|
|
|
|||||||
|
|||||||||
Volume 272, Number 52, Issue of December 26, 1997
pp. 32723-32726
(Received for publication, October 3, 1997, and in revised form, October 23, 1997)
From the Target Discovery Department and the
ABSTRACT We have isolated a novel gene, hKCa4,
encoding an intermediate conductance, calcium-activated potassium
channel from a human lymph node library. The translated protein
comprises 427 amino acids, has six transmembrane segments, S1-S6, and
a pore motif between S5 and S6. hKCa4 shares 41-42% similarity at the
amino acid level with three small conductance calcium-activated
potassium channels cloned from brain. Northern blot analysis of primary human T lymphocytes reveals a 2.2-kilobase transcript that is highly
up-regulated in activated compared with resting cells, concomitant with
an increase in KCa current. hKCa4 transcript is also
detected by Northern blots or by polymerase chain reaction in placenta,
prostate, thymus, spleen, colon, and many cell lines of hematopoietic
origin. Patch-clamp recordings of hKCa4-transfected HEK 293 cells reveal a large voltage-independent, inwardly rectifying potassium
current that is blocked by externally applied tetraethylammonium (Kd = 30 ± 7 mM), charybdotoxin
(Kd = 10 ± 1 nM), and
clotrimazole (Kd = 387 ± 34 nM),
but is resistant to apamin, iberiotoxin, kaliotoxin, scyllatoxin
(Kd > 1 µM), and margatoxin
(Kd > 100 nM). Single hKCa4 channels have a conductance of 33 ± 2 picosiemens in symmetrical potassium solutions. The channel is activated by intracellular calcium
(Kd = 270 ± 8 nM) with a highly
cooperative interaction of approximately three calcium ions per
channel. These properties of the cloned channel are very similar to
those reported for the native KCa channel in activated human T
lymphocytes, indicating that hKCa4 encodes this channel
type.
INTRODUCTION Potassium channels play a critical role in modulating calcium
signaling of lymphocytes (1). Human T lymphocytes express at least two
types of potassium channels (2): those that open in response to changes
in membrane potential (Kv
channels)1 and those that are
activated following elevations of intracellular calcium levels (KCa
channels). The predominant Kv channel in human T cells is encoded by
Kv1.3, a Shaker-related voltage-gated potassium channel gene. Kv1.3 has been characterized extensively at the molecular
and physiological level and plays a vital role in controlling T cell
proliferation, mainly by maintaining the resting membrane potential of
the cell (3). Upon T cell activation, there is at most a 2-fold
increase in Kv1.3 currents. The predominant KCa channel on human T
lymphocytes is of intermediate conductance, is voltage-insensitive, and
is potently blocked by the scorpion venom peptide, charybdotoxin (CTX;
Ref. 4). Unlike Kv1.3, KCa currents are up-regulated dramatically
(10-25-fold) following mitogenic or antigenic stimulation and are
thought to play a significant role in post-activation and secondary
immune phenomena (4, 5). KCa channels with biophysical and
pharmacological properties very similar to the T lymphocyte channel
also have been identified in red blood cells (Gardos channel; Ref. 6),
macrophages (7), neutrophils (8), and B lymphocytes (9), as well as in
other peripheral tissues. However, the molecular identity of this
channel type was hitherto unknown. We report the cloning and
characterization of an intermediate conductance, CTX-sensitive KCa
channel, which we call hKCa4, from a human lymph node
cDNA library. We present convergent molecular, biophysical, and
pharmacological evidence that hKCa4 encodes the predominant
KCa channel in human T cells.
EXPERIMENTAL PROCEDURES We performed a BLAST search of a
proprietary EST data base (licensed from Incyte
Pharmaceuticals, Palo Alto, CA) for unannotated potassium channel
sequences using the pore sequence of hKv2.1, a Shab-related
K+ channel (PASFWWATITMTTVGYGDIYP; Ref. 10). Two
overlapping clones of interest were identified, and their sequences
were determined (Applied Biosystems PRISMTM377 automated sequencer).
Both of these clones were from a cDNA library of adherent
mononuclear cells, which came from a pool of male and female
donors.
A
32P-labeled DNA fragment from one of the above clones,
corresponding to nucleotides 262-1265 in Fig. 1A, was used
as a probe to screen ~600,000 recombinant plaques from a human lymph
node Computer analysis of the hKCa4 sequence was done using
Lasergene software (DNAstar, Inc., Madison, WI). Alignments with other potassium channel sequences were performed using the CLUSTAL algorithm, and these were used to create a dendrogram. The gap penalty and the gap
length penalty were 10 each. Hydropathy plots were according to
Kyte-Doolittle criteria, averaging over a nine-residue window. Post-translational modification sites were identified using pattern searches within the Protean program. Patterns were derived from the
Prosite data base, and the threshold for matching was 100%.
Mononuclear
cells were isolated from whole blood (obtained from healthy donors) on
Ficoll-Hypaque density gradients. Contaminating red blood cells were
removed by hypotonic lysis for 45 s in 0.2% saline followed by an
equal volume of 1.6% saline to bring saline back to physiological
concentration. Monocytes and B cells were removed using M450 Pan-B
(CD19) and M450 (CD14) Dynabeads according to the Dynal protocol (Lake
Success, NY). Remaining cells were assumed to be mainly T cells
(typically 80-90% as assessed by fluorescence-activated cell sorter
analysis). T cells were cultured overnight at 37 °C, 5%
CO2, in complete RPMI 1640 medium containing 10% fetal
bovine serum and 1 × penicillin/streptomycin (Life Technologies, Inc.). The cells then were activated with 10 µg/ml final
concentration phytohemagglutinin (Sigma) in complete RPMI for 48-72
h.
