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Seema Mohamed

Researcher at Albany College of Pharmacy and Health Sciences

Publications -  17
Citations -  1399

Seema Mohamed is an academic researcher from Albany College of Pharmacy and Health Sciences. The author has contributed to research in topics: Angiogenesis & Tube formation. The author has an hindex of 12, co-authored 17 publications receiving 1315 citations. Previous affiliations of Seema Mohamed include Wilmington University & DuPont.

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Integrin alphaVbeta3 contains a cell surface receptor site for thyroid hormone that is linked to activation of mitogen-activated protein kinase and induction of angiogenesis.

TL;DR: It is suggested that T(4) binds to alpha(V)beta(3) near the RGD recognition site and show that hormone-binding to alpha (V) beta(3), a cell surface receptor for thyroid hormone, has physiological consequences.
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Proangiogenic Action of Thyroid Hormone Is Fibroblast Growth Factor–Dependent and Is Initiated at the Cell Surface

TL;DR: Thyroid hormone is shown to be a proangiogenic factor, initiated at the plasma membrane, is MAPK dependent and mediated by FGF2.
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Novel small molecule alpha v integrin antagonists: comparative anti-cancer efficacy with known angiogenesis inhibitors.

TL;DR: It is demonstrated that potent selective av antagonist can target endothelial cells, tumor cells, inhibit angiogenesis and inhibit tumor growth and the apoptotic index increased significantly in the SM256 and SG545-treated groups, suggesting increased cell death contributed to decreased tumor volumes.
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Inhibition of endothelial cell tube formation by the low molecular weight heparin, tinzaparin, is mediated by tissue factor pathway inhibitor.

TL;DR: The results suggest that the inhibitory effect of the LMWH tinzaparin on endothelial tube formation is associated with stimulation of the release of TFPI, but not to anti-Factor Xa activity.
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Anti-angiogenic mechanisms and efficacy of the low molecular weight heparin, tinzaparin: anti-cancer efficacy.

TL;DR: It is demonstrated that tinzaparin is a potent inhibitor of angiogenesis regardless of the angiogenic factor and suggest that its effect is mediated via cellular release of tissue factor pathway inhibitor (TFPI).