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RESEARCH
INTERESTS:
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Established in 1993, my lab is interested in
the regulation and structure-function
relationships of contractile and
cytoskeleton proteins.
Muscle (cardiac, skeletal and smooth)
contraction and non-muscle cell motility
play vital roles in physiological activities
and pathological conditions. Our research is
focused on actin thin filament-associated
regulatory proteins: troponin and calponin,
to study their regulation and
structure-function relationships. Molecular
biology and genetic approaches are used to
investigate protein isoform evolution and
expression as well as to provide engineered
protein constructs for functional
characterization. Biochemical, biophysical
and immunochemical methods are used in
studying protein structure and function.
Cell culture systems and transgenic/gene
knock-out/knock-in mouse models are
developed for integrative functional
characterizations at cellular, organ and
whole animal levels. |
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ONGOING PROJECTS:
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Regulation and function of troponin T
isoforms:
Biochemical and biophysical studies are
performed to investigate the functional
significance of various troponin T isoforms
in the Ca2+-regulation of cardiac
and skeletal muscle contraction and
diseases. The studies are focused on the
abnormal cardiac troponin T splicing
variants found in dilated cardiomyopathy and
a slow skeletal muscle troponin T mutation
that causes a lethal type of nemaline
myopathy. This line of study is currently
funded by NIH grants R01HL078773 and
R01AR048816. |
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Post-translational regulation of troponin
during muscle adaptation and diseases:
Proteolytic modification of troponin I and
troponin T is studied for functional
significance and therapeutic values in the
Ca2+-regulation of myocardial
contraction in adaptation to hemodynamic
stresses, myocardial ischemia-reperfusion
injury, heart failure, and skeletal muscle
fatigue. This line of study is currently
funded by NIH grant R01HL098945 and a Group
Incubator Grant from WSU Office of Vice
President for Research. |
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Mechanical tension regulation and function
of calponin:
To study calponin's function as a troponin
analog in smooth muscle and non-muscle
cells, we are investigating their role in
the fine-tuning of smooth muscle
contractility, non-muscle motility, and the
function of actin cytoskeleton during
development, tissue remodeling and
cytokinesis. The study is focused on
mechanical tension regulated calponin gene
expression and protein degradation in
epithelial, endothelial, fibroblast,
macrophages and smooth muscle cells. This
line of study is currently funded by NIH
grant R01HL086720. |
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SELECTED
PUBLICATIONS
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A complete list of Dr. Jin's publications can be
found at
PubMed-Jin
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Barbato, J.C., Huang, Q.-Q., Hossain, M.M.,
Bond, M., and Jin, J.-P. (2005)
Proteolytic N-Terminal Truncation of Cardiac
Troponin I Facilitates Ventricular
Relaxation and Enhances Heart Function.
J. Biol. Chem.
280:6602-6609. |
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Wang, X., Huang, Q.-Q. Breckenridge, M.T.,
Chen, A., Crawford, T.O., Morton, D.H.,
and Jin, J.-P. (2005) Cellular fate
of truncated slow skeletal muscle troponin T
produced by Glu180 nonsense
mutation in Amish nemaline myopathy.
J. Biol. Chem. 280:13241-13249.
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Hossain, M.M., Crish, J.F., Eckert R.L.,
Lin, J.J.-C., and Jin, J.-P. (2005)
H2-calponin is regulated by mechanical
tension and modifies the function of actin
cytoskeleton.
J. Biol. Chem.
280:42442-53. |
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Brotto, M.A.P. Biesiadecki, B.J.
Brotto, L.S., Nosek T.M. and.
Jin, J.-P. (2006) Coupled Expression of
Troponin T and Troponin I Isoforms in Single
Skeletal Muscle Fibers Correlating to
Contractility. Am. J. Physiol. Cell
Physiol. 290:C567-C576. |
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Zhang, Z., Biesiadecki, B.J., and Jin,
J.-P. (2006) Selective removal
of the N-terminal variable region of cardiac
troponin T in ischemia-reperfusion by
myofibril-associated
m-calpain
cleavage. Biochemistry
45:11681-94. |
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Hossain, M.M., Smith, P.G., Wu, K., and
Jin, J.-P. (2006) Cytoskeletal tension
regulates both expression and degradation of
h2-calponin in lung alveolar cells.