T cell
poly(A)+ RNA was isolated using Invitrogen's FastTrack 2.0 kit (Carlsbad, CA). 0.9 µg each of resting and activated T cell RNA
(equivalent to 12 × 107 resting and 1 × 107 activated T cells) was resolved by electrophoresis
through a 1% agarose gel containing 2.2 M formaldehyde,
with 3 µg of RNA ladder as a size marker (Life Technologies, Inc.).
RNA was transferred for 6 h to positively charged nylon membrane
(Hybond-N+, Amersham Life Science, Inc.), followed by UV
cross-linking.
Twenty-five to forty ng (9-15 × 106 cpm) of
32P-labeled polymerase chain reaction fragment
corresponding to nucleotides 262-702 of hKCa4 (Fig.
1A) was used to probe multiple tissue Northern blots (~2
µg RNA/lane, CLONTECH) and a T cell blot. Blots
were hybridized for 1.5 h at 68 °C and washed two times in
0.1 × SSC + 0.1% SDS at 50 °C, then exposed to film 3-14
days using two intensifying screens. Laser densitometry was used to
quantitate relative band intensities on the T cell blot. The same blot,
when probed with A ~1.3-kb
SmaI/ScaI fragment containing the coding region
of hKCa4 was cloned into pcDNA3 vector (Invitrogen) at
the EcoRV site. This cloning strategy introduced an
additional methionine and two amino acids (G, A) upstream and in-frame
with the authentic initiator methionine. Approximately 3 × 105 HEK 293 cells (ATCC, Rockville, MD) were transfected
with 5 µg of hKCa4 gene in pcDNA3 vector along with 1 µg of green fluorescent protein (GFP) in pEGFP-C1 vector
(CLONTECH) using the LipoTAXI transfection kit
(Stratagene, La Jolla, CA) as per the manufacturer's instructions.
Currents were recorded 24-72 h later.
Currents were recorded with an
Axopatch 200A amplifier (Axon Instruments, Foster City, CA) using the
whole cell, cell-attached, and inside-out configurations (12).
Transfected HEK cells were selected for recording by the presence of
GFP epifluorescence (excitation: 485/22 nm, emission: 505 nm).
Thin-wall borosilicate glass pipettes were fabricated, sylgarded, and
fire-polished to a DC resistance of 2-8 M For whole cell recording, the pipette solution contained (in
mM) 160 potassium aspartate, 2 MgCl2, 5 HEPES,
and 1.6 EGTA with either 0.8 CaCl2 (calculated
[Ca2+]free = 100 nM; Eqcal
software, Biosoft Corp, Cambridge, United Kingdom) or 1.6 CaCl2 (calculated [Ca2+]free = 1 µM) at pH 7.2 (by KOH) and osmolality ~315 mOsm (by sucrose). Cells were perfused locally with a solution containing 160 KCl, 2 CaCl2, 1 MgCl2, 5 HEPES, and 5 glucose
at pH 7.4 (by KOH) and osmolality ~325 mOsm. In K+
selectivity experiments, equimolar Na+ was substituted for
K+. For cell-attached patches, the pipette
solution contained 160 KCl, 2 CaCl2, 1 MgCl2,
and 10 HEPES at pH 7.4 (by NaOH) and osmolality ~325 mOsm. Cells were
perfused with Ringer solution (160 NaCl, 4.5 KCl, 1 MgCl2,
5 HEPES, and 2 CaCl2 at pH 7.4) ± 1 µM
ionomycin. For excised inside-out patches, the pipette
solution contained 160 KCl, 2 CaCl2, 1 MgCl2,
and 10 HEPES at pH 7.4 (by KOH) and osmolality ~325 mOsm. The local
perfusion solution (cytoplasmic face) contained 160 K aspartate, 2 MgCl2, 5 HEPES, and 10 EGTA at pH 7.2 (by KOH) and
osmolality ~329 mOsm with CaCl2 added at concentrations
that yielded the calculated [Ca2+]free
specified. Perfusion solutions were delivered locally using a solenoid
valve system (13). Toxins were purchased from Sigma and were diluted in
solution containing 0.01% bovine serum albumin.
RESULTS AND DISCUSSION We obtained a 2.2-kb cDNA clone from a human lymph node
[View Larger Version of this Image (85K GIF file)]
[View Larger Version of this Image (57K GIF file)]
Northern blot analysis of hKCa4 revealed a strong signal at
~2.2 kb in activated human T lymphocytes, placenta, prostate, and
colon (Fig. 2, A and B). Moderate signal was
observed in spleen, thymus, and peripheral blood leukocytes (Fig.
2A); there was no detectable signal in brain. Minor
transcripts of larger sizes also were seen in some tissues (Fig.
2A).
The hKCa4 gene, when co-transfected with a reporter gene for
GFP into HEK 293 cells, produced a calcium-dependent
K+ current with strong inward rectification in symmetrical
K+ solutions upon perfusion of 1 µM ionomycin
(Fig. 3A). Current induced by
ionomycin was blocked completely by 100 nM CTX, but unaffected (i.e. <10% change in amplitude) by 1 µM apamin (n = 2). Internal dialysis with
a solution containing 1 µM
[Ca2+]free also activated a stable large
current (15.4 ± 2.4 nS slope conductance between
[View Larger Version of this Image (17K GIF file)]
Cell-attached recordings revealed single channel openings during
perfusion with Ringer solution containing 1 µM ionomycin. Channels showed a unitary conductance of 33 ± 2 pS
(n = 3; Fig. 4A) measured during voltage
ramps between
[View Larger Version of this Image (35K GIF file)]
We provide strong molecular, biophysical, and pharmacological evidence
that hKCa4 encodes the calcium-activated potassium channel
in T lymphocytes: (a) the clone was identified from a lymph
node library, which is enriched for activated T cells; (b) Northern blot analysis of resting and activated T cells revealed ~10-fold up-regulation of transcript levels, with a corresponding increase in current levels (Fig. 2, B and C); and
(c) the electrophysiological properties of the hKCa4
currents are essentially indistinguishable from those reported for T
cells (1, 4), including inward rectification in high potassium
solution, block by CTX and TEA, single-channel conductance, and
Kd for calcium dependence (Fig. 4D).
hKCa4 may also encode the KCa channels found in other cells
of hematopoietic origin (6-9), because the properties reported for the
channel from these cells is compatible with our data on the
hKCa4 clone heterologously expressed in HEK 293 cells. In addition, we were able to amplify a 1-kb band using
hKCa4-specific primers and to confirm sequence from many
cell lines of hematopoietic origin (e.g. U937, fetal liver
cells, Jurkats, etc.). Our results do not rule out possible association
of hKCa4 with accessory proteins; such interactions as well as
variations in post-translational modifications, could account for the
subtle differences in reported properties in different cell types
(6-9; 15). Further biochemical studies could address these issues.
