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035			_a(RuTPU)RU\TPU\network\3544
071	6	0	_a10.1161/circresaha.107.156463
090			_a639140
100			_a20150224a2007 k y0engy50 ba
101	0		_aeng
135			_adrcn ---uucaa
181		0	_ai
182		0	_ab
200	1		_aAbl silencing inhibits CAS-Mediated process and constriction in resistance arteries _fYa. J. Anfinogenova [et al.]
203			_aText _celectronic
300			_aTitle screen
320			_a[References: 44 tit.]
330			_aThe tyrosine phosphorylated protein Crk-associated substrate (CAS) has previously been shown to participate in the cellular processes regulating dynamic changes in the actin architecture and arterial constriction. In the present study, treatment of rat mesenteric arteries with phenylephrine (PE) led to the increase in CAS tyrosine phosphorylation and the association of CAS with the adapter protein CrkII. CAS phosphorylation was catalyzed by Abl in an in vitro study. To determine the role of Abl tyrosine kinase in arterial vessels, plasmids encoding Abl short hairpin RNA (shRNA) were transduced into mesenteric arteries by chemical loading plus liposomes. Abl silencing diminished increases in CAS phosphorylation on PE stimulation. Previous studies have shown that assembly of the multiprotein compound containing CrkII, neuronal Wiskott–Aldrich Syndrome Protein (N-WASP) and the Arp2/3 (Actin Related Protein) complex triggers actin polymerization in smooth muscle as well as in nonmuscle cells. In this study, Abl silencing attenuated the assembly of the multiprotein compound in resistance arteries on contractile stimulation. Furthermore, the increase in F/G-actin ratios (an index of actin assembly) and constriction on contractile stimulation were reduced in Abl-deficient arterial segments compared with control arteries. However, myosin regulatory light chain phosphorylation (MRLCP) elicited by contractile activation was not inhibited in Abl-deficient arteries. These results suggest that Abl may play a pivotal role in mediating CAS phosphorylation, the assembly of the multiprotein complex, actin assembly, and constriction in resistance arteries. Abl does not participate in the regulation of myosin activation in arterial vessels during contractile stimulation.
461			_tCirculation Research
463			_tVol. 101, iss. 4 _v[P. 420–428] _d2007
610	1		_aэлектронный ресурс
610	1		_aтруды учёных ТПУ
610	1		_atyrosine kinase
610	1		_atyrosine kinase
610	1		_acontraction
610	1		_avascular smooth muscle
610	1		_aadapter protein
701		1	_aAnfinogenova _bYa. J. _cmedic _cLecturer of Tomsk Polytechnic University, Doctor of medical sciences _f1970- _gYana Jonovna _2stltpush _3(RuTPU)RU\TPU\pers\33592
701		0	_aRuping Wang
701		0	_aQing-fen Li
701		1	_aSpinelli _bA. M.
701		1	_aTang _bD. D.
801		2	_aRU _b63413507 _c20150317 _gRCR
856	4		_uhttp://circres.ahajournals.org/content/101/4/420.short
942			_cCF