The gene TOM1L1 (target of myb1 like 1 membrane trafficking) is mapped to human chromosome 17q23. The protein has a VHS (Vps27p/Hrs/Stam) domain at the N-terminal, a GAT (GGA (Golgi-localizing, γ-adaptin ear domain homology, ADP-ribosylation factor (Arf)-binding protein and Tom) domain at the center and interaction motifs at the C-terminal.
Immunogen
immunized with a TOM1L1 fusion protein.
Biochem/physiol Actions
TOM1L1 (target of myb1 like 1 membrane trafficking) is an adaptor protein, which is involved in vesicular trafficking as well as intracellular signaling. It negatively controls the mitogenic and transforming functions in fibroblasts by working as a substrate for SRC (tyrosine protein kinase). It is involved in EGF (epidermal growth factor)-mediated internalization of EGF receptor. TOM1L1 is downregulated in cutaneous squamous cell carcinoma and esophageal squamous cell carcinoma.
Physical form
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.
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Src-family tyrosine kinases (SFKs) play critical roles in regulating cellular differentiation and proliferation. Src-activating and signaling molecule (Srcasm) is a novel molecule that down-regulates SFK activity and promotes cell differentiation. The aim of this study was to determine whether Srcasm
Although many proteins have been shown to participate in ligand-stimulated endocytosis of EGF receptor (EGFR), the adaptor protein responsible for interaction of activated EGFR with endocytic machinery remains elusive. We show here that EGF stimulates transient tyrosine phosphorylation of Tom1L1
Mediators of inflammation, 2009, 416298-416298 (2010-02-26)
TOM1L (target of Myb-1 Like) was identified as a binding partner for the full length and catalytically-active Lck in a yeast 2-hybrid screening assay. Here we show that in Jurkat T cells stimulated by CD3/CD28 coligation where the expression of
Chromosome 17 is severely rearranged in breast cancer. Whereas the short arm undergoes frequent losses, the long arm harbors complex combinations of gains and losses. In this work we present a comprehensive study of quantitative anomalies at chromosome 17 by
The non-receptor tyrosine kinase SRC is frequently deregulated in human colorectal cancer (CRC), and SRC increased activity has been associated with poor clinical outcomes. In nude mice engrafted with human CRC cells, SRC over-expression favors tumor growth and is accompanied
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