SEMA 3C drives cancer growth by transactivating multiple receptor tyrosine kinases via Plexin B1
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چکیده
منابع مشابه
SEMA3C drives cancer growth by transactivating multiple receptor tyrosine kinases via Plexin B1
Growth factor receptor tyrosine kinase (RTK) pathway activation is a key mechanism for mediating cancer growth, survival, and treatment resistance. Cognate ligands play crucial roles in autocrine or paracrine stimulation of these RTK pathways. Here, we show SEMA3C drives activation of multiple RTKs including EGFR, ErbB2, and MET in a cognate ligand-independent manner via Plexin B1. SEMA3C expre...
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Semaphorin 3A (Sema3A) binds to neuropilin-1 (NP1) and activates the transmembrane Plexin to transduce a repulsive axon guidance signal. Here, we show that Sema3 signals are transduced equally effectively by PlexinA1 or PlexinA2, but not by PlexinA3. Deletion analysis of the PlexinA1 ectodomain demonstrates that the sema domain prevents PlexinA1 activation in the basal state. Sema-deleted Plexi...
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BACKGROUND Human Plexin-B1 is expressed in two truncated forms. The long form encodes a trans-membranal protein, while the short form, which is bound to the cell surface and partially secreted, possibly serves as a decoy receptor. Plexin receptors are trans-membrane proteins. The sema domain, found in the extracellular region, is common to all plexins, semaphorins, and the scatter factor recept...
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Tight control of cell proliferation and morphogenesis in conjunction with programmed cell death (apoptosis) is required to ensure normal tissue patterning. Alterations that cause an imbalance of the cellular signals that control these events may promote cell growth, suppress apoptosis, and enhance cell invasion, resulting in oncogenesis. Many of these signals are regulated by receptor tyrosine ...
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ژورنال
عنوان ژورنال: EMBO Molecular Medicine
سال: 2018
ISSN: 1757-4676,1757-4684
DOI: 10.15252/emmm.201707689