progress
has been made during the past few years in our understanding of the
adipocyte differentiation program. This review will focus on the roles
of the CAAT/enhancer binding protein
(C/EBP)1 and peroxisome
proliferator-activated receptor (PPAR) families of transcription
factors in the differentiation program. The reader is referred to other
recent reviews (1-3) for references too numerous to include in this
Minireview.
Our understanding of adipocyte differentiation derives largely from
studies with preadipose cell lines in culture, notably the C3H10T1/2
and NIH 3T3 fibroblastic cell lines and the 3T3-L1 and 3T3-F442A
preadipocyte lines (1). Treatment of multipotent C3H10T1/2 cells with
5-azacytidine gives rise to cells committed to the myogenic,
adipogenic, or chondrogenic lineages. This is consistent with the view
that the adipose lineage arises from the same multipotent stem cell
population of mesodermal origin that gives rise to the muscle and
cartilage lineages (1). When appropriately induced with hormonal agents
(e.g. glucocorticoid, insulin-like growth factor-1, and
cyclic AMP or factors that mimic these agents) committed preadipocytes
differentiate into adipocytes in culture. A large body of evidence
shows that differentiation of 3T3 preadipocytes faithfully mimics the
in vivo process giving rise to cells that possess virtually
all of the biochemical and morphological characteristics of adipocytes
(2). Following hormonal induction, confluent preadipocytes undergo
mitotic clonal expansion, become growth arrested, and then coordinately
express adipocyte gene products (1).
Several transcription factors have been identified, which act
cooperatively and sequentially to trigger the terminal differentiation program (3-5). These include members of the C/EBP and PPAR families. The sequence of expression of certain of these transcription factors during differentiation is outlined in Fig. 1. It should
be noted that these patterns differ somewhat depending upon the
differentiation protocol and preadipocyte cell line employed,
e.g. 3T3-L1 versus 3T3-F442A versus
NIH 3T3 cells.
The C/EBP Family Three members of the C/EBP family of transcription factors,
i.e. C/EBP Convincing evidence shows that C/EBP In view of its anti-mitotic activity, C/EBP Another probable function of C/EBP An increasing body of evidence
indicates that C/EBP Ectopic expression of liver activator protein, the activating isoform
of C/EBP Given that C/EBP Another member of the C/EBP family of
transcription factors, CHOP-10 (GADD153), heterodimerizes avidly with
other C/EBP isoforms, notably C/EBP The PPAR Family The PPARs, a subgroup of the nuclear hormone receptors, have
recently been implicated in the transcriptional activation of adipocyte
differentiation. It has been shown that PPAR activators can induce
adipocyte differentiation, not only of preadipocytes (21-23) but also
myoblasts (24) and multipotent C3H10T1/2 stem cells (25). Moreover
ectopic expression of certain PPARs in the presence of activators can
induce adipogenesis in NIH 3T3 fibroblasts (26, 27). In addition, PPAR
response elements (PPREs) have been identified in a number of adipocyte
genes known to be transcriptionally activated during adipocyte
differentiation. These include genes encoding adipose fatty
acid-binding protein (28), phosphoenolpyruvate carboxykinase (29),
lipoprotein lipase (30), and stearoyl-CoA desaturase 1 (31).
PPAR Members of the PPAR family are activated by long chain fatty acids,
fatty acid metabolites, and certain hypolipidemic drugs and
plasticizers (32, 37). While a few of these agents have recently been
identified as true ligands of one or more of the PPARs, other
activators may act indirectly. Certain thiazolidinediones, as well as
prostaglandin J2 derivatives (e.g.
15-deoxy- PPAR PPAR It has been reported that the level of PPAR The adipogenic potential
of the different PPARs has been assessed by transfection into a variety
of cell lines that have the capacity to undergo adipogenesis (26, 27,
43, 44, 46). When compared directly by ectopic expression in NIH 3T3
cells, PPAR Although ectopic expression of PPAR Cross-talk with the Retinoic Acid Signaling Pathway? Retinoic acid (RA) has long been recognized as a potent inhibitor
(effective concentration ranging from 3 nM to 10 mM) of adipocyte differentiation in several different cell
lines (22, 41, 48-53). The effects of retinoids are known to be
mediated by two types of nuclear hormone receptors, retinoic acid
receptors (RARs) and retinoid X receptors (RXRs) (reviewed in Ref. 54). All-trans-RA is a ligand for RAR (Kd in
the 0.5 nM range), whereas its isomerization product,
9-cis-RA, is a ligand for both RAR and RXR (55). Studies
with RAR- and RXR-specific agonists and antagonists indicate that
inhibition of adipocyte differentiation by RA is mediated by an RAR(s)
(41, 53). Like a number of other non-steroid nuclear hormone receptors,
members of the RAR subfamily bind, as heterodimers with an RXR partner,
to imperfect repeats of a hexad consensus. Depending upon the spacing
between repeats, the RXR-RAR dimer acts either as a
RA-dependent transcriptional activator or as a
RA-independent repressor (34).
