Abl Interactor 1 Binds to Sos and Inhibits Epidermal Growth Factor- and v-Abl-Induced Activation of Extracellular Signal-Regulated Kinases

Fan, Pang-Dian; Goff, Stephen P.

doi:10.1128/mcb.20.20.7591-7601.2000

Cited by 66 publications

(80 citation statements)

References 38 publications

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“…42,43 Abi-1 and Sos1 form a trimeric complex with Eps8 that mediates transduction of signals from Ras to Rac 44 and is required for the inhibition of growth factor-and v-Ablmediated activation of Erk. 45 MLL fusion proteins including the AF4 family and AF6 are also involved in Ras signaling, [46][47][48] and N-ras and K-ras mutation have been reported for leukemia patients with t(11; 17)(q23; q25) and other MLL translocations. 49,50 The pathologic significance of the Ras-mediated pathways in MLL leukemogenesis is further strengthened by the identification of EEN SH3 domain as a critical transformation domain, which is sufficient for MLL-EEN-mediated myeloid transformation (C.W.S.…”

Section: Discussionmentioning

confidence: 99%

Identification and characterization of EBP, a novel EEN binding protein that inhibits Ras signaling and is recruited into the nucleus by the MLL-EEN fusion protein

Yam

Jin

et al. 2004

Blood

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Section: Discussionmentioning

confidence: 99%

Identification and characterization of EBP, a novel EEN binding protein that inhibits Ras signaling and is recruited into the nucleus by the MLL-EEN fusion protein

Yam

Jin

et al. 2004

Blood

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“…In transient transfection assays, the fulllength Abi-1 protein potently blocked v-Abl induced activation of Erk2, a signaling kinase downstream of the Ras eector molecule (Fan and Go, 2000). This inhibition of Ras signaling is a plausible means by which the full-length protein blocks v-Abl transformation.…”

Section: Discussionmentioning

confidence: 93%

“…To test this notion directly, cell lines were engineered to overexpress a mutant of Abi-1 lacking the C-terminal SH3 domain (AbiD394 ± 475; (Fan and Go, 2000)). This mutant, here termed Abi-1DSH3, fails to interact with P160 v-Abl in vitro and in vivo, and fails to inhibit Erk2 activation by EGF (Fan and Go, 2000;Shi et al, 1995). The coding region for Abi-1DSH3 was inserted into the pMT21 plasmid to direct the expression of the protein with a myc epitope tag at the C-terminus.…”

Section: The Sh3 Domain Of Abi-1 Is Required For Inhibition Of Transfmentioning

confidence: 99%

“…Abi-1 may also interact with the cytoskeletal components such as dynamin and synaptojanin (So et al, 2000). More recently, Abi-1 has also been shown to directly associate with Sos, the guanosine exchange factor important for Ras activation (Fan and Go, 2000;Scita et al, 1999). Whether this association normally is associated with a positive or negative signal is not known.…”

Section: Introductionmentioning

confidence: 99%

“…Whether this association normally is associated with a positive or negative signal is not known. However, the highlevel overexpression of Abi-1 can have signi®cant negative regulatory eects on EGF-mediated signaling (Fan and Go, 2000;Shi et al, 1995). Thus, overexpression of Abi-1 can reduce and delay the activation of the extracellular response kinases (Erks) that normally follows EGF exposure.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Inhibition of v-Abl transformation in 3T3 cells overexpressing different forms of the Abelson interactor protein Abi-1

et al. 2001

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The abi-1 gene encodes a protein that binds and is phosphorylated by the Abelson protein tyrosine kinase. Constructs expressing a full-length abi-1 cDNA, and a smaller cDNA arising from an alternatively spliced form, were generated and tested for their eect on transformation of NIH3T3 cells by the Abelson murine leukemia virus. Overexpression of both forms of the protein strongly inhibited transformation by the wild-type P160 strain of the virus, but not by the non-interacting mutant P90A strain. The inhibition required the SH3 domain of Abi-1, suggesting that a direct interaction was required for the eect. Rare breakthrough P160 transformants of the Abi-1 overexpressing lines were found to have downregulated Abi-1 protein levels by a post-transcriptional mechanism. Oncogene (2001) 20, 4926 ± 4934.

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Generation of branched actin networks: assembly and regulation of the N‐WASP and WAVE molecular machines

2010

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The Arp2/3 complex is a molecular machine that generates branched actin networks responsible for membrane remodeling during cell migration, endocytosis, and other morphogenetic events. This machine requires activators, which themselves are multiprotein complexes. This review focuses on recent advances concerning the assembly of stable complexes containing the most-studied activators, N-WASP and WAVE proteins, and the level of regulation that is provided by these complexes. N-WASP is the paradigmatic auto-inhibited protein, which is activated by a conformational opening. Even though this regulation has been successfully reconstituted in vitro with isolated N-WASP, the native dimeric complex with a WIP family protein has unique additional properties. WAVE proteins are part of a pentameric complex, whose basal state and activated state when bound to the Rac GTPase were recently clarified. Moreover, this review attempts to put together diverse observations concerning the WAVE complex in the conceptual frame of an in vivo assembly pathway that has gained support from the recent identification of a precursor.

show abstract

Abl Interactor 1 Binds to Sos and Inhibits Epidermal Growth Factor- and v-Abl-Induced Activation of Extracellular Signal-Regulated Kinases

Cited by 66 publications

References 38 publications

Identification and characterization of EBP, a novel EEN binding protein that inhibits Ras signaling and is recruited into the nucleus by the MLL-EEN fusion protein

Identification and characterization of EBP, a novel EEN binding protein that inhibits Ras signaling and is recruited into the nucleus by the MLL-EEN fusion protein

Inhibition of v-Abl transformation in 3T3 cells overexpressing different forms of the Abelson interactor protein Abi-1

Generation of branched actin networks: assembly and regulation of the N‐WASP and WAVE molecular machines

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