Výsledky vyhledávání - "Brenda, Litchie"

Transactivation of the Insulin-Like Growth Factor-I Receptor by Angiotensin II Mediates Downstream Signaling from the Angiotensin II Type 1 Receptor to Phosphatidylinositol 3-Kinase

Autor: Ben Storie, Brenda Litchie, Peter Zahradka, Gail Helwer

Publikováno v: Endocrinology. 145:2978-2987

Angiotensin II (AngII) activates phosphatidylinositol 3-kinase (PI3-kinase), a known effector of receptor tyrosine kinases. Treatment of smooth muscle cells with AngII has also been shown to promote phosphorylation of various tyrosine kinase receptor

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e2f16f6d919ae1f399d6f0d08918b2ef
https://doi.org/10.1210/en.2004-0029

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Endogenous mono-ADP-ribosylation mediates smooth muscle cell proliferation and migration via protein kinase N-dependent induction of c-fos expression

Autor: Shawn Thomas, Peter Zahradka, Natalia Yurkova, Lorraine Yau, Brenda Litchie, Benjamin Storie

Publikováno v: European Journal of Biochemistry. 270:101-110

ADP-ribosylation has been coupled to intracellular events associated with smooth muscle cell vasoreactivity, cytoskeletal integrity and free radical damage. Additionally, there is evidence that ADP-ribosylation is required for smooth muscle cell prol

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_________::727ee0eaab2a05d2bfb2281451b38043
https://doi.org/10.1046/j.1432-1033.2003.03366.x

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Activation of MMP-2 in response to vascular injury is mediated by phosphatidylinositol 3-kinase-dependent expression of MT1-MMP

Autor: Brenda Litchie, Shawn Thomas, David Wilson, Jeffrey P. Werner, Peter Zahradka, Greg Harding, Natalia Yurkova

Publikováno v: American journal of physiology. Heart and circulatory physiology. 287(6)

Phosphatidylinositol 3-kinase (PI3K) is required for smooth muscle cell (SMC) proliferation. This study reports that inhibitors of PI3K also prevent SMC migration and block neointimal hyperplasia in an organ culture model of restenosis. Inhibition of

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::bd09825c354b2f27f851561ceb51a551
https://pubmed.ncbi.nlm.nih.gov/15297252

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MIBG, an inhibitor of arginine-dependent mono(ADP-ribosyl)ation, prevents differentiation of L6 skeletal myoblasts by inhibiting expression of myogenin and p21(cip1)

Autor: Peter Zahradka, Brenda Litchie, Lorraine Yau

Publikováno v: Experimental cell research. 301(2)

The development of skeletal muscle is controlled by a highly synchronized series of cellular events, and various signals from both inside and outside the cell play a role in the switch from multipotential mesodermal stem cells to muscle fibers. Meta-

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6461e65a8d7eeb7166dcbadb6a8b773e
https://pubmed.ncbi.nlm.nih.gov/15530866

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Activation of peroxisome proliferator-activated receptors alpha and gamma1 inhibits human smooth muscle cell proliferation

Autor: Peter, Zahradka, Natalia, Yurkova, Brenda, Litchie, Michael C, Moon, Dario F, Del Rizzo, Carla G, Taylor

Publikováno v: Molecular and cellular biochemistry. 246(1-2)

Atherosclerotic lesions occur as a result of excess lipid deposition within the vascular tissues. The peroxisome proliferator-activated receptors (PPARs) present in adipose and hepatic tissues have been shown to promote fatty acid oxidation and lipid

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=pmid________::528fa1d1490e694c4d25b96b0ca8474f
https://pubmed.ncbi.nlm.nih.gov/12841350

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Activation of peroxisome proliferator-activated receptors α and γ1 inhibits human smooth muscle cell proliferation

Autor: Natalia Yurkova, Peter Zahradka, Carla G. Taylor, Michael C. Moon, Dario F. Del Rizzo, Brenda Litchie

Publikováno v: Vascular Biochemistry ISBN: 9781461350101

Atherosclerotic lesions occur as a result of excess lipid deposition within the vascular tissues. The peroxisome proliferatoractivated receptors (PPARs) present in adipose and hepatic tissues have been shown to promote fatty acid oxidation and lipid

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_________::5dd0d00beb2ed7e111fc01dc33f4bb92
https://doi.org/10.1007/978-1-4615-0298-2_15

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NF-kappaB activation is essential for angiotensin II-dependent proliferation and migration of vascular smooth muscle cells

Autor: Jeffrey P. Werner, Peter Zahradka, Brenda Litchie, Gail Helwer, Shawn Thomas, Shelly Buhay

Publikováno v: Journal of molecular and cellular cardiology. 34(12)

Angiotensin II (AngII) functions as a stress hormone under conditions of stretch, pressure and injury to stimulate smooth muscle cell migration and proliferation. Since the cellular response to stress is mediated in part by the transcription factor N

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3ed87b504fad54db2a4d1b13161017fb
https://pubmed.ncbi.nlm.nih.gov/12505059

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Endogenous mono-ADP-ribosylation mediates smooth muscle cell proliferation and migration via protein kinase N-dependent induction of c-fos expression

Autor: Lorraine, Yau, Brenda, Litchie, Shawn, Thomas, Benjamin, Storie, Natalia, Yurkova, Peter, Zahradka

Publikováno v: European journal of biochemistry. 270(1)

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=pmid________::bbea5308829d053e760ca250f169c246
https://pubmed.ncbi.nlm.nih.gov/12492480

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Platelet-derived growth factor-induced expression of c-fos in human vascular smooth muscle cells: implications for long-term graft patency

Autor: Natalia Yurkova, Brenda Litchie, Dario F. Del Rizzo, Michael C. Moon, Peter Zahradka

Publikováno v: The Annals of thoracic surgery. 74(1)

Background . The internal mammary artery (IMA) has been shown to have a significantly superior long-term patency rate when compared with the saphenous vein (SV) graft. Cultured smooth muscle cells (SMCs) from the IMA are more resistant to the mitogen

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::fad6b3af74c70a5761191b872e7147ac
https://pubmed.ncbi.nlm.nih.gov/12118809

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