The time window during which RA can inhibit adipocyte differentiation
is limited to the period immediately following induction of
differentiation with hormonal agents, preceding the expression of
C/EBP Cooperation among Members of the C/EBP and PPAR Families The induction of adipocyte differentiation involves the
cooperative interplay of members of the C/EBP and PPAR families. A model incorporating the best documented of these interactions is
presented in Fig. 2. C/EBP
C/EBP FOOTNOTES REFERENCES
Volume 272, Number 9,
Issue of February 28, 1997
pp. 5367-5370
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.
MINIREVIEW:
and
INTRODUCTION
The C/EBP Family
The PPAR Family
Cross-talk with the Retinoic Acid Signaling Pathway?
Cooperation among Members of the C/EBP and PPAR Families
FOOTNOTES
REFERENCES
Fig. 1.
Expression of C/EBP and PPAR family members
during differentiation of 3T3-L1 preadipocytes. The magnitude of
expression is indicated by the intensity of the horizontal
band corresponding to each transcription factor. The
differentiation protocol is as described (4).
[View Larger Version of this Image (85K GIF file)]
, C/EBP
, and C/EBP
, have been implicated
in the induction of adipocyte differentiation. These transcription
factors possess C-terminal basic region/leucine zipper (bZIP) domains,
which confer DNA binding ability (basic region) and the ability to
dimerize (leucine zipper), either as homodimers or as heterodimers,
with other family members. The structural features of the C/EBPs and cis-elements to which they bind have been reviewed (1,
2).
plays an
important role in the transcriptional activation of adipose
differentiation (1, 2). C/EBP is expressed just before the
transcription of most adipocyte-specific genes is initiated. Moreover,
the proximal promoters of many of these genes contain C/EBP binding
sites, which have been shown to mediate the activation of reporter gene expression. Attempts to determine whether constitutive expression of
C/EBP could initiate the adipocyte differentiation program were
complicated by the fact that C/EBP blocks mitosis of preadipocytes. However, by placing the C/EBP gene under the control of the Lac repressor (6) or using a retroviral vector (7), it was demonstrated that expression of C/EBP is sufficient to induce differentiation of
3T3-L1 preadipocytes into adipocytes without the use of external hormonal inducers. Definitive proof that C/EBP is required for adipocyte differentiation was obtained by showing that expression of
antisense C/EBP RNA in 3T3-L1 preadipocytes prevented
differentiation (8). Consistent with this finding, disruption of the
C/EBP gene gave rise to mice that failed to develop white adipose
tissue (9). Taken together these findings proved that C/EBP is both required and sufficient to induce adipocyte differentiation.
may serve to terminate
the mitotic clonal expansion that occurs early in the differentiation
program. The point in the program at which mitosis ceases coincides
with the onset of expression of C/EBP and the transcriptional
activation of adipocyte genes. Ectopic expression of C/EBP was
recently shown to stimulate the expression of two growth
arrest-associated proteins, GADD45 (10) and p21(WAF-1/CIP-1/SDI-1) (11), the latter of which is a cyclin-dependent kinase
inhibitor directly involved in growth arrest.
in the differentiation program is
maintenance of the terminally differentiated state through autoactivation of its own gene. Several lines of evidence support this
role. The murine C/EBP gene promoter possesses a specific C/EBP
binding site, which can mediate activation of reporter gene transcription by either C/EBP or C/EBP (12, 13). Strong support
for autoactivation by C/EBP derives from the fact that expression of
C/EBP antisense RNA not only blocks expression of the C/EBP but
also the transcription of the C/EBP gene (8). Furthermore, inducible
or ectopic expression of C/EBP is sufficient to activate expression
of the endogenous C/EBP gene (6, 7). It is also possible that
C/EBP, which is expressed much earlier in the differentiation
program than C/EBP, transcriptionally activates the C/EBP gene
through the C/EBP binding site (see below).
and C/EBP
and possibly C/EBP function early
(i.e. prior to C/EBP) as transcriptional activators in
the sequence of events leading to adipocyte differentiation (Fig. 1).