The significant up-regulation of hKCa4 transcript levels
during T cell activation highlights the importance of these channels in
early activation and post-activation immune responses. Engagement of
the T cell receptor by mitogen or antigen evokes an increase in
intracellular calcium concentration leading to membrane
hyperpolarization (rather than depolarization) caused by opening of KCa
channels (1). This event, in turn, maximizes the electrical driving force for calcium influx through calcium release-activated channels, facilitating sustained calcium oscillations required for cell proliferation, cytokine production, and the expression of immune function (1, 4, 5). Blockade of both KCa and Kv channels has been
reported to cause profound inhibition of T cell proliferation (17),
whereas blockade of KCa channels is sufficient to prevent secondary
immune responses (5). With the identification and characterization of
hKCa4, it is now possible to dissect the molecular mechanisms by which calcium-activated potassium channels control leukocyte development and activation.
FOOTNOTES ACKNOWLEDGEMENTS We thank Susan Li and Jianming Zhou for help
with library screening, Lee Hirata for DNA sequencing and primer
synthesis, and Trevor J. Hallam and David Silberstein for scientific
support and helpful discussions.
Note Added in Proof During review of this manuscript, two
papers were published describing a gene similar to hKCa4.
The clone of Joiner et al. (Joiner, W. J., Wang, L. Y.,
Tang, M. D., and Kaczmarek, L. K. (1997) Proc. Natl. Acad. Sci.
U. S. A. 94, 11013-11018) had functional properties that
differed significantly from ours. The sequence of Ishii et
al. (Ishii, T. M., Silvia, C., Hirschberg, B., Bond, C. T.,
Adelman, J. P., and Maylie, J. (1997) Proc. Natl. Acad. Sci.
U. S. A. 94, 11651 REFERENCES
COMMUNICATION:
A Novel Gene, hKCa4, Encodes the Calcium-activated
Potassium Channel in Human T Lymphocytes*
, and
Respiratory, Inflammatory, and Neurological Diseases
Department, Zeneca Pharmaceuticals, Wilmington, Delaware 19850
ABSTRACT
INTRODUCTION
EXPERIMENTAL PROCEDURES
RESULTS AND DISCUSSION
FOOTNOTES
ACKNOWLEDGEMENTS
Note Added in Proof
REFERENCES
gt10 cDNA library (CLONTECH).
Hybridizations were at 42° C overnight. Filters were washed twice in
1 × SSC (150 mM NaCl, 15 mM
Na3 citrate, pH 7.0) and 0.5% SDS at 65 °C for 1 h
and exposed to x-ray film overnight. Of 38 doubly positive clones, 10 were subjected to two rounds of plaque purification and rescreening.
Inserts were amplified using -specific primers, and amplicons were
sequenced directly by automated sequencing as above. Six clones had
hKCa4 sequence information, and three were full length. One
full-length clone was subcloned and sequenced entirely on both strands
and used for subsequent expression constructs.
-actin, revealed 2.0-kb bands in both lanes,
confirming the integrity of the RNA.
. The resistance of patch
seals was >10 G. Liquid junction potentials were corrected for in
all experiments, and series resistance compensation of >70% was used
where maximal current was >0.5 nA. Voltage clamp protocols were
implemented and data acquisition performed with pClamp 6.0 software
(Axon Instruments.). Currents were low pass-filtered (
3 db at 1 kHz) and then digitized at 3-8 kHz as computer files with a TL-1 interface (Scientific Solutions, Solon, OH). Currents were measured with p-Clamp
software, and iterative curve fittings were performed with either
p-Clamp or Origin software (Version 3.73; Microcal Inc., Northampton,
MA).
library using a probe derived from an EST sequence that was identified from a data base search for novel potassium channels. The clone has 400 bp of 5
-UTR, 1.3 kb of coding region, and 540 bp of 3-UTR (Fig.
1A). We have mapped the entire
transcript of the predominant 2.2-kb band seen in Northern blots from
various tissues (see Fig. 2), because
four independent clones started with the same 5-UTR sequence (±15
bp), and the 3-UTR ended with a polyadenylation signal followed by a
poly(A) tail. We also detected an in-frame stop codon upstream of the
initiator ATG in all four clones, ruling out the existence of alternate
upstream initiator ATG codons. The translated protein comprises 427 amino acids. Hydropathy plot analysis reveals a short intracellular N
terminus, followed by six transmembrane segments (S1-S6) and a long
intracellular C terminus (Fig. 1B). The loop between S5 and
S6 contains the highly conserved GYG sequence characteristic of all
cloned potassium channel pores (10). The hKCa4 protein has one
consensus N-linked glycosylation site between S5 and the
pore and several sites for serine-threonine phosphorylation. There are
no consensus EF hand motifs in hKCa4. A comparison of the amino acid
sequence of hKCa4 with representative members of the K+
channel superfamily reveals that it is most similar to the small conductance KCa channels (hSK1, rSK2, rSK3) recently cloned from brain
(14). However, it shares only 41-42% amino acid identity with them,
warranting placement within a distinct subfamily (Fig. 1C).
