Gene targeting of BPAG1: Abnormalities in mechanical strength and cell migration in stratified epithelia and neurologic degeneration

Guo, Lifei; Degenstein, Linda; Dowling, James J.; Yu, Qian-Chun; Wollmann, Robert L.; Perman, Benjamin; Fuchs, Elaine

doi:10.1016/0092-8674(95)90333-x

Cited by 420 publications

(423 citation statements)

References 38 publications

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“…Included in this list are laminin g2, laminin a3, integrin a 6 , integrin b 6 , BPAG-1, Ecadherin, P-cadherin, desmoglein, cytokeratin 6, and cytokeratin 14 (Lersch and Fuchs, 1988;Breuss et al, 1993;Karpati et al, 1993;Tryggvason, 1993;Koch and Franke, 1994;Guo et al, 1995;Borradori and Sonnenberg, 1996). On the other hand, genes that are up-regulated in HPV-transformed cells are more diverse.…”

Section: Discussionmentioning

confidence: 99%

Characterization of transformation related genes in oral cancer cells

Chang

Park²,

Denny

et al. 1998

Oncogene

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A cDNA representational di erence analysis (cDNA-RDA) and an arrayed ®lter technique were used to characterize transformation-related genes in oral cancer. From an initial comparison of normal oral epithelial cells and a human papilloma virus (HPV)-immortalized oral epithelial cell line, we obtained 384 di erentially expressed gene fragments and arrayed them on a ®lter. Two hundred and twelve redundant clones were identi®ed by three rounds of back hybridization. Sequence analysis of the remaining clones revealed 99 unique clones corresponding to 69 genes. The expression of these transformation related gene fragments in three nontumorigenic HPV-immortalized oral epithelial cell lines and three oral cancer cell lines were simultaneously monitored using a cDNA array hybridization. Although there was a considerable cell line-to-cell line variability in the expression of these clones, a reliable prediction of their expression could be made from the cDNA array hybridization. Our study demonstrates the utility of combining cDNA-RDA and arrayed ®lters in highthroughput gene expression di erence analysis. The di erentially expressed genes identi®ed in this study should be informative in studying oral epithelial cell carcinogenesis.

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Section: Discussionmentioning

confidence: 99%

Characterization of transformation related genes in oral cancer cells

Chang

Park²,

Denny

et al. 1998

Oncogene

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“…Loss of the plakins plectin and BP230 affects hemidesmosome formation and induces mechanical fragility of the skin, but to a lesser extent than integrin loss, since plaques could still be seen. In BP230 KO mice, keratins fail to attach to defective hemidesmosomes, whereas in plectin KO mice, they are absent only in areas undergoing blistering and histolysis (Guo et al, 1995;Andra et al, 1997). In contrast, human patients with mutations affecting BP180 display milder hemidesmosome defects (McGrath et al, 1995).…”

Section: Initial Hemidesmosome Assemblymentioning

confidence: 99%

The making of hemidesmosome structures in vivo

Zhang

Labouesse

2010

Developmental Dynamics

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Hemidesmosomes are evolutionarily conserved attachment complexes linked to intermediate filaments that connect epithelial cells to the extracellular matrix. They provide tissue integrity and resistance to mechanical forces. Alterations in hemidesmosome structures are responsible for skin blistering, carcinoma invasion, and wound-healing defects. Valuable information about hemidesmosome assembly and disassembly has been obtained from in vitro cell culture studies. However, how these processes take place in vivo still remains elusive. Here, we discuss recent data about the formation and reorganization of hemidesmosomes in several in vivo model systems, particularly zebrafish and Caenorhabditis elegans, focusing on various factors affecting their dynamics. Mechanisms found in different organisms reveal that hemidesmosome formation and maintenance in vivo are carefully controlled by ECM protein folding, ECM-receptor expression and trafficking, and by post-translational modification of hemidesmosome components. These findings validate and extend the in vitro studies, and shed light on our understanding about hemidesmosomes across species.

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“…These functional differences arise from the expression of multiple tissue-specific isoforms, as illustrated by the phenotypes of the various dt alleles. Comparison of two alleles, dt J and dt Alb , both of which display the neuropathy phenotype, demonstrated protein expression in the epithelium of the former, but not the latter, consistent with the respective lack and presence of hemidesmosome abnormalities in the two strains [53]. Further analysis of mRNA expression levels among various dt alleles has shown that transcription is reduced for all Dst regions in dt Alb , dt Tg4 , and dt 24J mice, but in dt 27J mice, reductions were observed for regions found only in neural and muscle isoforms.…”

Section: Allelic Seriesmentioning

confidence: 58%

Mouse Forward Genetics in the Study of the Peripheral Nervous System and Human Peripheral Neuropathy

Douglas

Popko

2008

Neurochem Res

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Forward genetics, the phenotype-driven approach to investigating gene identity and function, has a long history in mouse genetics. Random mutations in the mouse transcend bias about gene function and provide avenues towards unique discoveries. The study of the peripheral nervous system is no exception; from historical strains such as the trembler mouse, which led to the identification of PMP22 as a human disease gene causing multiple forms of peripheral neuropathy, to the more recent identification of the claw paw and sprawling mutations, forward genetics has long been a tool for probing the physiology, pathogenesis, and genetics of the PNS. Even as spontaneous and mutagenized mice continue to enable the identification of novel genes, provide allelic series for detailed functional studies, and generate models useful for clinical research, new methods, such as the piggyBac transposon, are being developed to further harness the power of forward genetics.

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Gene targeting of BPAG1: Abnormalities in mechanical strength and cell migration in stratified epithelia and neurologic degeneration

Cited by 420 publications

References 38 publications

Characterization of transformation related genes in oral cancer cells

Characterization of transformation related genes in oral cancer cells

The making of hemidesmosome structures in vivo

Mouse Forward Genetics in the Study of the Peripheral Nervous System and Human Peripheral Neuropathy

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