Induction of differentiation by treating growth-arrested 3T3-L1
preadipocytes with exogenous hormonal inducers provokes an immediate,
albeit transient, burst of expression of C/EBP and C/EBP (3).
Concomitantly, the preadipocytes re-enter the cell cycle undergoing
several rounds of mitotic clonal expansion and then again become
growth-arrested as expression of C/EBP and terminal differentiation
ensues. Two of the differentiation inducers appear to be responsible
for activating expression of C/EBP and C/EBP, i.e.
cAMP for C/EBP and glucocorticoid for C/EBP (14). It should be
noted that both C/EBP and C/EBP are also expressed at high levels
in actively dividing preadipocytes (in the absence of exogenous
differentiation inducers), and upon achieving growth arrest at
confluence, expression of both decreases.2
Thus, it is uncertain whether expression of C/EBP and C/EBP following "induction" is the cause or the effect of re-entry into the cell cycle. Nevertheless, it is clear that conditions, which cause
expression of either of these isoforms, accelerate adipogenesis in
3T3-L1 preadipocytes. In addition to the differentiation-associated induction of expression of C/EBP described above, this transcription factor may also be regulated by post-translational modification (Ref.
15, and references therein) and by interaction with molecular chaperones (16). Whether these modifications and structural changes
play a role in the activation of C/EBP during adipocyte differentiation is not known.
, accelerates differentiation, whereas ectopic overexpression of liver inhibitory protein, the truncated
dominant-negative isoform of C/EBP (which lacks the transactivation
domain), blocks differentiation initiated by exogenous inducers (14).
The fact that liver inhibitory protein interrupts the differentiation
program at a point prior to the induction of C/EBP suggests that it
acts at an early stage, most likely by forming inactive heterodimers with liver activator protein. Ectopic expression of C/EBP in NIH 3T3
fibroblasts, which normally do not respond to the exogenous hormonal
inducers, appears to cause commitment to the adipose lineage. When
subsequently stimulated with hormonal inducers, the "committed"
adipoblasts undergo differentiation into adipocytes (14, 17, 18).
Curiously, however, PPAR
but not C/EBP was detected in these
cells (14, 17), suggesting that in these cells, overexpression of
C/EBP may substitute for C/EBP as a transactivator for some
adipocyte genes.
is an early participant in the differentiation
program, the question of its site of action is raised. The results
above suggest that C/EBP may be involved in the induction of PPAR
(see below). Since the C/EBP gene promoter contains a C/EBP binding
site (12, 13) that can mediate transactivation by members of the C/EBP
family (13),2 it is possible that C/EBP acts as a
transcriptional activator of the C/EBP gene. The role of C/EBP,
which has much lower adipogenic potential than C/EBP, remains
uncertain, but recent results suggest that it may act synergistically
with C/EBP in the induction of PPAR (18).
and C/EBP. However, the basic
region responsible for DNA binding deviates considerably in sequence
from that of other C/EBP proteins; hence, CHOP-C/EBP dimers bind only
to a subset of C/EBP sites (19). Thus, CHOP-10 acts as a
dominant-negative inhibitor of transcription activated by C/EBP dimers.
Nevertheless, CHOP-10 has the capacity to activate transcription by
binding to other response elements. When ectopically expressed in
3T3-L1 preadipocytes, CHOP-10 inhibits adipocyte differentiation.
Expression of CHOP-10 by preadipocytes in culture can be induced by
cellular stresses including glucose starvation (20). Such perturbations or the ectopic expression of CHOP-10 inhibit preadipocyte
differentiation (20). Thus, although CHOP-10 has the capacity to abort
or forestall adipocyte differentiation under certain stress conditions,
it is uncertain whether CHOP-10 functions in this manner under normal circumstances. CHOP-10 might have a metabolic function in fully differentiated adipocytes. Thus, the dramatic rise in expression of
CHOP-10 following glucose depletion may down-regulate the transcription of adipose genes regulated by C/EBP through inactive heterodimer formation and, thereby, inhibit energy storage.
