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