The amino acid sequence of hKCa4 is 11-14% similar to the other
cloned six-transmembrane K+ channels (Kv, SLO, HERG, and
KVLQT1; Ref. 10). In a recent abstract, J. P. Adelman reported
cloning an intermediate-conductance KCa channel from a human pancreatic
cDNA library; sequence information was not published (15).
Fig. 1.
hKCa4 sequence. A,
nucleotide and predicted amino acid sequence of hKCa4
(GenBankTM accession number AF022797). Predicted transmembrane regions
are boxed and shaded. Consensus sites for glycosylation are indicated by a triangle, serine-threonine
phosphorylation sites are circled, the polyadenylation
signal is underlined, and the stop codon is indicated by an
asterisk. B, hydropathy plot of hKCa4 protein
showing six predicted transmembrane segments and a pore between S5 and
S6. C, amino acid dendrogram of hKCa4 with the recently
cloned small conductance KCa channels, hSK1, rSK2 and rSK3. Percent
similarity of each channel to hKCa4 is shown.
Fig. 2.
Northern blot analysis of hKCa4
message. A, a predominant 2.2 kb band was detected in
multiple tissues. B, the band was also detected in resting
and activated human T lymphocytes, showing up-regulation of message
after activation. C, patch-clamp analysis of representative
T cells that were subjected to Northern blot in B, showing
up-regulation of KCa channel currents on activation. Each superimposed
current trace was elicited by a 200-ms voltage ramp from 100 to +40
mV (Ehold = 50 mV). Trace 1,
resting T cell; trace 2, resting T cell plus 100 nM CTX; trace 3, activated T cell; trace
4, activated T cell plus 100 nM CTX. Components of Kv
and KCa currents are indicated.
100 and 30
mV; n = 11) with similar characteristics. Control
current during ramps in symmetrical 160 mM K+
converged with current elicited during 100 nM CTX perfusion
close to 0 mV (e.g. Fig. 3A), supporting
K+ selectivity of the channel. K+ selectivity
was evaluated further by examining reversal potentials of control
versus CTX currents over a range of different
K+(out) concentrations (Fig. 3C).
Reversal potential shifted 57 mV per 10-fold increase in
K+(out), in close agreement with the predicted
Nernstian value for a K+-selective channel. Pharmacological
evaluation (Fig. 3B) revealed that this current was
inhibited by CTX (Kd = 10 ± 1 nM) and tetraethylammonium (TEA; Kd = 30 ± 7 mM), but insensitive to margatoxin (Kd
>100 nM), apamin, iberiotoxin, kaliotoxin, and scyllatoxin
(Kd >1 µM, n = 2-3
each). Clotrimazole, a drug that is reported to block KCa channels in
erythrocytes and thymocytes in the low micromolar range (16), blocked
hKCa4 currents with a Kd of 387 ± 34 nM. Untransfected HEK 293 cells or cells transfected
with GFP alone showed very small CTX-resistant currents in response to
voltage ramps during dialysis with 1 µM
[Ca2+]free (conductance < 0.1 nS;
n = 8).
Fig. 3.
KCa currents in HEK 293 cells transfected
with hKCa4 gene. A, dependence of whole cell
current on 1 µM ionomycin perfusion and blockade by CTX
(100 nM). Superimposed currents were evoked by 200-ms
voltage ramps from 100 to +30 mV (Ehold = 50
mV). The pipette solution contained 100 nM
[Ca2+]free, and the bath solution contained
160 mM K+. B,
concentration-dependent blockade of KCa current by CTX,
TEA, and clotrimazole (CLT). Protocol was the same as in
A, except that [Ca2+]free was
buffered to 1 µM in the pipette, and ionomycin was
omitted from the bath. Currents were measured at 95 mV on the ramp
and normalized between control amplitude and that obtained during perfusion with 100 nM CTX in the same experiment. Each
point is the mean ± S.E. of three to five experiments.
Solid lines represent fits to a Hill equation of the
following form: 100/[1 + (Kd/x)n], where x is
concentration, Kd the concentration producing 50%
inhibition, and n is the slope factor of the line. See text for fitting parameters. C, K+ selectivity of
hKCa4 current. Each point represents the voltage (mean ± S.E.;
n = 3-6), where control current converged with current in CTX during voltage ramps at the designated
K+(out) concentration. The solid
line is a linear regression to the data (slope 57 mV).
120 and 30 mV with pipettes containing 160 mM K+ and a unitary conductance of 9 ± 1 pS (n = 3) with pipettes containing 4.5 mM
K+. Pipette potentials between 100 and +20 mV had no
apparent effect on the probability of channel openings
(Po) during ramps (e.g. Fig.
4A) or steps. The inside-out configuration in symmetrical K+ also revealed single channels of similar conductance
with gating that clearly depended on the
[Ca2+]free at the cytoplasmic face of the
patch (Fig. 4B). The Po with different [Ca2+]free varied considerably
between cells, but never exceeded ~0.5. Fitting the open probability
versus [Ca2+]free revealed an
activation Kd = 270 ± 8 nM
Ca2+ with a Hill coefficient of 2.7 ± 0.2, indicative
of a highly cooperative interaction between calcium ions and the
channel (Fig. 4C).
Fig. 4.
Unitary conductance and calcium sensitivity
of hKCa4 channels. A, single-channel current (openings are
down) from a cell-attached patch containing two channels with 160 K+ in the pipette. The bath contained Ringer with 1 µM ionomycin. The patch was ramped over 100 ms from 120
to +60 mV. A blank trace (i.e. no channel openings) was
digitally subtracted. The dashed line represents a slope
conductance of 31 pS. B, representative traces obtained from
an inside-out patch excised from an hKCa4-transfected cell
(Ehold = 80 mV). The pipette contained 160 mM K+, and the patch was perfused with the
[Ca2+]free indicated. C,
relationship between open probability and cytoplasmic
[Ca2+]free determined using the experimental
protocol in B. Single channel open probabilities were
determined by the relative areas of peaks in second-order Gaussian fits
to amplitude frequency histograms (patches contained one apparent
channel). Points are the mean ± S.E. from the designated number
of experiments. Solid line is a fit to the Hill equation
described in Fig. 3B for the range of 10 nM to
600 nM [Ca2+]free. D,
summary table of data obtained from experiments shown in Figs. 3 and 4
for hKCa4 expressed in HEK cells compared with published data for the
human T cell KCa channel.