, the first member of the PPAR family to be identified, was
cloned as an orphan receptor activated by agents that induce peroxisome
proliferation, primarily in the liver. Subsequently, PPAR (also
referred to as PPAR, NUC1, and FAAR) and PPAR were cloned by low
stringency screening (32). These subtypes share a high degree of amino
acid sequence similarity, both within their DNA- and ligand-binding
domains (33). This is reflected in functional similarities in that the
receptors are activated by structurally related compounds and bind as
heterodimers with a retinoid X receptor partner to a PPRE (imperfect
6-base pair direct repeats of the sequence RGGTCA spaced by 1 base pair
and referred to as DR-1; reviewed in Ref. 34). Nevertheless, the three
PPAR subtypes appear to serve different roles in vivo. They
exhibit markedly different tissue distributions (35, 36), have
differing affinities for different PPREs (27), and are activated to
different extents by different activators/ligands (26, 27, 33, 37).
12,14-prostaglandin J2), were shown
to be ligands of PPAR (25, 26, 38). Leukotriene B4 was identified as
a PPAR ligand (39), and recently, carbaprostacyclin was reported to
be a ligand of PPAR and PPAR and 8(S)-HETE to be a
ligand of PPAR.3 Notably, all naturally
occurring ligands identified to date are derived from arachidonic acid.
The diversity of the ligands so far identified suggests that other
ligands are likely to be found.
is the most adipose-specific of the PPARs. It
is expressed at the highest level in adipose tissue and adipocyte cell lines and at low levels, or not at all, in other tissues and cell lines
(26, 32, 35). Two isoforms of PPAR, i.e. PPAR1 and PPAR2, are generated by alternative splicing and alternate
translation initiation (28, 40, 41). Although PPAR2 appears to be
more adipose-specific than PPAR1 (42), functional differences
between the two isoforms have not been detected. Expression of PPAR
is induced concomitantly with (or perhaps preceding (43)) and prior to
the transcriptional activation of most adipocyte genes.
and PPAR
is expressed in many tissues and
cell lines including adipose tissue and adipocyte cell lines (33, 35,
44). There are conflicting reports concerning changes in the expression
of PPAR during adipocyte differentiation, e.g. it has
been reported that the level of PPAR remains relatively constant
during differentiation (43)4 and also that
its expression is activated early in the differentiation program (44).
These discrepancies may be due to the fact that the various cell lines
used in these studies were arrested at different stages of preadipocyte
development when they were originally cloned (2) and therefore might
differ in their ability to express the different PPAR genes.
increases during
adipocyte differentiation (22). Relative to the high level of PPAR
in brown adipose tissue, however, the level in white adipose tissue and
adipocyte cell lines is extremely low (33, 35) suggesting that this
isoform plays a minor role in adipocytes from white adipose tissue.
Consistent with this notion, targeted disruption of the mouse PPAR
gene revealed that its major role is the regulation of peroxisomal
-oxidation rather than adipose development (45).
was by far the most adipogenic, PPAR was less so, and
PPAR was inactive (27). The finding that PPAR is the most
adipogenic is consistent with its adipose-specific expression and with
the fact that thiazolidinediones, which are high affinity ligands of
PPAR, are potent inducers of adipocyte differentiation (25). Furthermore, a prostaglandin derivative
(15-deoxy-12,14-prostaglandin J2), which is
a ligand of PPAR, stimulates adipogenesis of the pluripotent
C3H10T1/2 cell line (38) and of NIH 3T3 cells when PPAR is expressed
ectopically (26). Precursors of
15-deoxy-12,14-prostaglandin J2 also
activate adipocyte differentiation, but to a lesser extent (26, 38).
However, it has not been determined, as yet, whether this prostaglandin
is present in vivo.
fails to induce adipogenesis in
NIH 3T3 cells, this receptor appears to up-regulate expression of a
subset of adipose-specific genes in these and certain other cell types
(23, 27, 44). The fact that PPAR activators stimulate adipogenesis of
3T3-L1 preadipocytes (22) as well as myoblasts (47), which express
PPAR constitutively (but not detectable levels of other PPARs),
suggests that PPAR may have the capacity to initiate adipocyte
differentiation in at least some cell culture models. Antisense RNA
and/or gene knockout experiments to disrupt expression of PPAR and
PPAR would be useful to determine whether these isoforms actually
play the roles tentatively ascribed to them in adipose determination
and differentiation.
