Use your antibodies-online credentials, if available.
Keine Produkte auf Ihrer Vergleichsliste.
Ihr Warenkorb ist leer.
TGM5 encodes a member of the transglutaminase family. Zusätzlich bieten wir Ihnen Transglutaminase 5 Antikörper (58) und und viele weitere Produktgruppen zu diesem Protein an.
Showing 4 out of 4 products:
Acral PSS (APSS) (OMIM 609796), typically non-inflammatory, is confined to distal extremities with localized exfoliation of the epidermis. It is caused by mutations in the TGM5 gene, encoding transglutaminase 5 or in the CTSA gene, encoding cystatin A and it is inherited in autosomal recessive pattern
We report both European and non-European families with acral peeling skin syndrome carrying mutations in the TGM5 gene. In 5 patients, we found 3 novel mutations: c.1001+2_1001+3del, c.1171G>A and c.1498C>T.
Data trebles the number of TMG5 mutations and provides further evidence that pCly113Cys is a founder mutation in the European population.
study concludes polymorphisms of TGM5, PPAP2B and PSMA4 are not major contributors tonon-small cell lung cancer susceptibility in never-smoking hinese population, this primarily can be attributed to the significantly distinct genetic background of Asian populations from western populations
Genetic variation in the epidermal transglutaminase genes is not associated with atopic dermatitis.
TGM5 mutations impact epidermal differentiation in acral peeling skin syndrome.
analysis of a recurrent mutation in the TGM5 gene in European patients with acral peeling skin syndrome
Acral peeling skin syndrome with TGM5 gene mutations may resemble epidermolysis bullosa simplex in young individuals.
transglutaminase 5 contributes, as a secondary effect, to the hyperkeratotic phenotype in ichthyosis (both vulgaris and lamellar) and in psoriasis.
Results demonstrate that transglutaminase 5 is able to induce cell death when intracellularly overexpressed.
Data show that transglutaminase (TGase) 5 is acetylated at the N-terminal end, is active upon treatment with phorbol acetate, and co-localises with vimentin intermediate filaments.
Transglutaminase 5 is expressed during hair follicle homeostasis.
A homozygous missense mutation in TGM5 abolishes epidermal TGM5 activity and causes acral peeling skin syndrome.
TG5 full-length enzyme has very low enzymatic activity, while the 53-kDa proteolytically processed form is highly active.
A missense mutation in TGM5 causes acral peeling skin syndrome in a Tunisian family.
This gene encodes a member of the transglutaminase family. The encoded protein catalyzes formation of protein cross-links between glutamine and lysine residues, often resulting in stabilization of protein assemblies. This reaction is calcium dependent. Mutations in this gene have been associated with acral peeling skin syndrome.
, protein-glutamine gamma-glutamyltransferase 5-like
, TGase X
, protein-glutamine gamma-glutamyltransferase 5
, transglutaminase V
, transglutaminase X
, TGase 5