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Stem cell factor apoptosis protein

Q331S6] 2) Casein kinase-1 binding partner (CK1 BP) 3) Stem cell factor apoptosis response protein-1 (SCF ARP1), isoform a (55861) [15881]... [Pg.116]

Dysbindin-2B has been identified as both stem cell factor apoptosis response protein 1 (SCF ARP1) by Lucas et al. (2005) and as a casein kinase 1 binding partner (CK1BP) by Yin et al. (2006). SCF ARP1 is expressed in bone marrow-derived myelomonocytic stem cells upon induction of apoptosis by withdrawal of stem cell growth factor SCF (Lucas et al., 2005). Programmed cell death via apoptosis controls stem cell numbers during hematopoietic cell development (Domen 2001). Since apoptosis is similarly important in development of neurons (Kuan et al., 2000 Buss and Oppenheim, 2004), dysbindin-2B may play a role in nervous system development (see also Section 2.2.33.1). [Pg.125]

Further discussion of the dysbindin family is limited to dysbindin-1 since little is known about other family members apart from the fact that dysbindin-2B is a casein kinase 1 binding partner and a stem cell factor apoptosis response protein. In contrast, much has been learned about dysbindin-1 since its discovery was reported by Benson et al. (2001). It is the only member of the dysbindin family known to exist in invertebrates, specifically the fruit fly, and may thus date back 600 million years. Unlike all other dysbindin paralogs, it contains a coiled coil domain (CCD) allowing extensive interactions with other proteins. A leucine zipper motif in the CCD changed in the course of evolution in a manner permitting more durable interactions with binding partners. [Pg.218]

Yan W, Suominen J, Samson M, Jegou B, Toppari J. 2000. Involvement of Bcl-2 family proteins in germ cell apoptosis during testicular development in the rat and pro-survival effect of stem cell factor on germ cells in vitro. Mol. Cell Endocrinol. 165 115-29... [Pg.146]

Imatinib is a protein-tyrosine-kinase inhibitor. Imatinib inhibits proliferation and induces apoptosis in BCR-ABL positive cell lines as well as fresh leukemic cells from Philadelphia chromosome-positive (Ph-r) chronic myeloid leukemia (CML). Imatinib inhibits tumor growth of BCR-ABL transfected murine myeloid cells and BCR-ABL positive leukemia lines derived from CML patients in blast crisis. It also inhibits the receptor tyrosine kinases for platelet-derived growth factor (PDGF) and stem cell factor (SCF), c-Kit, and inhibits PDGF- and SCF-mediated cellular events. It is indicated in the treatment of newly diagnosed adult patients with Ph-t CML in chronic phase patients with Ph-t CML in blast crisis, accelerated phase, or in chronic phase after failure of interferon-alpha treatment children with Ph-t chronic phase CML whose disease has recurred after stem cell transplant or who are resistant to interferon-alpha therapy and treatment of gastrointestinal stromal tumors (GIST). [Pg.339]


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