§
To whom correspondence should be addressed. Tel.: 302-886-5708;
Fax: 302-886-2766; E-mail: jayashree.aiyar{at}phwilm.zeneca.com.
1
The abbreviations used are: Kv, voltage-gated
potassium; KCa, calcium-activated potassium; CTX, charybdotoxin; TEA,
tetraethylammonium; UTR, untranslated region; kb, kilobase; bp, base
pair; GFP, green fluorescent protein; S, siemens.
11656) differed by two amino acids in
critical regions of the protein. Neither paper established a connection
to lymphocytes.
Volume 272, Number 52,
Issue of December 26, 1997
pp. 32723-32726
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  B. Fioretti, L. Catacuzzeno, L. Sforna, F. Aiello, F. Pagani, D. Ragozzino, E. Castigli, and F. Franciolini Histamine hyperpolarizes human glioblastoma cells by activating the intermediate-conductance Ca2+-activated K+ channel Am J Physiol Cell Physiol, July 1, 2009; 297(1): C102 - C110. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. G. Romanenko, K. S. Roser, J. E. Melvin, and T. Begenisich The role of cell cholesterol and the cytoskeleton in the interaction between IK1 and maxi-K channels Am J Physiol Cell Physiol, April 1, 2009; 296(4): C878 - C888. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Heitzmann and R. Warth Physiology and Pathophysiology of Potassium Channels in Gastrointestinal Epithelia Physiol Rev, July 1, 2008; 88(3): 1119 - 1182. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. G. Meuth, S. Bittner, P. Meuth, O. J. Simon, T. Budde, and H. Wiendl TWIK-related Acid-sensitive K+ Channel 1 (TASK1) and TASK3 Critically Influence T Lymphocyte Effector Functions J. Biol. Chem., May 23, 2008; 283(21): 14559 - 14570. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J.-Z. Sheng and A. P. Braun Small- and intermediate-conductance Ca2+-activated K+ channels directly control agonist-evoked nitric oxide synthesis in human vascular endothelial cells Am J Physiol Cell Physiol, July 1, 2007; 293(1): C458 - C467. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 V. G. Romanenko, T. Nakamoto, A. Srivastava, T. Begenisich, and J. E. Melvin Regulation of membrane potential and fluid secretion by Ca2+-activated K+ channels in mouse submandibular glands J. Physiol., June 1, 2007; 581(2): 801 - 817. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 V. H. John, T. J. Dale, E. C. Hollands, M. X. Chen, L. Partington, D. L. Downie, H. J. Meadows, and D. J. Trezise Novel 384-Well Population Patch Clamp Electrophysiology Assays for Ca2+-Activated K+ Channels J Biomol Screen, February 1, 2007; 12(1): 50 - 60. [Abstract] [PDF]
|
|
|
|
 |
|
 V. Kaushal, P. D. Koeberle, Y. Wang, and L. C. Schlichter The Ca2+-Activated K+ Channel KCNN4/KCa3.1 Contributes to Microglia Activation and Nitric Oxide-Dependent Neurodegeneration J. Neurosci., January 3, 2007; 27(1): 234 - 244. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Leroy, A. Prive, J.-C. Bourret, Y. Berthiaume, P. Ferraro, and E. Brochiero Regulation of ENaC and CFTR expression with K+ channel modulators and effect on fluid absorption across alveolar epithelial cells Am J Physiol Lung Cell Mol Physiol, December 1, 2006; 291(6): L1207 - L1219. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. M. Shah, M. Javadzadeh-Tabatabaie, D. C. H. Benton, C. R. Ganellin, and D. G. Haylett Enhancement of Hippocampal Pyramidal Cell Excitability by the Novel Selective Slow-Afterhyperpolarization Channel Blocker 3-(Triphenylmethylaminomethyl)pyridine (UCL2077) Mol. Pharmacol., November 1, 2006; 70(5): 1494 - 1502. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G Cruse, S M Duffy, C E Brightling, and P Bradding Functional KCa3.1 K+ channels are required for human lung mast cell migration Thorax, October 1, 2006; 61(10): 880 - 885. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. Romanenko, T. Nakamoto, A. Srivastava, J. E. Melvin, and T. Begenisich Molecular Identification and Physiological Roles of Parotid Acinar Cell Maxi-K Channels J. Biol. Chem., September 22, 2006; 281(38): 27964 - 27972. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Thompson and T. Begenisich Membrane-delimited Inhibition of Maxi-K Channel Activity by the Intermediate Conductance Ca2+-activated K Channel J. Gen. Physiol., January 30, 2006; 127(2): 159 - 169. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Beeton and K. G. Chandy Potassium Channels, Memory T Cells, and Multiple Sclerosis Neuroscientist, December 1, 2005; 11(6): 550 - 562. [Abstract] [PDF]
|
|
|
|
 |
|
 I. Grgic, I. Eichler, P. Heinau, H. Si, S. Brakemeier, J. Hoyer, and R. Kohler Selective Blockade of the Intermediate-Conductance Ca2+-Activated K+ Channel Suppresses Proliferation of Microvascular and Macrovascular Endothelial Cells and Angiogenesis In Vivo Arterioscler. Thromb. Vasc. Biol., April 1, 2005; 25(4): 704 - 709. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Begenisich, T. Nakamoto, C. E. Ovitt, K. Nehrke, C. Brugnara, S. L. Alper, and J. E. Melvin Physiological Roles of the Intermediate Conductance, Ca2+-activated Potassium Channel Kcnn4 J. Biol. Chem., November 12, 2004; 279(46): 47681 - 47687. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. Visan, Z. Fajloun, J.-M. Sabatier, and S. Grissmer Mapping of Maurotoxin Binding Sites on hKv1.2, hKv1.3, and hIKCa1 Channels Mol. Pharmacol., November 1, 2004; 66(5): 1103 - 1112. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. A. Pardo Voltage-Gated Potassium Channels in Cell Proliferation Physiology, October 1, 2004; 19(5): 285 - 292. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
