Wiley
0892-6638
1530-6860
Cơ quản chủ quản: John Wiley & Sons Inc. , WILEY
Lĩnh vực:
BiochemistryMedicine (miscellaneous)GeneticsBiotechnologyMolecular Biology
Các bài báo tiêu biểu
Expression of human collagenase-3 (MMP-13) by fetal skin fibroblasts is induced by transforming growth factor β via p38 mitogen-activated protein kinase
Tập 15 Số 6 - Trang 1098-1100 - 2001
Intramitochondrial hydrogen sulfide production by 3‐mercaptopyruvate sulfurtransferase maintains mitochondrial electron flow and supports cellular bioenergetics
Tập 27 Số 2 - Trang 601-611 - 2013
Mechanism of Ca<sub>v</sub>1.2 channel modulation by the amino terminus of cardiac β<sub>2</sub>‐subunits ABSTRACT L‐type calcium channels are composed of a pore, α1c (CaV 1.2), and accessory β‐ and α2 δ‐subunits. The β‐subunit core structure was recently resolved at high resolution, providing important information on many functional aspects of channel modulation. In this study we reveal differential novel effects of five ß2 ‐subunits isoforms expressed in human heart ( β 2a‐e ) on the single L‐type calcium channel current. These splice variants differ only by amino‐terminal length and amino acid composition. Single‐channel modulation by β2 ‐subunit isoforms was investigated in HEK293 cells expressing the recombinant L‐type ion conducting pore. All β2 ‐subunits increased open probability, availability, and peak current with a highly consistent rank order (ß2a ≈ ß2b >ß2e ≈ ß2c >ß2d ). We show graded modulation of some transition rates within and between deep‐closed and inactivated states. The extent of modulation correlates strongly with the length of amino‐terminal domains. Two mutant ß2 ‐subunits that imitate the natural span related to length confirm this conclusion. The data show that the length of amino termini is a relevant physiological mechanism for channel closure and inactivation, and that natural alternative splicing exploits this principle for modulation of the gating properties of calcium channels.—Herzig, S., Khan, I. F. Y., Gründemarin, D., Matthes, J., Ludwig, A., Michels, G., Hoppe, U. C., Chaudhuri, D., Schwartz, A., Yue, D. T., Hullin, R. Mechanism of Cav1.2 channel modulation by the amino terminus of cardiac ß2‐sub‐units. FASEB J. 21, 1527–1538 (2007)
Tập 21 Số 7 - Trang 1527-1538 - 2007
VEGF‐A promotes tissue repair‐associated lymphatic vessel formation via VEGFR‐2 and the α1β1 and α2β1 integrins ABSTRACT Vascular endothelial growth factor‐A (VEGF‐A) is strongly up‐regulated in wounded cutaneous tissue and promotes repair‐associated angiogenesis. However, little is known about its role in lymphatic regeneration of the healing skin. We studied wound healing in transgenic mice that overexpress VEGF‐A specifically in the epidermis and in wild‐type mice in the absence or presence of inhibitors of VEGF‐A signaling. Surprisingly, transgenic overexpression of VEGF‐A in the skin promoted lymphangiogenesis at the wound healing site, whereas systemic blockade of VEGFR‐2 prevented lymphatic vessel formation. Studies in cultured lymphatic endothelial cells revealed that VEGF‐A induced expression of the α1 and α2 integrins, which promoted their in vitro tube formation and their haptotactic migration toward type I collagen. VEGF‐A‐induced lymphatic endothelial cord formation and haptotactic migration were suppressed by anti‐α1 and anti‐α2 integrin blocking antibodies, and systemic blockade of the α1 and α2 integrins inhibited VEGF‐A‐driven lymphangiogenesis in vivo. We propose that VEGF‐A promotes lymphatic vasculature formation via activation of VEGFR‐2 and that lineage‐specific differences of integrin receptor expression contribute to the distinct dynamics of wound‐associated angiogenesis and lymphangiogenesis.
Tập 18 Số 10 - Trang 1111-1113 - 2004
Abnormal small heat shock protein interactions involving neuropathy‐associated HSP22 (HSPB8) mutants
Tập 20 Số 12 - Trang 2168-2170 - 2006
Cysteine/cystine couple is a newly recognized node in the circuitry for biologic redox signaling and control
Tập 18 Số 11 - Trang 1246-1248 - 2004