(41, 50, 51). RA does not interfere with the induction of
expression of C/EBP but blocks the expression of C/EBP and PPAR and is able to repress expression of PPAR even after it is
induced (41). The mechanism by which RA inhibits adipocyte differentiation is not well understood. However, recent findings suggest that the inhibition of differentiation is not due to
RXR-RAR-mediated stimulation of an inhibitory gene(s). Rather, liganded
RAR appears to interfere with transcriptional activation by C/EBP
and C/EBP, possibly by competing with these transcription factors
for a common and limiting cofactor (56). Thus, it is possible that RA
blocks C/EBP-activated expression of the PPAR and C/EBP genes
(see above) and, thereby, differentiation.
and C/EBP are expressed
immediately following hormonal induction of differentiation. Several
lines of evidence implicate C/EBP in the activation of expression of both PPAR and C/EBP. While C/EBP can also induce expression of
PPAR (56), C/EBP is probably the initial inducer since it is
expressed before C/EBP in the differentiation program. In addition
to activating the expression of PPAR, C/EBP is believed to be a
transactivator of the C/EBP gene. Once transcription of the C/EBP
gene has been initiated its continued expression is assured through
transcriptional autoactivation. This mechanism is believed to be
responsible, at least in part, for maintaining expression of adipocyte
genes transactivated by C/EBP in the terminally differentiated
state.
Fig. 2.
Model illustrating the regulatory interplay
among transcription factors involved in adipocyte differentiation.
Arrows indicate activation of expression either directly or
indirectly. Broken lines with arrowheads indicate
activations where the mechanism is less well understood. The
thickness of arrows depicts the relative importance of the activation. Inhibition by
all-trans-retinoic acid mediated by RAR is indicated by a
red arrow and an encircled "
" symbol.
[View Larger Version of this Image (52K GIF file)]
and PPAR appear to act synergistically by triggering the
adipocyte differentiation program and reciprocally activating transcription of one another (Fig. 2). This is supported by the finding
that ectopic expression of either C/EBP or PPAR in myoblasts and
NIH 3T3 fibroblasts promotes only partial differentiation, while
co-expression of both factors provokes "full" differentiation, i.e. the same rate and extent of differentiation produced by
hormonal inducers (27, 43, 46). Cooperative interaction between
C/EBP and PPAR is evidenced by the fact that ectopic expression
of either transcription factor alone induces expression of the other (43, 56). This may involve reciprocal gene activation, i.e. transactivation of the C/EBP gene by PPAR and vice
versa. It is also of interest that C/EBP and PPAR act
cooperatively in the transcriptional activation of other adipocyte
genes. The 422/aP2 and the phosphoenolpyruvate carboxykinase gene
promoters both possess C/EBP and PPAR binding sites, which mediate
transactivation by the corresponding transacting factors (5). Thus,
there appear to be two levels of cooperative interplay between members
of the C/EBP and PPAR families during adipocyte differentiation,
i.e. they reciprocally activate expression of one another
and subsequently, they activate some adipocyte genes.
Supported by a grant from the Danish Natural Science Research
Council. Present address: Dept. of Molecular Biology, Odense University, Campusvej 55, DK-5320 Odense M, Denmark.
§
Supported by Research Grant DK 38418 from the NIDDK, National
Institutes of Health. To whom correspondence should be addressed: Dept.
of Biological Chemistry, The Johns Hopkins University School of
Medicine, 512 Wood Basic Science Bldg., 725 N. Wolfe St., Baltimore, MD 21205. Tel.: 410-955-3554; Fax: 410-955-0903; E-mail: DAN. LANE@QMAIL.BS.JHU.EDU.
1
The abbreviations used are: C/EBP, CAAT/enhancer
binding protein; PPAR, peroxisome proliferator-activated receptor;
PPRE, PPAR response element; RA, retinoic acid; RAR, retinoic acid
receptor; RXR, retinoid X receptor.
2
P. Cornelius and M. D. Lane, unpublished
results.
3
R. M. Evans, personal communication.
4
S. Mandrup, unpublished results.
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.
