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2 LC-gamma2-deficient cells reconstituted with Src homology domain 2 (SH2) domain mutant PLC-gamma2 did
3 ontaining a functional point mutation in the Src homology domain 2 (SH2) led to more rapid dephosphor
4 resulted in the tyrosine phosphorylation of Src homology domain 2 (SH2)-containing phosphatase-2 (SH
6 ine phosphorylation and association with the Src homology domain 2 (SH2)-containing protein tyrosine
7 By contrast, SOCS-2 and cytokine-inducible Src homology domain 2 (SH2)-containing protein up-regula
8 er in a pathway downstream of EGL-15 and the Src homology domain 2 (SH2)/SH3-adaptor protein SEM-5/GR
9 factor receptor binding protein 2 (Grb2) and Src homology domain 2 containing (Shc) TbetaR-II, thereb
10 tory function of CEACAM1, was dependent upon src homology domain 2 containing phosphatase 1 activity,
12 the protein kinase A (PKA) pathway activates Src homology domain 2 containing protein tyrosine phosph
14 ion and VEGFR-2 deactivation, the latter via Src homology domain 2-containing (SH2-containing) tyrosi
15 B cells require the inositol 5-phosphatase, Src homology domain 2-containing inositol 5-phosphatase
16 ing protein tyrosine phosphatase (SHP) 2 and Src homology domain 2-containing inositol phosphatase 1
19 ion of both the receptor and the phosphatase Src homology domain 2-containing protein tyrosine phosph
20 rosine-phosphorylated CTLA-4, and associated Src homology domain 2-containing protein tyrosine phosph
21 g binding to DCIR induced phosphorylation of Src homology domain 2-containing protein tyrosine phosph
22 is the binding site for both SOCS-3 and for Src homology domain 2-containing tyrosine phosphatase 2
23 endent on protein tyrosine phosphatase SHP2 (Src homology domain 2-containing tyrosine phosphatase 2)
26 r(P)(19)) may function as a docking site for Src homology domain-2 (SH2) domain containing proteins d
27 ar sequence of FGFRL1 consists of a putative Src homology domain-2 (SH2)-binding motif adjacent to a
28 ressing both heme oxygenase-1 (HO-1) and the Src homology domain-2 containing tyrosine phosphatase-1
30 is mediated by an interaction of the second src homology domain 3 (SH3) domain of ponsin with the pr
31 proline rich, the hypothesis that it targets Src homology domain 3 (SH3) domains was tested, but muta
34 g mutant Myo5 proteins with deletions of the src homology domain 3 (SH3) or both TH2 and SH3 domains
36 e (GST) fusion proteins encoding the unique, Src homology domain 3 (SH3), and SH2 domains of Fyn, Hck
37 following either the loss or mutation of its Src homology domain 3 (SH3), resulting in both increased
38 mains [i.e., Src homology domain 2 (SH2) and Src homology domain 3 (SH3)] play a critical role in lin
39 evalence of modular protein domains, such as Src homology domain 3 and 2 (SH3 and SH2), among importa
40 l interfering RNA or myristoylated cortactin Src homology domain 3 blocking peptide attenuated ROS pr
41 cruitment of IRSp53 effector proteins to its Src homology domain 3 by promoting 14-3-3 binding in the
43 in Kalirin-9, with its Sec14p, spectrin, and Src homology domain 3 motifs, is essential for regulatin
45 a potential interaction motif for the Noxa1 Src homology domain 3, caused up-regulation of basal and
47 This domain is one of the rare examples of Src homology domain 3-like folds in bacterial proteins,
50 the native state ensemble of the C-terminal src homology domain-3 (C-SH3) from Caenorhabditis elegan
51 ntramolecular interactions of the PLC-gamma1 Src homology domains and/or by positioning it for phosph
52 toylation consensus sequence and SH3 and SH2 Src homology domains, but lacks a tyrosine kinase domain
54 at the cytoplasmic tail of CEACAM1 bound the src homology domain-containing phosphatase 1 and adaptor
55 development, whereas a tyrosine phosphatase Src homology domain-containing tyrosine phosphatase (Shp
56 In this study, we provide evidence that the Src-homology domain-containing adaptor Nck1 negatively r
57 terization of protein modules exemplified by Src Homology domains has revolutionized our understandin
59 se results fit a model which postulates that Src homology domain interactions are a molecular determi
60 Tyrosine kinase activity, a determinant of Src homology domain interactions, has a prominent effect
61 sented here suggest that, although cbl lacks src homology domains, it represents a novel intermediate
64 involve phosphotyrosine adapter molecules or src-homology domains of p85alpha, and extend to other st
66 intramolecular interactions of the enzyme's Src-homology domains SH2 and SH3, with concomitant displ
68 PI-3 kinase activation required a putative Src-homology domain (SH2) binding motif in the MyD88 Tol
70 Tyr-783 in the beta1 tail, and that the Arg Src homology domain then engages this phosphorylated reg
71 tion of two C-terminal Grb10 motifs (BPS and Src homology domains) with receptor phosphotyrosine resi
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