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1 zation (N-cadherin, PSD-95, RhoA, NCAM1, and integrin alpha1).
2 ted in glomeruli of Alport mice that express integrin alpha1.
3 hibitor or Rac1 inhibitor, or by deletion of integrin alpha1.
4  transcriptase-PCR showed mRNA expression of integrins alpha1, alpha2, alpha3, alpha4, alpha5, alpha7
5         CSE also increased the expression of integrins alpha1, alpha2, and alpha10 (collagen receptor
6                  Among those alpha subunits, integrins alpha1, alpha2, and the other four subunits be
7  significantly decreased their expression of integrin alpha1, an adhesion molecule highly expressed b
8 ted in reduced proliferation, migration, and integrin alpha1 and alpha2 integrin expression.
9  results indicate that NSP4 interaction with integrin alpha1 and alpha2 is an important component of
10 ti-integrin alpha2 and beta1 but not by anti-integrin alpha1 and alpha6.
11 We conclude that overexpression of mesangial integrin alpha1 and podocyte vimentin and integrin alpha
12                                              Integrins alpha1 and alpha2, which contributed only marg
13                                              Integrin alpha1-blocking and alpha2-blocking antibodies
14                  Furthermore, we showed that integrin alpha1 but not alpha2 subunits were expressed o
15     In both developing and adult muscle, the integrin alpha1 chain was selectively associated with pr
16 ition of purified integrin alpha1beta1 or an integrin alpha1 cytoplasmic peptide to which TCPTP has b
17                                              Integrin alpha1-deficient mice thus provide a geneticall
18 ked reduction of their proliferation on both integrin alpha1-dependent (collagenous) and independent
19 ive immunofluorescence showed an increase in integrin alpha1 expression in Alport mesangial cells and
20        In Alport mice that are also null for integrin alpha1 expression, expansion of the mesangial m
21       Mice with targeted inactivation of the integrin alpha1 gene (alpha1-KO mice) provide a model th
22                                        Thus, integrin alpha1 has a unique role among the collagen rec
23 nalysis, to examine solution dynamics of the integrin alpha1 I domain induced by the binding of dival
24 oblasts from normal and fibrotic dermis, and integrin alpha1 knockout mice maintain increased collage
25  tolerance and insulin sensitivity in HF-fed integrin alpha1-null (itga1(-/-)) and wild-type (itga1(+
26                 Previous work has shown that integrin alpha1-null Alport mice exhibit attenuated glom
27 evated in both integrin alpha1-null mice and integrin alpha1-null Alport mice relative to wild-type m
28 thesis, while overexpression of Cav-1 in the integrin alpha1-null MCs decreases EGFR-mediated ROS pro
29                         We further show that integrin alpha1-null MCs have increased levels of activa
30 ibition of ERK increases Cav-1 levels in the integrin alpha1-null MCs.
31                                              Integrin alpha1-null mesangial cells (MCs) have reduced
32                                              Integrin alpha1-null mesangial cells have constitutively
33 t studies, we describe the mechanism whereby integrin alpha1-null mesangial cells produce excessive R
34 d MMP-14, was significantly elevated in both integrin alpha1-null mice and integrin alpha1-null Alpor
35  in oxidative stress-mediated damage and why integrin alpha1-null mice are more susceptible to fibros
36 ecies (ROS) production, we demonstrated that integrin alpha1-null mice develop more severe glomerulos
37              We previously demonstrated that integrin alpha1-null mice develop worse fibrosis than wi
38                                              Integrin alpha1-null mice display marked delays in trans
39                                              Integrin alpha1-null mice have delayed-onset progressive
40           Finally, we show that glomeruli of integrin alpha1-null mice have reduced levels of Cav-1 a
41 showed previously that tumor angiogenesis in integrin alpha1-null mice is reduced compared to that of
42 f plasma levels of MMP-9 in either normal or integrin alpha1-null mice leads to decreased synthesis o
43                     We have observed that in integrin alpha1-null mice synthesis of MMP7 and MMP9 was
44                                 We have used integrin alpha1-null mice to investigate the role of thi
45             To investigate this possibility, integrin alpha1-null mice were crossed with KrasLA2 mice
46 i and cultured mesangial cells isolated from integrin alpha1-null mice, activation of the p38 and ERK
47 14 expression levels in mesangial cells from integrin alpha1-null mice.
48 , we used blocking antibodies against either integrin alpha1 or alpha2 subunits and VSMCs from mice t
49 port mice with Rac1 inhibitor or deletion of integrin alpha1 reduced mesangial cell process invasion
50 erstood, truncation and point mutants of the integrin alpha1 subunit cytoplasmic tail (amino acids 11
51      These results indicate that loss of the integrin alpha1 subunit decreases the incidence and grow
52 educed Cav-1 levels, and reexpression of the integrin alpha1 subunit increases Cav-1 levels, decrease
53                     To determine whether the integrin alpha1 subunit protects against impairments in
54  Cav-1 directly interacts with TCPTP and the integrin alpha1 subunit, 2) pCav-1 is a substrate of TCP

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