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A. M. Vertino, J. M. Taylor-Jones, K. A. Longo, E. D. Bearden, T. F. Lane, R. E. McGehee Jr., O. A. MacDougald, and C. A. Peterson Wnt10b Deficiency Promotes Coexpression of Myogenic and Adipogenic Programs in Myoblasts Mol. Biol. Cell, April 1, 2005; 16(4): 2039 - 2048. [Abstract] [Full Text] [PDF]
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J. E. Kim and J. Chen Regulation of Peroxisome Proliferator-Activated Receptor-{gamma} Activity by Mammalian Target of Rapamycin and Amino Acids in Adipogenesis Diabetes, November 1, 2004; 53(11): 2748 - 2756. [Abstract] [Full Text] [PDF]
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M. Kudo, A. Sugawara, A. Uruno, K. Takeuchi, and S. Ito Transcription Suppression of Peroxisome Proliferator-Activated Receptor {gamma}2 Gene Expression by Tumor Necrosis Factor {alpha} via an Inhibition of CCAAT/ Enhancer-binding Protein {delta} during the Early Stage of Adipocyte Differentiation Endocrinology, November 1, 2004; 145(11): 4948 - 4956. [Abstract] [Full Text] [PDF]
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K. Tominaga, C. Kondo, T. Kagata, T. Hishida, M. Nishizuka, and M. Imagawa The Novel Gene fad158, Having a Transmembrane Domain and Leucine-rich Repeat, Stimulates Adipocyte Differentiation J. Biol. Chem., August 13, 2004; 279(33): 34840 - 34848. [Abstract] [Full Text] [PDF]
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X. Su, D. J. Mancuso, P. E. Bickel, C. M. Jenkins, and R. W. Gross Small Interfering RNA Knockdown of Calcium-independent Phospholipases A2 {beta} or {gamma} Inhibits the Hormone-induced Differentiation of 3T3-L1 Preadipocytes J. Biol. Chem., May 21, 2004; 279(21): 21740 - 21748. [Abstract] [Full Text] [PDF]
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A. Gauthier, G. Vassiliou, F. Benoist, and R. McPherson Adipocyte Low Density Lipoprotein Receptor-related Protein Gene Expression and Function Is Regulated by Peroxisome Proliferator-activated Receptor gamma J. Biol. Chem., March 28, 2003; 278(14): 11945 - 11953. [Abstract] [Full Text] [PDF]
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S. R. Demaree, C. D. Gilbert, H. J. Mersmann, and S. B. Smith Conjugated Linoleic Acid Differentially Modifies Fatty Acid Composition in Subcellular Fractions of Muscle and Adipose Tissue but Not Adiposity of Postweanling Pigs J. Nutr., November 1, 2002; 132(11): 3272 - 3279. [Abstract] [Full Text] [PDF]
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B. Lecka-Czernik, E. J. Moerman, D. F. Grant, J. M. Lehmann, S. C. Manolagas, and R. L. Jilka Divergent Effects of Selective Peroxisome Proliferator-Activated Receptor-{gamma}2 Ligands on Adipocyte Versus Osteoblast Differentiation Endocrinology, June 1, 2002; 143(6): 2376 - 2384. [Abstract] [Full Text] [PDF]
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H. B. Hartman, X. Hu, K. X. Tyler, C. K. Dalal, and M. A. Lazar Mechanisms Regulating Adipocyte Expression of Resistin J. Biol. Chem., May 24, 2002; 277(22): 19754 - 19761. [Abstract] [Full Text] [PDF]
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J. Han, S. R. Farmer, J. L. Kirkland, B. E. Corkey, R. Yoon, T. Pirtskhalava, Y. Ido, and W. Guo Octanoate Attenuates Adipogenesis in 3T3-L1 Preadipocytes J. Nutr., May 1, 2002; 132(5): 904 - 910. [Abstract] [Full Text] [PDF]
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T. Imai, M. Jiang, P. Chambon, and D. Metzger Impaired adipogenesis and lipolysis in the mouse upon selective ablation of the retinoid X receptor alpha mediated by a tamoxifen-inducible chimeric Cre recombinase (Cre-ERT2) in adipocytes PNAS, December 22, 2000; (2000) 11528898. [Abstract] [Full Text]
