RPMI 1640 Medium, no phenol red, 500 mL - Citations

RPMI 1640 Medium, no phenol red, 500 mL - Citations

View additional product information for RPMI 1640 Medium, no phenol red - Citations (11835030, 11835055)

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Citations & References
Abstract
Inhibition of both paracrine and autocrine VEGF/ VEGFR-2 signaling pathways is essential to induce long-term remission of xenotransplanted human leukemias.
Authors Dias S; Hattori K; Heissig B; Zhu Z; Wu Y; Witte L; Hicklin D J; Tateno M; Bohlen P; Moore M A; Rafii S;
JournalProc Natl Acad Sci U S A
PubMed ID11553814
'Antiangiogenic agents block the effects of tumor-derived angiogenic factors (paracrine factors), such as vascular endothelial growth factor (VEGF), on endothelial cells (EC), inhibiting the growth of solid tumors. However, whether inhibition of angiogenesis also may play a role in liquid tumors is not well established. We recently have shown that ... More
Regulation of neural differentiation by normal and mutant (G654A, amyloidogenic) gelsolin.
Authors Westberg J A; Zhang K Z; Andersson L C;
JournalFASEB J
PubMed ID10463954
'Gelsolin belongs to a family of proteins that modulate the structural dynamics of cytoskeletal actin. Gelsolin activity is required for the redistribution of actin occurring during membrane ruffling, cell crawling, and platelet activation. A point mutation (G654A) in the gelsolin gene causes a dominantly inherited systemic amyloidosis called familial amyloidosis ... More
Inhibition of mitochondrial respiration by endogenous nitric oxide: a critical step in Fas signaling.
Authors Beltrán Belén; Quintero Marisol; García-Zaragozá Eugenia; O'Connor Enrique; Esplugues Juan V; Moncada Salvador;
JournalProc Natl Acad Sci U S A
PubMed ID12077295
We have found that activation of human adult T cell leukemia (Jurkat) cells with anti-Fas Ab leads, in a concentration-dependent manner, to an early burst of production of nitric oxide (NO), which inhibits cell respiration. This results in mitochondrial hyperpolarization, dependent on the hydrolysis of glycolytic ATP by the F1F(o)-ATPase ... More