Disease relevance of Itgb4

• These amplicons are not observed in DB hyperplasias or in tumors overexpressing wild-type PyMT and result in overexpression of Grb2 and Itgb4 [1].
• Integrin beta 4 mutations associated with junctional epidermolysis bullosa with pyloric atresia [2].
• Splicing modulation of integrin beta4 pre-mRNA carrying a branch point mutation underlies epidermolysis bullosa with pyloric atresia undergoing spontaneous amelioration with ageing [3].
• Genes highly correlated with invasion or peritoneal dissemination of gastric cancer, such as E-cadherin or integrin beta4, were down-regulated in both of the derivative cell lines analyzed in this study [4].
• Thus, the impaired function of integrin beta 4-mediated adhesion is considered to be an important factor in intravasation during metastasis [5].

High impact information on Itgb4

• Epithelial detachment due to absence of hemidesmosomes in integrin beta 4 null mice [6].
• Mutations in the genes encoding integrin beta 4 and chains of laminin-5 have been implicated in junctional epidermolysis bullosa [7].
• The cytoplasmic domain of the integrin beta4 subunit mediates both association with the hemidesmosomal cytoskeleton and recruitment of the signaling adaptor protein Shc [8].
• Cell cycle and adhesion defects in mice carrying a targeted deletion of the integrin beta4 cytoplasmic domain [8].
• Targeted deletion of the integrin beta4 signaling domain suppresses laminin-5-dependent nuclear entry of mitogen-activated protein kinases and NF-kappaB, causing defects in epidermal growth and migration [9].

Biological context of Itgb4

• Partial rescue of epithelial phenotype in integrin beta4 null mice by a keratin-5 promoter driven human integrin beta4 transgene [10].
• Analyses using anti-integrin antibodies indicated that the dysadhesion phenotype in Int-3LL cells was associated with integrin beta 4 dysfunction, which is known to produce epithelial detachment [5].
• Our data suggested that PC-PLC had an important role in regulating neural cell survival, and PC-PLC might perform its function by upregulating the expressions of integrin beta4 and Rb protein [11].

Anatomical context of Itgb4

• Integrin beta 1 was expressed on granulosa and large luteal cells, but integrin beta 4 was undetectable [12].
• Study of mRNA in wild-type keratinocytes transfected with IGTB4 minigenes containing intron 31 with or without mutation 3986-19T-->A, confirmed the causative role of the intronic mutation in PA-JEB, and highlighted the influence of feeders on the maturation process of the mutated beta4 pre-mRNA [3].
• Integrin beta 4 subunit is present in association with alpha 6 chain on both normal and transformed epithelial cells [13].
• The basement membrane proteins including laminin, type IV collagen, type VII collagen, integrin alpha6, and integrin beta4 were all detected at the dermal-epidermal junction, which showed a continuous structure in the 4 weeks after grafting [14].

Associations of Itgb4 with chemical compounds

• We have generated a conditional knockout mouse strain, in which the gene encoding the beta4 integrin subunit (Itgb4) was inactivated only in small stretches of the skin [15].

Other interactions of Itgb4

• Furthermore, the addition of Matrigel to the hepatoblast culture upregulated the expression of cytokeratin 7 and 19, integrin beta4, and HNF1beta, which are known to be expressed in cholangiocytes [16].

Analytical, diagnostic and therapeutic context of Itgb4

• Integrin beta 1 subunit could be detected by immunofluorescence on all cell types of embryonic mouse kidney, but we could not detect integrin beta 4 subunit in embryonic kidney by immunofluorescence or by in situ hybridization [17].

References