Orfali, ODonovan, Nyhan, Britschgi, Tschan, Cahill, Mongan, Gudas, McKenna: "Induction of autophagy is a key component of all-trans-retinoic acid-induced differentiation in leukemia cells and a potential target for pharmacologic modulation." in: Experimental hematology, Vol. 43, Issue 9, pp. 781-93.e2, (2015) (PubMed).
GABARAPL2 antikoerper, atg8 antikoerper, gef2 antikoerper, gate16 antikoerper, gate-16 antikoerper, Gef2 antikoerper, ATG8 antikoerper, ATG8C antikoerper, GATE-16 antikoerper, GATE16 antikoerper, GEF-2 antikoerper, GEF2 antikoerper, zgc:92319 antikoerper, 0610012F20Rik antikoerper, 2900019O08Rik antikoerper, AI173605 antikoerper, GABA type A receptor associated protein like 2 antikoerper, GABA(A) receptor-associated protein like 2 antikoerper, GABA(A) receptor-associated protein like 2 L homeolog antikoerper, gamma-aminobutyric acid (GABA) A receptor-associated protein-like 2 antikoerper, GABARAPL2 antikoerper, gabarapl2 antikoerper, Gabarapl2 antikoerper, gabarapl2.L antikoerper
Hintergrund
Membrane proteins located on vesicles (v-SNAREs) and on the target membrane (t-SNAREs) mediate specific recognition and, possibly, fusion between a transport vesicle and its target membrane. The activity of SNARE molecules is regulated by several soluble cytosolic proteins. We have cloned a bovine brain cDNA encoding a conserved 117 amino acid polypeptide, denoted Golgi-associated ATPase Enhancer of 16 kDa (GATE-16), that functions as a soluble transport factor. GATE-16 interacts with N-ethylmaleimidesensitive factor (NSF) and significantly stimulates its ATPase activity. It also interacts with the Golgi v-SNARE GOS-28 in an NSF-dependent manner. We propose that GATE-16 modulates intra-Golgi transport through coupling between NSF activity and SNAREs activation.