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ABL1 — SOAT1

Text-mined interactions from Literome

Limnander et al., Mol Cell 2004 (Cell Transformation, Neoplastic) : SOCS-1 is expressed in v-Abl transformed cells but is unable to inhibit v-Abl mediated Jak-Stat signaling
Ahmed et al., Oncogene 1998 : Our results indicate that although both constitutively activated cEpoR and BCR-ABL oncogenes induce growth-factor independence in Ba/F3 cells, only BCR-ABL is able to protect cells from etoposide and serum-deprivation induced apoptosis and induce a strong constitutive activation of STAT factors, suggesting a role for these molecules in the anti-apoptotic activity of BCR-ABL
Danial et al., Mol Cell Biol 1998 (Neoplasms, Experimental) : We propose that Jak1 is a mediator of v-Abl induced STAT activation and v-Abl induced proliferation in BAF/3 cells, and may be important for efficient transformation of immature B cells by the v-abl oncogene