U. Banderali, H. Klein, L. Garneau, M. Simoes, L. Parent, and R. Sauve New Insights on the Voltage Dependence of the KCa3.1 Channel Block by Internal TBA J. Gen. Physiol., September 27, 2004; 124(4): 333 - 348. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Ouadid-Ahidouch, M. Roudbaraki, P. Delcourt, A. Ahidouch, N. Joury, and N. Prevarskaya Functional and molecular identification of intermediate-conductance Ca2+-activated K+ channels in breast cancer cells: association with cell cycle progression Am J Physiol Cell Physiol, July 1, 2004; 287(1): C125 - C134. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Jager, T. Dreker, A. Buck, K. Giehl, T. Gress, and S. Grissmer Blockage of Intermediate-Conductance Ca2+-Activated K+ Channels Inhibit Human Pancreatic Cancer Cell Growth in Vitro Mol. Pharmacol., March 1, 2004; 65(3): 630 - 638. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Hayashi, C. Kunii, T. Takahata, and T. Ishikawa ATP-dependent regulation of SK4/IK1-like currents in rat submandibular acinar cells: possible role of cAMP-dependent protein kinase Am J Physiol Cell Physiol, March 1, 2004; 286(3): C635 - C646. [Abstract] [Full Text]
|
|
|
|
 |
|
 R. Kohler, H. Wulff, I. Eichler, M. Kneifel, D. Neumann, A. Knorr, I. Grgic, D. Kampfe, H. Si, J. Wibawa, et al. Blockade of the Intermediate-Conductance Calcium-Activated Potassium Channel as a New Therapeutic Strategy for Restenosis Circulation, September 2, 2003; 108(9): 1119 - 1125. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. F. Hoffman, W. Joiner, K. Nehrke, O. Potapova, K. Foye, and A. Wickrema The hSK4 (KCNN4) isoform is the Ca2+-activated K+ channel (Gardos channel) in human red blood cells PNAS, June 10, 2003; 100(12): 7366 - 7371. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. S. L. Faber and P. Sah Calcium-Activated Potassium Channels: Multiple Contributions to Neuronal Function Neuroscientist, June 1, 2003; 9(3): 181 - 194. [Abstract] [PDF]
|
|
|
|
 |
|
 K A Bowley, M J Morton, M Hunter, and G I Sandle Non-genomic regulation of intermediate conductance potassium channels by aldosterone in human colonic crypt cells Gut, June 1, 2003; 52(6): 854 - 860. [Abstract] [Full Text]
|
|
|
|
|
|
C. A. Syme, K. L. Hamilton, H. M. Jones, A. C. Gerlach, L. Giltinan, G. D. Papworth, S. C. Watkins, N. A. Bradbury, and D. C. Devor Trafficking of the Ca2+-activated K+ Channel, hIK1, Is Dependent upon a C-terminal Leucine Zipper J. Biol. Chem., February 28, 2003; 278(10): 8476 - 8486. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. A. Castle, D. O. London, C. Creech, Z. Fajloun, J. W. Stocker, and J.-M. Sabatier Maurotoxin: A Potent Inhibitor of Intermediate Conductance Ca2+-Activated Potassium Channels Mol. Pharmacol., February 1, 2003; 63(2): 409 - 418. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Nehrke, C. C. Quinn, and T. Begenisich Molecular identification of Ca2+-activated K+ channels in parotid acinar cells Am J Physiol Cell Physiol, February 1, 2003; 284(2): C535 - C546. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Koegel, S. Kaesler, R. Burgstahler, S. Werner, and C. Alzheimer Unexpected Down-regulation of the hIK1 Ca2+-activated K+ Channel by Its Opener 1-Ethyl-2-benzimidazolinone in HaCaT Keratinocytes. INVERSE EFFECTS ON CELL GROWTH AND PROLIFERATION J. Biol. Chem., January 24, 2003; 278(5): 3323 - 3330. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Takahata, M. Hayashi, and T. Ishikawa SK4/IK1-like channels mediate TEA-insensitive, Ca2+-activated K+ currents in bovine parotid acinar cells Am J Physiol Cell Physiol, January 1, 2003; 284(1): C127 - C144. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Q.-H. Liu, B. K. Fleischmann, B. Hondowicz, C. C. Maier, L. A. Turka, K. Yui, M. I. Kotlikoff, A. D. Wells, and B. D. Freedman Modulation of Kv Channel Expression and Function by TCR and Costimulatory Signals during Peripheral CD4+ Lymphocyte Differentiation J. Exp. Med., October 7, 2002; 196(7): 897 - 909. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Simoes, L. Garneau, H. Klein, U. Banderali, F. Hobeila, B. Roux, L. Parent, and R. Sauve Cysteine Mutagenesis and Computer Modeling of the S6 Region of an Intermediate Conductance IKCa Channel J. Gen. Physiol., June 24, 2002; 120(1): 99 - 116. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. H. Clarson, V. H. J. Roberts, S. L. Greenwood, and A. C. Elliott ATP-stimulated Ca2+-activated K+ efflux pathway and differentiation of human placental cytotrophoblast cells Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2002; 282(4): R1077 - R1085. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. A Cowley and P. Linsdell Characterization of basolateral K+ channels underlying anion secretion in the human airway cell line Calu-3 J. Physiol., February 1, 2002; 538(3): 747 - 757. