On the Molecular Organization, Diversity and Functions of Desmosomal Proteins

Steinberg, Malcolm S.; Shida, Hisato; Giudice, George J.; Shida, Mariko; Patel, Nipam H.; Blaschuk, Orest W.

doi:10.1002/9780470513408.ch2

Cited by 32 publications

(8 citation statements)

References 38 publications

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“…Here, we analyzed mouse epithelial tissues, specifically focusing on desmosome structures. We were able to detect fine details which were comparable to previous findings (Al-Amoudi et al, 2007; Franke Garrod, 1993;Garrod et al, 2002;Runswick et al, 2001;Steinberg et al, 1987). An overview projection and a tomographic slice through a desmosome are shown in Fig.…”

Section: Structural Preservation Of Desmosomes In Stratified Epithelisupporting

confidence: 91%

“…In addition, we examined stratified epithelial tissue from mouse tongue. Epidermal tissue has been extensively used for studies of desmosomes and their components, by various means (Frank et al, 2001;Garrod, 1993;Garrod et al, 2002;Giudice et al, 1984;Koulu et al, 1984;Runswick et al, 2001;Steinberg et al, 1987). The process, from tissue fixation to acquisition of 3D volumes, is outlined in Fig.…”

Section: Resultsmentioning

confidence: 99%

“…These adhesions play an important role in tissue morphogenesis, and display a characteristic laminated structure. The fine structure of desmosomes, including the identity and localization of their diverse components, has been well-documented (Franke et al, 1987;Garrod, 1993;Garrod et al, 2002;Giudice et al, 1984;Koulu et al, 1984;Steinberg et al, 1987), enabling us to compare the structural information attained with the VFS-cryoET approach, to that obtained by other methods (Al-Amoudi et al, 2007;Delva et al, 2009;Franke et al, 1987;Garrod and Chidgey, 2008;Giudice et al, 1984;Koulu et al, 1984;Steinberg et al, 1987). Here, we analyzed mouse epithelial tissues, specifically focusing on desmosome structures.…”

Section: Structural Preservation Of Desmosomes In Stratified Epithelimentioning

confidence: 99%

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Reconstructing adhesion structures in tissues by cryo-electron tomography of vitrified frozen sections

Bokstad

Sabanay

Dahan

et al. 2012

Journal of Structural Biology

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Section: Structural Preservation Of Desmosomes In Stratified Epithelisupporting

confidence: 91%

Section: Resultsmentioning

confidence: 99%

Section: Structural Preservation Of Desmosomes In Stratified Epithelimentioning

confidence: 99%

See 1 more Smart Citation

Reconstructing adhesion structures in tissues by cryo-electron tomography of vitrified frozen sections

Bokstad

Sabanay

Dahan

et al. 2012

Journal of Structural Biology

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“…5C and D), suggesting alternative mode(s) of XMRV entry in these cells. As a control for the siRNA knockdown, we similarly transfected the Ep156T cells with siRNA that targets the conserved region of the epithelial cell specific desmoglein-2 gene, which is a member of the cadherin superfamily of genes that mediate adhesion of intercellular junctions (i.e., desmosomes) (36), and showed significant knockdown of this gene (Fig. 5B), implying that the Ep156T primary epithelial cells were indeed susceptible to siRNA transfection and knockdown.…”

Section: Susceptibility Of Prostate Cancer and Noncancerous Cell Linementioning

confidence: 99%

Evaluation of Cellular Determinants Required for In Vitro Xenotropic Murine Leukemia Virus-Related Virus Entry into Human Prostate Cancer and Noncancerous Cells

Bhosle¹,

Suppiah²,

Molinaro³

et al. 2010

J Virol

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Prostate cancer is the most common male malignancy in Western countries and the second most common cause of cancer-related deaths in males worldwide (15,24). The known risk factors for prostate cancer are hormones (i.e., androgens), diet, sex, and race, as well as environmental and genetic factors (27). A recent study suggests that susceptibility to prostate cancer can be influenced by the genetic variations associated with an antagonistic coevolution, which occurs between a specific host locus (RNASEL), known to be involved in antiviral innate immune defense, and a viral pathogen (38). Indeed, several epidemiologic studies have supported the involvement of the RNASEL gene in the prostate cancer etiology (4,5,30,31), whereas other studies do not (9,22,34,43). Some studies have reported that individuals with a single mutated copy of the RNASEL gene have a 50% increased risk for prostate cancer, whereas those with homozygous mutant RNASEL alleles have a 2-fold-increased risk of prostate cancer (5).The RNASEL gene encodes for the RNase L protein, a constitutively expressed latent endoribonuclease, which mediates the interferon-inducible 2-5A system against viral and/or cellular double-stranded RNAs (8,16,20,23,49,50). The RNase L "Q" variant allele (R462Q) shows a 3-fold decrease in catalytic activity compared to the wild-type enzyme (5, 44). The possible association of mutant RNASEL alleles with human prostate cancers suggests an enhanced susceptibility of prostate tissues to a viral agent. This hypothesis has led to the recent identification of a new human retrovirus, xenotropic murine leukemia virus (MuLV)-related virus (XMRV), in 40% of prostate cancer patients with the QQ variant alleles of RNASEL compared to 1.5% among heterozygous (RQ) and wild-type (RR) RNASEL carriers (41). XMRV virus infection appears to be susceptible to inhibition by interferon and its downstream effector RNase L protein (7). However, a recent study has provided some evidence to show that XMRV infection is independent of the RNASEL genotype (34), suggesting that population differences and/or other environmental or genetic factors may influence the impact of RNASEL on prostate cancer development.The XMRV genome is 8,185 nucleotides in length and shares up to 95% overall nucleotide sequence identity with known xenotropic MuLVs (41). One receptor for xenotropic MuLVs is Xpr1, a 696-amino-acid protein with multiple transmembrane-spanning domains (2). Expression of this protein in Chinese hamster ovary (CHO) cells that are not known to express Xpr1 endogenously confers an enhanced susceptibility of these cells to xenotropic MuLV infection (2). Infection of hamster and mouse cells with XMRV-like virus that is derived from a prostate cancer cell line (22Rv1) also requires Xpr1 as a receptor (18). Earlier studies have demonstrated the importance of certain residues located within the putative third and fourth extracellular loops (ECL3 and ECL4) of Mus dunni's Xpr1 in conferring infection by xenotropic MuLVs (25). Furthermore, it has been shown ...

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“…These landmark studies provided a foundation for the Franke and Steinberg laboratories to characterize the transmembrane glycoproteins and cytoplasmic plaque proteins that linked the structure to the intermediate filament cytoskeleton, and to develop immunological tools for localizing specific components (Franke et al 1981;Kapprell et al 1985;Steinberg et al 1987). Collectively, these and other studies shaped our current view of how desmosomal components are organized.…”

mentioning

confidence: 99%