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T. Helledie, M. Antonius, R. V. Sørensen, A. V. Hertzel, D. A. Bernlohr, S. Kølvraa, K. Kristiansen, and S. Mandrup Lipid-binding proteins modulate ligand-dependent trans-activation by peroxisome proliferator-activated receptors and localize to the nucleus as well as the cytoplasm J. Lipid Res., November 1, 2000; 41(11): 1740 - 1751. [Abstract] [Full Text]
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C. Roh, G. Thoidis, S. R. Farmer, and K. V. Kandror Identification and characterization of leptin-containing intracellular compartment in rat adipose cells Am J Physiol Endocrinol Metab, October 1, 2000; 279(4): E893 - E899. [Abstract] [Full Text] [PDF]
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M. Classon, B. K. Kennedy, R. Mulloy, and E. Harlow Opposing roles of pRB and p107 in adipocyte differentiation PNAS, September 19, 2000; (2000) 190343597. [Abstract] [Full Text]
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P. Penfornis, S. Viengchareun, D. Le Menuet, F. Cluzeaud, M.-C. Zennaro, and M. Lombes The mineralocorticoid receptor mediates aldosterone-induced differentiation of T37i cells into brown adipocytes Am J Physiol Endocrinol Metab, August 1, 2000; 279(2): E386 - E394. [Abstract] [Full Text] [PDF]
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G. Mbalaviele, Y. Abu-Amer, A. Meng, R. Jaiswal, S. Beck, M. F. Pittenger, M. A. Thiede, and D. R. Marshak Activation of Peroxisome Proliferator-activated Receptor-gamma Pathway Inhibits Osteoclast Differentiation J. Biol. Chem., May 5, 2000; 275(19): 14388 - 14393. [Abstract] [Full Text] [PDF]
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R. K. Jaiswal, N. Jaiswal, S. P. Bruder, G. Mbalaviele, D. R. Marshak, and M. F. Pittenger Adult Human Mesenchymal Stem Cell Differentiation to the Osteogenic or Adipogenic Lineage Is Regulated by Mitogen-activated Protein Kinase J. Biol. Chem., March 24, 2000; 275(13): 9645 - 9652. [Abstract] [Full Text] [PDF]
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J. A. Engelman, A. H. Berg, R. Y. Lewis, A. Lin, M. P. Lisanti, and P. E. Scherer Constitutively Active Mitogen-activated Protein Kinase Kinase 6 (MKK6) or Salicylate Induces Spontaneous 3T3-L1 Adipogenesis J. Biol. Chem., December 10, 1999; 274(50): 35630 - 35638. [Abstract] [Full Text] [PDF]
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S. E. Ross, R. L. Erickson, N. Hemati, and O. A. MacDougald Glycogen Synthase Kinase 3 Is an Insulin-Regulated C/EBPalpha Kinase Mol. Cell. Biol., December 1, 1999; 19(12): 8433 - 8441. [Abstract] [Full Text] [PDF]
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S. Kim, P.-L. Mao, M. Gagliardi, and P.-A. Bedard C/EBPbeta (NF-M) Is Essential for Activation of the p20K Lipocalin Gene in Growth-Arrested Chicken Embryo Fibroblasts Mol. Cell. Biol., August 1, 1999; 19(8): 5718 - 5731. [Abstract] [Full Text] [PDF]
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C. Bastie, D. Holst, D. Gaillard, C. Jehl-Pietri, and P. A. Grimaldi Expression of Peroxisome Proliferator-activated Receptor PPARdelta Promotes Induction of PPARgamma and Adipocyte Differentiation in 3T3C2 Fibroblasts J. Biol. Chem., July 30, 1999; 274(31): 21920 - 21925. [Abstract] [Full Text] [PDF]
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J. E.-B. Reusch and D. J. Klemm Editorial: Nutrition and Fat Cell Differentiation Endocrinology, July 1, 1999; 140(7): 2935 - 2937. [Full Text]
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C. M. Smas, L. Chen, L. Zhao, M.-J. Latasa, and H. S. Sul Transcriptional Repression of pref-1 by Glucocorticoids Promotes 3T3-L1 Adipocyte Differentiation J. Biol. Chem., April 30, 1999; 274(18): 12632 - 12641. [Abstract] [Full Text] [PDF]