Biochemistry 45:15670-83. |
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Yu, Z.-B., Gao, F., Feng, H., and Jin,
J.-P. (2007) Differential regulation of
myofilament protein isoforms underlying the
contractility changes in skeletal muscle
unloading. Am. J. Physiol.:Cell
Physiol.,
292:C1192-203. |
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Biesiadecki, B., Chong, S.M., Nosek T.M.,
and Jin, J.-P. (2007) Troponin T Core
Structure and the Regulatory NH2-Terminal
Variable Region.
Biochemistry
46:1368-1379. |
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Jin, J.-P.,
Zhang, Z., and Bautista, J.A. (2007) Isoform
diversity, regulation and functional
adaptations of troponin and calponin.
Crit. Rev. in Eukar Gene Expr.
18:93-124 (invited review). |
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Huang, Q.-Q. Feng, H.-Z., Liu, J., Du, J.,
Stull, L.B., Moravec, C., Huang, X. and
Jin, J.-P. (2008) Co-expression of
skeletal and cardiac troponin T decreases
mouse cardiac function. Am J,
Physiol.:Cell Physiol. 294:C213-222.
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Feng, H.-Z., Biesiadecki, B.J., Yu, Z.-B.,
Hossain, M.M., and Jin,
J.-P.
(2008) Restricted N-terminal truncation of
cardiac troponin T: A novel mechanism for
functional adaptation to energetic crisis.
J. Physiol. (London)
586:3537-3550. |
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Wu, K., and Jin, J.-P. (2008)
Calponin in non-muscle cells. Cell
Biochem. Biophys. 52:139-148.
(invited review) |
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Larsson,, L., Wang, X., Yu, F.,
Höök, P., Borg, K., Chong, SM, and Jin
J.-P.
(2008) Adaptation by alternative RNA
splicing of slow troponin T isoforms in type
1 but not type 2 Charcot-Marie-Tooth
disease. Am. J. Physiol. Cell Physiol.
295:C722-31. |
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Huang, Q.-Q., Hossain, M.M., Wu, K., Parai.,
K., Pope, R.M., and Jin, J.-P. (2008)
Role of h2-calponin in regulating macrophage
motility and phagocytosis. J. Biol.
Chem. 283:25887-99. |
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Feng, H.-Z., Chen, M.,
Weinstein, L.S. and Jin, J.-P. (2008)
Removal of the N-terminal extension of
cardiac troponin I as a functional
compensation for myocardial
b-adrenergic
deficiency.
J. Biol. Chem.
283:33384-93. |
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Chong, S.M., and Jin, J.-P. (2009) To
Investigate Protein Evolution by Detecting
Suppressed Epitope Structures.
J. Mol. Evol.
68:448-60. |
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Jeong, E., Wang, X., Xu, K., Hossain, M.M.,
and Jin, J.-P. (2009)
Non-myofilament-associated troponin T
fragments induce apoptosis.
Am. J. Physiol. Heart Circ. Physiol.
297:H283-92. |
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Feng, H.-Z., Wei, B., and Jin, J.-P.
(2009)
Deletion of a genomic segment containing the
cardiac troponin I gene knocked down the
expression of slow troponin T gene and
impaired fatigue tolerance of diaphragm
muscle.
J. Biol. Chem.
284:31798–31806. |
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Feng, H.-Z. and Jin, J.-P. (2010)
Non-uniformity of Cardiac Troponin T Impairs
Heart Efficiency.
Am. J. Physiol. Heart Circ. Physiol.
299:H97-H105 |
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Wei, B., Gao, J., Huang, X.-P., and Jin,
J.-P. (2010) Mutual rescues between two
dominant-negative mutations in cardiac
troponin I and cardiac troponin T.
J. Biol. Chem.
285:27806-16. |
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Wei, B., and Jin, J.-P. (2011)
Troponin T Isoforms and Posttranscriptional
Modifications: Evolution, Regulation and
Function.
Arch Biochem Biophy.
505:144-154. (invited review) |
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Feng, H.-Z., Chen, M., Weinstein, L.S., and
Jin, J.-P. (2011) Fast-to-slow fiber
type switch increases fatigue resistance as
a compensatory adaptation in Gsa-deficient
soleus muscle. J Appl. Physiol.
111:834-843. |
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Zhang, Z., Akhter, S., Mottl S., and Jin,
J.-P. (2011) Ca2+-regulated
conformational change in the COOH terminus
of troponin I and binding to tropomyosin.
FEBS J.
278:3348-3359. |
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Zhang, Z., Feng, H.-Z., Jin, J.-P. (2011)
Structure of the NH(2)-terminal variable
region of cardiac troponin T determines its
sensitivity to restrictive cleavage in
pathophysiological adaptation.
Arch Biochem Biophys.
515:37-45. |
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