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1 d memory reported previously in mice lacking integrin alpha3.
2 plated on mAbs anti-integrin alpha5 or anti-integrin alpha3.
6 functionalized blocking antibodies (against integrins-alpha3, -alphaM, -alphaMbeta2) to both fibroti
7 artially explain the renal phenotype seen in integrin alpha3 and alpha3/alpha6 subunit-deficient anim
8 solated UB culture models indicate that both integrin alpha3 and alpha6 subunits play a direct role i
9 nd beta1 laminin chains; nidogen-1/entactin; integrin alpha3 and beta1 chains in diabetic and DR corn
10 are excellent tools for studying the role of integrin alpha3 and CD26 in the complex biology of pancr
11 he two novel mAbs KU44.22B and KU44.13A, are integrin alpha3 and CD26 respectively, with high levels
14 ted, including the major glomerular podocyte integrin alpha3 and the actin cytoskeleton-related gene
16 F, PDGF, and PDGF receptors, upregulation of integrins alpha3 and alpha5, and increased proliferation
18 inal neuron response to "activated" LN-1 are integrins alpha3 beta1 and alpha6 beta1; these are the s
20 o intracellular PKC helps to explain why the integrin alpha3 extracellular domain is needed for both
22 elop normally in mice with selective loss of integrin alpha3 in excitatory forebrain neurons, reachin
23 her, our data support a fundamental role for integrin alpha3 in regulating dendrite arbor stability,
24 identified a pathway involving activation of integrin alpha3 in TA cells that signals through an LATS
25 r adhesion molecules, including fibronectin, integrin alpha3, integrin beta1, integrin beta3, and cad
26 n phenotypes of laminin receptors, including integrin-alpha3, integrin-alpha6, integrin-alpha7, integ
28 re, gene-dosage experiments demonstrate that integrin alpha3 interacts functionally with the Arg nonr
31 al integrin alpha1 and podocyte vimentin and integrin alpha3 may be important features of glomerular
34 -2) and anti-invasive potential (decrease in integrin alpha3) of the combination of GHRH agonist and
39 sed an alanine-to-serine substitution in the integrin alpha3 subunit, thereby introducing an N-glycos
42 ession of wild-type Met, kinase-dead Met, or integrin alpha3 was sufficient to rescue death upon remo
43 on as follows: (i) a stronger interaction of integrin alpha3 with CD9 in KK47 than in YTS1; (ii) conv