Results 41 to 50 of about 14,267 (224)

Experience of rituximab therapy in pemphigus: A three-year retrospective study from a Sub-Himalayan State

open access: yesIndian Journal of Dermatology, 2022
Background: Pemphigus is a group of auto-immune blistering disorders, characterised clinically by mucocutaneous blisters and erosions and histopathologically by intra-epidermal acantholysis.
Ghanshyam Verma   +5 more
doaj   +1 more source

Protease inhibitors prevent plasminogen-mediated, but not pemphigus vulgaris-induced, acantholysis in human epidermis [PDF]

open access: yes, 2003
Pemphigus is an autoimmune blistering disease of the skin and mucous membranes. It is caused by autoantibodies directed against desmosomes, which are the principal adhesion structures between epidermal keratinocytes.
Besch, R.   +9 more
core   +1 more source

Desmoglein-1, differentiation, and disease [PDF]

open access: yesJournal of Clinical Investigation, 2013
Desmoglein-1 (DSG1), a desmosomal protein, maintains the structure of epidermis through its adhesive function. However, heterozygous mutations in DSG1 in humans result in abnormal differentiation, as does downregulation of DSG1 in human skin organ culture, suggesting that it may have important signaling functions. In this issue of the JCI, Harmon et al.
Christoph M, Hammers, John R, Stanley
openaire   +2 more sources

Differential Downregulation of E-Cadherin and Desmoglein by Epidermal Growth Factor

open access: yesDermatology Research and Practice, 2012
Modulation of cell : cell junctions is a key event in cutaneous wound repair. In this study we report that activation of the epidermal growth factor (EGF) receptor disrupts cel : cell adhesion, but with different kinetics and fates for the desmosomal ...
Miquella G. Chavez   +5 more
doaj   +1 more source

Desmosomal Junctions and Connexin-43 Remodeling in High-Pacing-Induced Heart Failure Dogs

open access: yesAnatolian Journal of Cardiology, 2023
Background: While desmosomal junctions and gap junction remodeling are among the arrhythmogenic substrates, the fate of desmosomal and gap junctions in high-pacing-induced heart failure remains unclear. This aim of this study was to determine the fate of
Qing Wang   +6 more
doaj   +1 more source

Nonischemic left ventricular scar and cardiac sudden death in the young [PDF]

open access: yes, 2016
Nonischemic Left Ventricular Scar (NLVS) is a pattern of myocardial injury characterized by midventricular and/or subepicardial gadolinium hyper enhancement at cardiac magnetic resonance, in absence of significant coronary artery disease.
CERBELLI, BRUNA   +10 more
core   +1 more source

Cortical tension regulates desmosomal morphogenesis

open access: yesFrontiers in Cell and Developmental Biology, 2022
Mechanical stability is a fundamental and essential property of epithelial cell sheets. It is in large part determined by cell-cell adhesion sites that are tightly integrated by the cortical cytoskeleton.
Marcin Moch   +2 more
doaj   +1 more source

c-Src/Cav1-dependent activation of the EGFR by Dsg2. [PDF]

open access: yes, 2016
The desmosomal cadherin, desmoglein 2 (Dsg2), is deregulated in a variety of human cancers including those of the skin. When ectopically expressed in the epidermis of transgenic mice, Dsg2 activates multiple mitogenic signaling pathways and increases ...
Brennan-Crispi, Donna M.   +8 more
core   +2 more sources

Sudden cardiac death in young athletes: Literature review of molecular basis [PDF]

open access: yes, 2020
Intense athletic training and competition can rarely result in sudden cardiac death (SCD). Despite the introduction of pre-participation cardiovascular screening, especially among young competitive athletes, sport-related SCD remains a debated issue ...
Barbara Lombardo   +5 more
core   +1 more source

Expression of Desmoglein 1 Compensates for Genetic Loss of Desmoglein 3 in Keratinocyte Adhesion [PDF]

open access: yesJournal of Investigative Dermatology, 2002
The desmoglein compensation hypothesis, namely that one desmoglein can compensate for loss of function of another, has been proposed to explain the tissue specificity of the autoantibody-induced loss of cell adhesion in pemphigus. To validate this hypothesis genetically, we used desmoglein-3 knockout mice (DSG3-/-) that lose their telogen hair ...
Hanakawa, Yasushi   +2 more
openaire   +2 more sources

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