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Ayabe, H. Wulff, D. Darmoul, M. D. Cahalan, K. G. Chandy, and A. J. Ouellette Modulation of Mouse Paneth Cell alpha -Defensin Secretion by mIKCa1, a Ca2+-activated, Intermediate Conductance Potassium Channel J. Biol. Chem., January 25, 2002; 277(5): 3793 - 3800. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Kunzelmann and M. Mall Electrolyte Transport in the Mammalian Colon: Mechanisms and Implications for Disease Physiol Rev, January 1, 2002; 82(1): 245 - 289. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. G. Shakkottai, I. Regaya, H. Wulff, Z. Fajloun, H. Tomita, M. Fathallah, M. D. Cahalan, J. J. Gargus, J.-M. Sabatier, and K. G. Chandy Design and Characterization of a Highly Selective Peptide Inhibitor of the Small Conductance Calcium-activated K+ Channel, SkCa2 J. Biol. Chem., November 9, 2001; 276(46): 43145 - 43151. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. M. Duffy, W. J. Lawley, E. C. Conley, and P. Bradding Resting and Activation-Dependent Ion Channels in Human Mast Cells J. Immunol., October 15, 2001; 167(8): 4261 - 4270. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Hosseini, D. C H Benton, P. M Dunn, D. H Jenkinson, and G. W J Moss SK3 is an important component of K+ channels mediating the afterhyperpolarization in cultured rat SCG neurones J. Physiol., September 1, 2001; 535(2): 323 - 334. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Khanna, L. Roy, X. Zhu, and L. C. Schlichter K+ channels and the microglial respiratory burst Am J Physiol Cell Physiol, April 1, 2001; 280(4): C796 - C806. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C.-C. Shieh, M. Coghlan, J. P. Sullivan, and M. Gopalakrishnan Potassium Channels: Molecular Defects, Diseases, and Therapeutic Opportunities Pharmacol. Rev., December 1, 2000; 52(4): 557 - 594. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Kohler, C. Degenhardt, M. Kuhn, N. Runkel, M. Paul, and J. Hoyer Expression and Function of Endothelial Ca2+-Activated K+ Channels in Human Mesenteric Artery : A Single-Cell Reverse Transcriptase-Polymerase Chain Reaction and Electrophysiological Study In Situ Circ. Res., September 15, 2000; 87(6): 496 - 503. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Steinmetz, S. Bierer, P. Hollah, K. H. Rahn, and E. Schlatter Heterogenous Vascular Effects of AP5A in Different Rat Resistance Arteries Are Due to Heterogenous Distribution of P2X and P2Y1 Purinoceptors J. Pharmacol. Exp. Ther., September 1, 2000; 294(3): 1182 - 1187. [Abstract] [Full Text]
|
|
|
|
|
|
H. Wulff, M. J. Miller, W. Hansel, S. Grissmer, M. D. Cahalan, and K. G. Chandy Design of a potent and selective inhibitor of the intermediate-conductance Ca2+-activated K+ channel, IKCa1: A potential immunosuppressant PNAS, July 5, 2000; 97(14): 8151 - 8156. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. L. Pena, S. H. Chen, S. F. Konieczny, and S. G. Rane Ras/MEK/ERK Up-regulation of the Fibroblast KCa Channel FIK Is a Common Mechanism for Basic Fibroblast Growth Factor and Transforming Growth Factor-beta Suppression of Myogenesis J. Biol. Chem., April 28, 2000; 275(18): 13677 - 13682. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. A. Syme, A. C. Gerlach, A. K. Singh, and D. C. Devor Pharmacological activation of cloned intermediate- and small-conductance Ca2+-activated K+ channels Am J Physiol Cell Physiol, March 1, 2000; 278(3): C570 - C581. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. M. Fanger, A. L. Neben, and M. D. Cahalan Differential Ca2+ Influx, KCa Channel Activity, and Ca2+ Clearance Distinguish Th1 and Th2 Lymphocytes J. Immunol., February 1, 2000; 164(3): 1153 - 1160. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Rauer, M. D. Lanigan, M. W. Pennington, J. Aiyar, S. Ghanshani, M. D. Cahalan, R. S. Norton, and K. G. Chandy Structure-guided Transformation of Charybdotoxin Yields an Analog That Selectively Targets Ca2+-activated over Voltage-gated K+ Channels J. Biol. Chem., January 14, 2000; 275(2): 1201 - 1208. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. C. Gerlach, N. N. Gangopadhyay, and D. C. Devor Kinase-dependent Regulation of the Intermediate Conductance, Calcium-dependent Potassium Channel, hIK1 J. Biol. Chem., January 7, 2000; 275(1): 585 - 598. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. B. Neylon, R. J. Lang, Y. Fu, A. Bobik, and P. H. Reinhart Molecular Cloning and Characterization of the Intermediate-Conductance Ca2+-Activated K+ Channel in Vascular Smooth Muscle : Relationship Between KCa Channel Diversity and Smooth Muscle Cell Function Circ. Res., October 29, 1999; 85 (9): e33 - e43. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Lehmann-Horn and K. Jurkat-Rott Voltage-Gated Ion Channels and Hereditary Disease Physiol Rev, October 1, 1999; 79(4): 1317 - 1372. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. S. Jensen, N. Odum, N. K. Jorgensen, P. Christophersen, and S.-P. Olesen Inhibition of T cell proliferation by selective block of Ca2+-activated K+ channels PNAS, September 14, 1999; 96(19): 10917 - 10921. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Rauer, M. Pennington, M. Cahalan, and K. G. Chandy Structural Conservation of the Pores of Calcium-activated and Voltage-gated Potassium Channels Determined by a Sea Anemone Toxin J. Biol. Chem., July 30, 1999; 274(31): 21885 - 21892. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Khanna, M. C. Chang, W. J. Joiner, L. K. Kaczmarek, and L. C. Schlichter hSK4/hIK1, a Calmodulin-binding KCa Channel in Human T Lymphocytes. ROLES IN PROLIFERATION AND VOLUME REGULATION J. Biol. Chem., May 21, 1999; 274(21): 14838 - 14849. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
