acne vulgaris/proline

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Leht 1 alates 28 tulemused

Purification and properties of a proline iminopeptidase from Propionibacterium acnes.

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Proline iminopeptidase was extracted from the cells of a strain of Propionibacterium acnes and purified. The molecular weight was estimated to be about 120,000 by SDS-polyacrylamide gel electrophoresis. The enzyme showed the highest activity at 50 degrees C-55 degrees C and its optimum pH was found

Keratin 5-Cre-driven deletion of Ncstn in an acne inversa-like mouse model leads to a markedly increased IL-36a and Sprr2 expression.

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Familial acne inversa (AI) is an autoinflammatory disorder that affects hair follicles and is caused by loss-of-function mutations in γ-secretase component genes. We and other researchers showed that nicastrin (NCSTN) is the most frequently mutated gene in familial AI. In this study, we generated a

A peptide with a ProGln C terminus in the human saliva peptidome exerts bactericidal activity against Propionibacterium acnes.

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Nine proline-rich peptides ending with a proline-glutamine C terminus in a salivary peptidome were sequenced by matrix-assisted laser desorption ionization time of flight time of flight tandem mass spectrometry. A GPPPQGGRPQ peptide binds gram-positive Propionibacterium acnes and considerably

Novel PSTPIP1 gene mutation in a patient with pyogenic arthritis, pyoderma gangrenosum and acne (PAPA) syndrome.

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BACKGROUND Pyogenic arthritis, pyoderma gangrenosum, and acne (PAPA) syndrome is a rare autosomal dominant disease that usually presents in childhood with recurrent sterile arthritis. As the child ages into puberty, cutaneous features develop and arthritis subsides. We report the case of a now

Disease activity accounts for long-term efficacy of IL-1 blockers in pyogenic sterile arthritis pyoderma gangrenosum and severe acne syndrome.

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To provide a rationale for anti-IL-1 treatment in pyogenic sterile arthritis, pyoderma gangrenosum and acne (PAPA) by defining whether IL-1β secretion is enhanced; requires NLRP3; and correlates with proline-serine-threonine phosphatase-interacting protein 1 mutations, disease activity and/or the

Single amino acid charge switch defines clinically distinct proline-serine-threonine phosphatase-interacting protein 1 (PSTPIP1)-associated inflammatory diseases.

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BACKGROUND Hyperzincemia and hypercalprotectinemia (Hz/Hc) is a distinct autoinflammatory entity involving extremely high serum concentrations of the proinflammatory alarmin myeloid-related protein (MRP) 8/14 (S100A8/S100A9 and calprotectin). OBJECTIVE We sought to characterize the genetic cause and

Imaging findings of sterile pyogenic arthritis, pyoderma gangrenosum and acne (PAPA) syndrome: differential diagnosis and review of the literature.

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Pyogenic arthritis, pyoderma gangrenosum and acne (PAPA) syndrome is a rare autosomal-dominant autoinflammatory disease of incomplete penetrance and variable expression. PAPA syndrome is the result of a mutation in the proline serine threonine phosphatase-interacting protein 1 (PSTPIP1/CD2BP1) gene

Inflammation in mice ectopically expressing human Pyogenic Arthritis, Pyoderma Gangrenosum, and Acne (PAPA) Syndrome-associated PSTPIP1 A230T mutant proteins.

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Pyogenic Arthritis, Pyoderma Gangrenosum, and Acne Syndrome (PAPA syndrome) is an autoinflammatory disease caused by aberrant production of the proinflammatory cytokine interleukin-1. Mutations in the gene encoding proline serine threonine phosphatase-interacting protein-1 (PSTPIP1) have been linked

Proline-serine-threonine phosphatase interacting protein 1 inhibition of T-cell receptor signaling depends on its SH3 domain.

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Proline-serine-threonine phosphatase interacting protein 1 (PSTPIP1) is an adaptor protein associated with the cytoskeleton that is mainly expressed in hematopoietic cells. Mutations in PSTPIP1 cause the rare autoinflammatory disease called pyogenic arthritis, pyoderma gangrenosum, and acne. We

Pyoderma gangrenosum, acne and ulcerative colitis in a patient with a novel mutation in the PSTPIP1 gene.

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BACKGROUND Pyogenic sterile arthritis, pyoderma gangrenosum and acne (PAPA) syndrome is a rare hereditary, autosomal dominant, auto-inflammatory disease caused by mutations in the PSTPIP1 gene, which encodes proline-serine-threonine phosphatase interacting protein 1. The fact that PSTPIP1 is

Alarming consequences - autoinflammatory disease spectrum due to mutations in proline-serine-threonine phosphatase-interacting protein 1.

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To give an overview about the expanding spectrum of autoinflammatory diseases due to mutations in proline-serine-threonine phosphatase-interacting protein 1 (PSTPIP1) and new insights into their pathogenesis. In addition to classical pyogenic sterile arthritis, pyoderma gangrenosum, and acne (PAPA)

A common pathway in periodic fever syndromes.

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Familial Mediterranean fever (FMF) is an autosomal recessive disease due to mutations in pyrin, which normally inhibits pro-interleukin-1beta (IL-1beta) cytokine processing to the active form. A novel role for pyrin has been proposed by Shoham et al., who studied patients with an autosomal dominant

[PAPA syndrome with Crohn's disease and primary sclerosing cholangitis/autoimmune hepatitis overlap syndrome].

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BACKGROUND The PAPA syndrome, an acronym for pyogenic sterile arthritis, pyoderma gangraenosum and acne, is an autosomal dominant hereditary disease which is caused by a mutation in the PSTPIP1 ("proline-serine-threonine phosphatase interacting protein 1") gene located on chromosome 15 and encodes

Mutations in the PSTPIP1 gene and aberrant splicing variants in patients with pyoderma gangrenosum.

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BACKGROUND Pyoderma gangrenosum (PG) is a rare, noninfectious form of skin ulceration, typically accompanied by neutrophilic infiltration. Several familial cases have been reported, suggesting the involvement of genetic factors in the aetiology of PG. Two mutations (A230T and E250Q) in the PSTPIP1

PAPA spectrum disorders

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Pyogenic arthritis, pyoderma gangrenosum (PG) and acne (PAPA) syndrome is an autosomal dominant autoinflammatory syndrome due to mutations in proline-serine-threonine phosphatase interacting protein 1 (PSTPIP1) gene and presenting with cutaneous and articular manifestations. Other autoinflammatory

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