Anti-ITCH/AIP4 Antibody Picoband® Fluoro594 Conjugated

ITCH is an ubiquitin-conjugating enzyme. This gene encodes a member of the Nedd4 family of HECT domain E3 ubiquitin ligases. HECT domain E3 ubiquitin ligases transfer ubiquitin from E2 ubiquitin-conjugating enzymes to protein substrates, thus targeting specific proteins for lysosomal degradation. The encoded protein plays a role in multiple cellular processes including erythroid and lymphoid cell differentiation and the regulation of immune responses. Mutations in this gene are a cause of syndromic multisystem autoimmune disease. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene.

Receptor-type tyrosine-protein kinase FLT3; 2.7.10.1; FL cytokine receptor; Fetal liver kinase 2; FLK-2; Fms-like tyrosine kinase 3; FLT-3; Tyrosine-protein kinase receptor flk-2; CD135; Flt3; Flk-2, Flt-3

Tyrosine-protein kinase that acts as cell-surface receptor for the cytokine FLT3LG and regulates differentiation, proliferation and survival of hematopoietic progenitor cells and of dendritic cells. Promotes phosphorylation of SHC1 and AKT1, and activation of the downstream effector MTOR. Promotes activation of RAS signaling and phosphorylation of downstream kinases, including MAPK1/ERK2 and/or MAPK3/ERK1. Promotes phosphorylation of FES, FER, PTPN6/SHP, PTPN11/SHP-2, PLCG1, and STAT5A and/or STAT5B. Activation of wild-type FLT3 causes only marginal activation of STAT5A or STAT5B. Mutations that cause constitutive kinase activity promote cell proliferation and resistance to apoptosis via the activation of multiple signaling pathways.

1. Dorjbal B; Derse D; Lloyd P; Soheilian F; Nagashima K; Heidecker G. “The role of ITCH protein in human T-cell leukemia virus type 1 release”. J Biol Chem, 2011 Sep 9. 2. Rossi M; Inoue S; Walewska R; Knight RA; Dyer MJ; Cohen GM; Melino G. “Caspase cleavage of Itch in chronic lymphocytic leukemia cells”. Biochem Biophys Res Commun, 2009 Feb 13.

Membrane; Constitutively activated mutant forms with internal tandem duplications are less efficiently transported to the cell surface and a significant proportion is retained in an immature form in the endoplasmic reticulum lumen. The activated kinase is rapidly targeted for degradation (By similarity) . .