O. Zegarra-Moran, A. Rasola, M. Rugolo, A. M. Porcelli, B. Rossi, and L. J. V. Galietta HIV-1 Nef Expression Inhibits the Activity of a Ca2+-Dependent K+ Channel Involved in the Control of the Resting Potential in CEM Lymphocytes J. Immunol., May 1, 1999; 162(9): 5359 - 5366. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. G. Gallagher and B. D. Smith Dehydrated Hereditary Stomatocytosis Is Not Linked to the hIK1 Locus, a Gardos Channel Candidate, on Chromosome 19q13.2 Blood, March 15, 1999; 93(6): 2134 - 2135. [Full Text] [PDF]
|
|
|
|
|
|
C. M. Fanger, S. Ghanshani, N. J. Logsdon, H. Rauer, K. Kalman, J. Zhou, K. Beckingham, K. G. Chandy, M. D. Cahalan, and J. Aiyar Calmodulin Mediates Calcium-dependent Activation of the Intermediate Conductance Channel, IKCa1 J. Biol. Chem., February 26, 1999; 274(9): 5746 - 5754. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. R. Ehring, H. H. Kerschbaum, C. Eder, A. L. Neben, C. M. Fanger, R. M. Khoury, P. A. Negulescu, and M. D. Cahalan A Nongenomic Mechanism for Progesterone-mediated Immunosuppression: Inhibition of K+ Channels, Ca2+ Signaling, and Gene Expression in T Lymphocytes J. Exp. Med., November 2, 1998; 188(9): 1593 - 1602. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. S. Jensen, D. Strobak, P. Christophersen, T. D. Jorgensen, C. Hansen, A. Silahtaroglu, S.-P. Olesen, and P. K. Ahring Characterization of the cloned human intermediate-conductance Ca2+-activated K+ channel Am J Physiol Cell Physiol, September 1, 1998; 275(3): C848 - C856. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. H. Vandorpe, B. E. Shmukler, L. Jiang, B. Lim, J. Maylie, J. P. Adelman, L. de Franceschi, M. D. Cappellini, C. Brugnara, and S. L. Alper cDNA Cloning and Functional Characterization of the Mouse Ca2+-gated K+ Channel, mIK1. ROLES IN REGULATORY VOLUME DECREASE AND ERYTHROID DIFFERENTIATION J. Biol. Chem., August 21, 1998; 273(34): 21542 - 21553. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Desai, A. Peretz, H. Idelson, P. Lazarovici, and B. Attali Ca2+-activated K+ Channels in Human Leukemic Jurkat T Cells. MOLECULAR CLONING, BIOCHEMICAL AND FUNCTIONAL CHARACTERIZATION J. Biol. Chem., December 15, 2000; 275(51): 39954 - 39963. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Ghanshani, H. Wulff, M. J. Miller, H. Rohm, A. Neben, G. A. Gutman, M. D. Cahalan, and K. G. Chandy Up-regulation of the IKCa1 Potassium Channel during T-cell Activation. MOLECULAR MECHANISM AND FUNCTIONAL CONSEQUENCES J. Biol. Chem., November 17, 2000; 275(47): 37137 - 37149. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Pedarzani, J. Mosbacher, A. Rivard, L. A. Cingolani, D. Oliver, M. Stocker, J. P. Adelman, and B. Fakler Control of Electrical Activity in Central Neurons by Modulating the Gating of Small Conductance Ca2+-activated K+ Channels J. Biol. Chem., March 23, 2001; 276(13): 9762 - 9769. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. M. Fanger, H. Rauer, A. L. Neben, M. J. Miller, H. Rauer, H. Wulff, J. C. Rosa, C. R. Ganellin, K. G. Chandy, and M. D. Cahalan Calcium-activated Potassium Channels Sustain Calcium Signaling in T Lymphocytes. SELECTIVE BLOCKERS AND MANIPULATED CHANNEL EXPRESSION LEVELS J. Biol. Chem., April 6, 2001; 276(15): 12249 - 12256. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W. J. Joiner, R. Khanna, L. C. Schlichter, and L. K. Kaczmarek Calmodulin Regulates Assembly and Trafficking of SK4/IK1 Ca2+-activated K+ Channels J. Biol. Chem., October 5, 2001; 276(41): 37980 - 37985. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Wulff, G. A. Gutman, M. D. Cahalan, and K. G. Chandy Delineation of the Clotrimazole/TRAM-34 Binding Site on the Intermediate Conductance Calcium-activated Potassium Channel, IKCa1 J. Biol. Chem., August 17, 2001; 276(34): 32040 - 32045. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Q.-H. Liu, D. A. Williams, C. McManus, F. Baribaud, R. W. Doms, D. Schols, E. De Clercq, M. I. Kotlikoff, R. G. Collman, and B. D. Freedman HIV-1 gp120 and chemokines activate ion channels in primary macrophages through CCR5 and CXCR4 stimulation PNAS, April 25, 2000; 97(9): 4832 - 4837. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. Cowley and P. Linsdell Characterization of basolateral K+ channels underlying anion secretion in the human airway cell line Calu-3 J. Physiol., December 19, 2001; (2001) 200101330. [Abstract] [PDF]
|
|
|
|
|
|
R. Kohler, S. Brakemeier, M. Kuhn, C. Behrens, R. Real, C. Degenhardt, H.-D. Orzechowski, A. R. Pries, M. Paul, and J. Hoyer Impaired Hyperpolarization in Regenerated Endothelium After Balloon Catheter Injury Circ. Res., July 20, 2001; 89(2): 174 - 179. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| All ASBMB Journals | Molecular and Cellular Proteomics |
| Journal of Lipid Research | ASBMB Today |