1,721,002 research outputs found
THE MSP RECEPTOR REGULATES ALPHA6BETA4 AND ALPHA3BETA1 INTEGRINS VIA 14-3-3 PROTEINS IN KERATINOCYTE RE-EPITHELIZATION
No full textCirculating fragments of myelin-associated alpha 6 beta 4 integrin in Guillain-Barré syndrome
No full textGuillain-Barré-Strohl syndrome (GBS) is an acute peripheral neuropathy causing reversible myelin damage. alpha 6 beta 4 is a laminin receptor of Schwann cells and myelin. Along with myelin breakdown, alpha 6 beta 4 immunoreactivity might be detected in patients' sera and provide a marker for monitoring GBS course. MAbs to beta 4 and alpha 6 were used in an ELISA test to detect protein in GBS serum samples as in normal individuals. In 66% GBS patients, alpha 6 beta 4 immunoreactivity was detected while controls were negative. The level of beta 4 was followed in different patients and found to fluctuate, always being positive in at least one sample. Treatment lowered immunoreactivity in two beta 4-positive GBS sera. Then, circulating alpha 6 beta 4 fragments represent a novel marker of extensive peripheral myelin damage and may be used to validate clinical diagnosis of GBS, evaluate its course and activity
Transforming Growth-Factor (TGF)-Beta(1) Enhances Alpha(5)Beta(1) And Alpha(V)Beta(5) Integrin Expression And Migration Of Normal Human Keratinocytes
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Distribution of integrins and extracellular matrix proteins in vulvar squamous cell carcinomas.
No full textWe report the topography of integrins and some basement membrane zone (BMZ) proteins in normal vulvar skin and in seven cases of vulvar squamous carcinoma (VSC). In vulvar epidermis integrin chains alpha 2, alpha 3 and beta 1 lined the lateral surface of basal cells, while the heterodimer alpha 6 beta 4 was detected only at their basal domain. The location of alpha 6 beta 4 exactly matched BMZ identified by kalinin, laminin and collagen type IV. In VSC this pattern was subverted since both beta 1 integrins and alpha 6 beta 4 became pericellular. In particular, alpha 6 beta 4 lost its coherence with the residual organization of BMZ. In fact, BMZ components displayed their normal pattern were this was preserved, and so were fibronectin and tenascin in the stroma underlying the tumor. Furthermore, alpha 5 beta 1, the prototype fibronectin receptor that is not normally exposed in vulvar epidermal cells, became detectable pericellularly in VSC tumor cells. Alteration of integrin polarized topography appears to be typical of VSC cells as well as of other tumor epidermal cells. This alteration may be easily shown by immunohistochemistry on routinely collected frozen biopsies. It may then represent a tool for the early diagnosis of VSC that provides a quick and easy complement of traditional histology
Fibronectin modulates the effects of HIV-1 Tat on the growth of murine Kaposi's sarcoma-like cells through the down-regulation of tyrosine phosphorylation
No full textHIV-1 Tat plays a role in the pathogenesis of Kaposi's sarcoma. We therefore investigated the effect of Tat on the growth of murine Kaposi's sarcoma-like spindle (TTB) cells derived from dermal lesions. We observed that Tat and a peptide corresponding to the carboxyl-terminal region (Tat65-80) containing an RGD sequence inhibit TTB cell proliferation only when cells are cultured on fibronectin. This inhibitory effect correlates with redistribution of the alpha(v) integrin subunit on the surface of TTB cells and with down-regulation of tyrosine phosphorylation of specific substrates due to an increased tyrosine phosphatase activity. Indeed, phenylarsine oxide, a potent inhibitor of phosphotyrosine phosphatases, prevented the effects of Tat on TTB cells. We therefore argue that the action of Tat on TTB cells is mediated by the RGD motif through an integrin-based cell signaling pathway involving the activity of phosphotyrosine phosphatase(s), which would lead to a decrease in the levels of phosphotyrosine-containing proteins, among which is erk-2/p42MAPK
Transforming Growth-Factor-Beta-1 Modulates Beta-1 And Beta-5 Integrin Receptors And Induces The De-Novo Expression Of The Alpha-V-Beta-6 Heterodimer In Normal Human Keratinocytes - Implications For Wound-Healing.
No full textThe molecular mechanism underlying the promotion of wound healing by TGF-beta 1 is incompletely understood. We report that TGF-beta 1 regulates the regenerative/migratory phenotype of normal human keratinocytes by modulating their integrin receptor repertoire. In growing keratinocyte colonies but not in fully stratified cultured epidermis, TGF-beta 1: (a) strongly upregulates the expression of the fibronectin receptor alpha 5 beta 1, the vitronectin receptor alpha v beta 5, and the collagen receptor alpha 2 beta 1 by differentially modulating the synthesis of their alpha and beta subunits; (b) downregulates the multifunctional alpha 3 beta 1 heterodimer; (c) induces the de novo expression and surface exposure of the alpha v beta 6 fibronectin receptor; (d) stimulates keratinocyte migration toward fibronectin and vitronectin; (e) induces a marked perturbation of the general mechanism of polarized domain sorting of both beta 1 and beta 4 dimers; and (f) causes a pericellular redistribution of alpha v beta 5. These data suggest that alpha 5 beta 1, alpha v beta 6, and alpha v beta 5, not routinely used by keratinocytes resting on an intact basement membrane, act as ''emergency'' receptors, and uncover at least one of the molecular mechanisms responsible for the peculiar integrin expression in healing human wounds. Indeed, TGF-beta 1 reproduces the integrin expression pattern of keratinocytes located at the injury site, particularly of cells in the migrating epithelial tongue at the leading edge of the wound. Since these keratinocytes are inhibited in their proliferative capacity, these data might account for the apparent paradox of a TGF-beta 1-dependent stimulation of epidermal wound healing associated with a growth inhibitory effect on epithelial cells
Phosphorylation of p27BBP/eIF6 and its association with the cytoskeleton are developmentally regulated in Xenopus oogenesis
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Cell-cell and cell-matrix adhesion structures may influence the growth pattern of chronic lymphoid malignancies
No full textNo abstract availabl
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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