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1 ntial for its binding with the cytodomain of beta4 integrin.
2 th the upregulation of MMP-9 and cleavage of beta4 integrin.
3 atic MNNG-HOS cells have increased levels of beta4 integrin.
4 p63 was rescued by signalling downstream of beta4 integrin.
5 s, epitope-tagged PMP22 forms a complex with beta4 integrin.
6 e.g. hCLCA2, mCLCA5, mCLCA1, and bCLCA2) and beta4 integrin.
7 if within the extracellular I-like domain of beta4 integrin.
8 essed in endothelia, failed to interact with beta4 integrin.
9 elial cells, which express little endogenous beta4 integrin.
10 autoantibodies in OCP sera specific for the beta4 integrin.
11 y up-regulated genes, including survivin and beta4-integrin.
12 was positive, yet attenuated, for alpha6 and beta4 integrins.
13 uced the expression of hemidesmosomal alpha6/beta4-integrins.
16 epithelial cells upregulate and internalize beta4-integrin along with its matrix substrate, laminin.
17 bnormalities in the expression of the alpha6 beta4 integrin, an integral component of hemidesmosomes.
18 dc)-1 engaging the cytoplasmic domain of the beta4 integrin and coupling of the integrin to human epi
19 eviously uncharacterized interaction between beta4 integrin and ezrin, a membrane-cytoskeletal linker
20 portantly, the concomitant overexpression of beta4 integrin and FAK significantly correlates with mal
21 physical and functional interactions between beta4 integrin and FAK that influence breast cancer mali
23 a4 integrin, which, in turn, recruits FAK to beta4 integrin and leads to FAK activation and signaling
24 inflammation was delayed, and expression of beta4 integrin and p21 was reduced in lysates of constit
25 cular arrest of cancer cells via adhesion to beta4 integrin and promote early, intravascular, metasta
26 However, the amount of Rac1 associating with beta4 integrin and the activity of both Rac1 and cofilin
27 transfected constructs encoding the mutated beta4 integrins and a GFP-conjugated wild type beta4 int
28 e following levels: p < 0.001 for alpha6 and beta4 integrins and the beta3 chain of laminin 5; p < 0.
29 In these same cells, BPAG1e, the truncated beta4 integrin, and type XVII collagen (Col XVII), a tra
30 three signaling pathways (NF-kappaB, alpha6-beta4-integrin, and IL-1) as differentially upregulated
35 uring early stages of myelination, PMP22 and beta4 integrin are coexpressed at the cell surface and c
36 also a functional connection between CD9 and beta4 integrins, as evidenced by anti-CD9 antibody effec
37 es and JEB keratinocytes, induced to express beta4 integrin, assemble laminin-332 in linear tracks ov
39 keratinocytes also display reduced levels of beta4 integrins at the cell surface but increased total
42 odia, and directed migration are restored in beta4 integrin-deficient cells by inducing expression of
43 typical of confluent, stationary cells, and beta4 integrin dynamics are reduced in knockdown cells c
46 Our analysis revealed that manipulation of beta4 integrin expression and signaling impacted SPARC e
53 escribes a pro-metastatic EGFR/Src-dependent beta4 integrin/FAK complex that is involved in breast ca
55 tegrin expression by shRNA and disruption of beta4 integrin function by transfection of dominant-nega
56 ta4 integrins and a GFP-conjugated wild type beta4 integrin (GFP-beta4WT) into 804G cells, which asse
63 The corresponding CLCA-binding domain of the beta4 integrin is localized to the specific determining
66 The alpha6beta4 integrin (referred to as "beta4" integrin) is a receptor for laminins that promote
67 e gene encoding the hemidesmosome-associated beta4 integrin (ITGB4), and in the gene for the hemidesm
70 d a mutation within the I-like domain of the beta4 integrin, lying outside the SDL region (GFP-beta4V
71 ncreased proliferation (Ki-67) and adhesion (beta4 integrin) markers, and induced inflammatory cell i
72 ense mutation in the extracellular domain of beta4 integrin may affect ligand binding or dimerization
73 We report here that alphaE-catenin inhibits beta4 integrin-mediated activation of SRC tyrosine kinas
75 of either primary human keratinocytes (NHK), beta4 integrin-null human keratinocytes (beta4-), or tho
76 ve in keratinocytes exhibiting deficiency in beta4 integrin or knockdown of the plakin protein Bullou
81 , re-expression of alpha6 integrin increases beta4 integrin protein at the cell surface, which result
83 stiffness and composition is sensed through beta4 integrin, Rac1, and the PI3K pathway, and suggest
85 ng that the clustering of alpha6beta4 with a beta4 integrin-specific antibody promotes p53-dependent
86 -catenin involves negative regulation of the beta4 integrin-SRC signaling pathway and that SRC-mediat
87 h Sdc1 engages the cytoplasmic domain of the beta4 integrin subunit allowing HER2-dependent motility
89 provide evidence that the SDL segment of the beta4 integrin subunit is required for ligand binding an
91 n of the alpha2beta1 integrin, the alpha6 or beta4 integrin subunit was expressed in our Mm5MT model.
92 their ability to increase expression of the beta4 integrin subunit, a component of the alpha6beta4 i
94 of patients with MMP and OCP recognize only beta4 integrin subunit, and sera of OP patients recogniz
95 cicatricial pemphigoid (OCP) sera recognize beta4 integrin subunit, oral pemphigoid sera recognize a
97 he notion of close association of the alpha6 beta4 integrin subunits and further attest to the critic
98 ults in up-regulation of both the alpha6 and beta4 integrin subunits but no change in the alpha1, alp
99 rther investigate the role of the alpha6 and beta4 integrin subunits in mediating the phenotypic chan
102 generated point mutations within the SDL of beta4 integrin tagged with green fluorescent protein (GF
103 mammary tumors lacking functional beta1 and beta4 integrin through activation of NFkappaB, and overe
104 was also shown to colocalize with Rab27B and beta4 integrin to early adhesion initiation sites in spr
105 in ECS cells, where it interacts with alpha6/beta4 integrin to stimulate FAK and Src signaling, leadi
106 ative genes, 14-3-3sigma, S100P, S100A6, and beta4 integrin, to neoplastic cells in pancreatic tumors
108 an keratinocytes (beta4-), or those in which beta4 integrin was reexpressed (beta4+), were tracked du
109 unction by transfection of dominant-negative beta4 integrin was sufficient to revert this highly meta
111 y inducing expression of a truncated form of beta4 integrin, which lacks binding sites for BPAG1e and
112 ing triggers the tyrosine phosphorylation of beta4 integrin, which, in turn, recruits FAK to beta4 in
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