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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 naling decreased tECM-mediated expression of integrin alpha1, alpha2, and beta1 in hASCs.
5  transcriptase-PCR showed mRNA expression of integrins alpha1, alpha2, alpha3, alpha4, alpha5, alpha7
6         CSE also increased the expression of integrins alpha1, alpha2, and alpha10 (collagen receptor
7                  Among those alpha subunits, integrins alpha1, alpha2, and the other four subunits be
8 involved significantly greater expression of integrins alpha1, alphav, beta1, and beta5 in cells with
9  significantly decreased their expression of integrin alpha1, an adhesion molecule highly expressed b
10 ted in reduced proliferation, migration, and integrin alpha1 and alpha2 integrin expression.
11  results indicate that NSP4 interaction with integrin alpha1 and alpha2 is an important component of
12 ocal adhesion kinase signaling downstream of integrin alpha1 and alpha2, and inhibition of collagen I
13 ti-integrin alpha2 and beta1 but not by anti-integrin alpha1 and alpha6.
14 We conclude that overexpression of mesangial integrin alpha1 and podocyte vimentin and integrin alpha
15                                              Integrins alpha1 and alpha2, which contributed only marg
16                                              Integrin alpha1-blocking and alpha2-blocking antibodies
17                  Furthermore, we showed that integrin alpha1 but not alpha2 subunits were expressed o
18     In both developing and adult muscle, the integrin alpha1 chain was selectively associated with pr
19 ition of purified integrin alpha1beta1 or an integrin alpha1 cytoplasmic peptide to which TCPTP has b
20                                              Integrin alpha1-deficient mice thus provide a geneticall
21 ked reduction of their proliferation on both integrin alpha1-dependent (collagenous) and independent
22 e intrinsically disordered cytosolic tail of Integrin-alpha1 displaces the TCPTP autoinhibitory tail,
23 ive immunofluorescence showed an increase in integrin alpha1 expression in Alport mesangial cells and
24        In Alport mice that are also null for integrin alpha1 expression, expansion of the mesangial m
25       Mice with targeted inactivation of the integrin alpha1 gene (alpha1-KO mice) provide a model th
26                                        Thus, integrin alpha1 has a unique role among the collagen rec
27 nalysis, to examine solution dynamics of the integrin alpha1 I domain induced by the binding of dival
28 oblasts from normal and fibrotic dermis, and integrin alpha1 knockout mice maintain increased collage
29  tolerance and insulin sensitivity in HF-fed integrin alpha1-null (itga1(-/-)) and wild-type (itga1(+
30                 Previous work has shown that integrin alpha1-null Alport mice exhibit attenuated glom
31 evated in both integrin alpha1-null mice and integrin alpha1-null Alport mice relative to wild-type m
32 thesis, while overexpression of Cav-1 in the integrin alpha1-null MCs decreases EGFR-mediated ROS pro
33                         We further show that integrin alpha1-null MCs have increased levels of activa
34 ibition of ERK increases Cav-1 levels in the integrin alpha1-null MCs.
35                                              Integrin alpha1-null mesangial cells (MCs) have reduced
36                                              Integrin alpha1-null mesangial cells have constitutively
37 t studies, we describe the mechanism whereby integrin alpha1-null mesangial cells produce excessive R
38 d MMP-14, was significantly elevated in both integrin alpha1-null mice and integrin alpha1-null Alpor
39  in oxidative stress-mediated damage and why integrin alpha1-null mice are more susceptible to fibros
40 ecies (ROS) production, we demonstrated that integrin alpha1-null mice develop more severe glomerulos
41              We previously demonstrated that integrin alpha1-null mice develop worse fibrosis than wi
42                                              Integrin alpha1-null mice display marked delays in trans
43                                              Integrin alpha1-null mice have delayed-onset progressive
44           Finally, we show that glomeruli of integrin alpha1-null mice have reduced levels of Cav-1 a
45 showed previously that tumor angiogenesis in integrin alpha1-null mice is reduced compared to that of
46 f plasma levels of MMP-9 in either normal or integrin alpha1-null mice leads to decreased synthesis o
47                     We have observed that in integrin alpha1-null mice synthesis of MMP7 and MMP9 was
48                                 We have used integrin alpha1-null mice to investigate the role of thi
49             To investigate this possibility, integrin alpha1-null mice were crossed with KrasLA2 mice
50 i and cultured mesangial cells isolated from integrin alpha1-null mice, activation of the p38 and ERK
51 14 expression levels in mesangial cells from integrin alpha1-null mice.
52 , we used blocking antibodies against either integrin alpha1 or alpha2 subunits and VSMCs from mice t
53  and AGEs displayed diminished expression of integrin alpha1, PDGF-R1beta and connexin-43.
54 port mice with Rac1 inhibitor or deletion of integrin alpha1 reduced mesangial cell process invasion
55 erstood, truncation and point mutants of the integrin alpha1 subunit cytoplasmic tail (amino acids 11
56      These results indicate that loss of the integrin alpha1 subunit decreases the incidence and grow
57 educed Cav-1 levels, and reexpression of the integrin alpha1 subunit increases Cav-1 levels, decrease
58                     To determine whether the integrin alpha1 subunit protects against impairments in
59  Cav-1 directly interacts with TCPTP and the integrin alpha1 subunit, 2) pCav-1 is a substrate of TCP