A
Abdullah Yalcin
Researcher at Uludağ University
Publications - 23
Citations - 1561
Abdullah Yalcin is an academic researcher from Uludağ University. The author has contributed to research in topics: Glycolysis & PFKFB4. The author has an hindex of 11, co-authored 23 publications receiving 1358 citations. Previous affiliations of Abdullah Yalcin include University of Louisville & Hacettepe University.
Papers
More filters
Journal ArticleDOI
Small-molecule inhibition of 6-phosphofructo-2-kinase activity suppresses glycolytic flux and tumor growth
Brian F. Clem,Sucheta Telang,Amy L. Clem,Abdullah Yalcin,Jason B. Meier,Alan Simmons,Mary Ann Rasku,Sengodagounder Arumugam,William L. Dean,John W. Eaton,Andrew N. Lane,John O. Trent,Jason Chesney +12 more
TL;DR: 3PO markedly attenuates the proliferation of several human malignant hematopoietic and adenocarcinoma cell lines and is selectively cytostatic to ras-transformed human bronchial epithelial cells relative to normal human bronachial epithel cells.
Journal ArticleDOI
Regulation of glucose metabolism by 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatases in cancer.
TL;DR: These studies suggest that selective depletion of intracellular F2,6BP in cancer cells may suppress glycolytic flux and decrease their survival, growth and invasiveness.
Journal ArticleDOI
Nuclear targeting of 6-phosphofructo-2-kinase (PFKFB3) increases proliferation via cyclin-dependent kinases.
Abdullah Yalcin,Abdullah Yalcin,Brian F. Clem,Alan Simmons,Andrew N. Lane,Kristin K. Nelson,Amy L. Clem,Erin Brock,Deanna Siow,Binks W. Wattenberg,Sucheta Telang,Jason Chesney +11 more
TL;DR: An unexpected role for PFKFB3 in nuclear signaling is demonstrated and it is indicated that Fru-2,6-BP may couple the activation of glucose metabolism with cell proliferation.
Journal ArticleDOI
Ras transformation requires metabolic control by 6-phosphofructo-2-kinase.
Sucheta Telang,Abdullah Yalcin,Amy L. Clem,Richard Bucala,Andrew N. Lane,John W. Eaton,Jason Chesney +6 more
TL;DR: Data indicate that the PFKFB3 protein product may serve as an essential downstream metabolic mediator of oncogenic ras, and it is proposed that pharmacologic inhibition of this enzyme should selectively suppress the high rate of glycolysis and growth by cancer cells.
Journal ArticleDOI
6-Phosphofructo-2-kinase (PFKFB3) promotes cell cycle progression and suppresses apoptosis via Cdk1-mediated phosphorylation of p27
Abdullah Yalcin,Abdullah Yalcin,Brian F. Clem,Yoannis Imbert-Fernandez,Selahattin C. Ozcan,Sabire Peker,Julie O'Neal,Alden C. Klarer,Amy L. Clem,Sucheta Telang,Jason Chesney +10 more
TL;DR: It is demonstrated that siRNA silencing of endogenous PFKFB3 inhibits Cdk1 activity, which in turn stabilizes p27 protein levels causing cell cycle arrest at G1/S and increased apoptosis in HeLa cells.