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Y. Umayahara, J. Billiard, C. Ji, M. Centrella, T. L. McCarthy, and P. Rotwein CCAAT/Enhancer-binding Protein delta Is a Critical Regulator of Insulin-like Growth Factor-I Gene Transcription in Osteoblasts J. Biol. Chem., April 9, 1999; 274(15): 10609 - 10617. [Abstract] [Full Text] [PDF]
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T. Thomas, F. Gori, S. Khosla, M. D. Jensen, B. Burguera, and B. L. Riggs Leptin Acts on Human Marrow Stromal Cells to Enhance Differentiation to Osteoblasts and to Inhibit Differentiation to Adipocytes Endocrinology, April 1, 1999; 140(4): 1630 - 1638. [Abstract] [Full Text]
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J. B. Hansen, R. K. Petersen, B. M. Larsen, J. Bartkova, J. Alsner, and K. Kristiansen Activation of Peroxisome Proliferator-activated Receptor gamma Bypasses the Function of the Retinoblastoma Protein in Adipocyte Differentiation J. Biol. Chem., January 22, 1999; 274(4): 2386 - 2393. [Abstract] [Full Text] [PDF]
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Q.-Q. Tang, M.-S. Jiang, and M. D. Lane Repression of transcription mediated by dual elements in the CCAAT/enhancer binding protein alpha gene PNAS, December 9, 1997; 94(25): 13571 - 13575. [Abstract] [Full Text] [PDF]
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M. Lu, J. Seufert, and J. F. Habener Pancreatic beta -Cell-specific Repression of Insulin Gene Transcription by CCAAT/Enhancer-binding Protein beta . INHIBITORY INTERACTIONS WITH BASIC HELIX-LOOP-HELIX TRANSCRIPTION FACTOR E47 J. Biol. Chem., November 7, 1997; 272(45): 28349 - 28359. [Abstract] [Full Text] [PDF]
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N. Hemati, S. E. Ross, R. L. Erickson, G. E. Groblewski, and O. A. MacDougald Signaling Pathways through Which Insulin Regulates CCAAT/Enhancer Binding Protein alpha (C/EBPalpha ) Phosphorylation and Gene Expression in 3T3-L1 Adipocytes. CORRELATION WITH GLUT4 GENE EXPRESSION J. Biol. Chem., October 10, 1997; 272(41): 25913 - 25919. [Abstract] [Full Text] [PDF]
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D. Shao and M. A. Lazar Peroxisome Proliferator Activated Receptor gamma , CCAAT/ Enhancer-binding Protein alpha , and Cell Cycle Status Regulate the Commitment to Adipocyte Differentiation J. Biol. Chem., August 22, 1997; 272(34): 21473 - 21478. [Abstract] [Full Text] [PDF]
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M. Nishizuka, K. Honda, T. Tsuchiya, T. Nishihara, and M. Imagawa RGS2 Promotes Adipocyte Differentiation in the Presence of Ligand for Peroxisome Proliferator-activated Receptor gamma J. Biol. Chem., August 3, 2001; 276(32): 29625 - 29627. [Abstract] [Full Text] [PDF]
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Y. Lin, H. Lee, A. H. Berg, M. P. Lisanti, L. Shapiro, and P. E. Scherer The Lipopolysaccharide-activated Toll-like Receptor (TLR)-4 Induces Synthesis of the Closely Related Receptor TLR-2 in Adipocytes J. Biol. Chem., August 4, 2000; 275(32): 24255 - 24263. [Abstract] [Full Text] [PDF]
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G. Elberg, J. M. Gimble, and S. Y. Tsai Modulation of the Murine Peroxisome Proliferator-activated Receptor gamma 2 Promoter Activity by CCAAT/Enhancer-binding Proteins J. Biol. Chem., September 1, 2000; 275(36): 27815 - 27822. [Abstract] [Full Text] [PDF]
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A. K. Ghosh, R. Lacson, P. Liu, S. B. Cichy, A. Danilkovich, S. Guo, and T. G. Unterman A Nucleoprotein Complex containing CCAAT/Enhancer-binding Protein beta Interacts with an Insulin Response Sequence in the Insulin-like Growth Factor-binding Protein-1 Gene and Contributes to Insulin-regulated Gene Expression J. Biol. Chem., March 9, 2001; 276(11): 8507 - 8515. [Abstract] [Full Text] [PDF]
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