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Human Polyclonal MEFV Primary Antibody pour WB - ABIN1881537
Cosan, Ustek, Oku, Duymaz-Tozkir, Cakiris, Abaci, Ocal, Aral, Gül: Association of familial Mediterranean fever-related MEFV variations with ankylosing spondylitis. dans Arthritis and rheumatism 2010
Show all 4 Pubmed References
Human Polyclonal MEFV Primary Antibody pour ELISA, WB - ABIN561791
Taskiran, Cetinkaya, Balci-Peynircioglu, Akkaya, Yilmaz: The effect of colchicine on pyrin and pyrin interacting proteins. dans Journal of cellular biochemistry 2012
Human Polyclonal MEFV Primary Antibody pour IP, WB - ABIN1169260
Papin, Cuenin, Agostini, Martinon, Werner, Beer, Grütter, Grütter, Tschopp: The SPRY domain of Pyrin, mutated in familial Mediterranean fever patients, interacts with inflammasome components and inhibits proIL-1beta processing. dans Cell death and differentiation 2007
Human Polyclonal MEFV Primary Antibody pour ELISA, WB - ABIN269824
Rabinovich, Livneh, Langevitz, Brezniak, Shinar, Pras, Shinar: Severe disease in patients with rheumatoid arthritis carrying a mutation in the Mediterranean fever gene. dans Annals of the rheumatic diseases 2005
Francisella induced microparticulate caspase-1/gasdermin-D activation is regulated by NLRP3 independent of Pyrin.
the present study was conducted to better definethe subset of late-onset disease in 10,370 Armenian FMFpatients by matchingMEFVmutational spectra and resultinggenotypes against the clinicodemographic profiles collectedfor these patients between 2005 and 2016
paper identifies two potential microbiota-derived metabolites, the bile acid analogues BAA485 and BAA473, as the first small molecules to activate the pyrin inflammasome. These results suggest that microbiota may be able to modulate this inflammatory process which, in turn, may contribute to the maintenance of intestinal homeostasis.
We performed genome-wide association studies in 1001 Turkish ankylosing spondylitis (AS) patients and 1011 Turkish controls, and 479 Iranian AS patients and 830 Iranian controls. An association of major effect was observed with a novel rare coding variant in MEFV (rs61752717, M694V).
the bile acid analogues BAA485 and BAA473 are the first small molecule activators of the pyrin inflammasome.
Sustained elevation of serum IL-18 may suggest the presence of persistent subclinical inflammation. Therefore, longitudinal examination of serum IL-18 may contribute to better follow-up of Familial Mediterranean fever patients with exon 10 mutations.
Clinical and Demographic Evaluation According to MEFV Genes in Patients with Familial Mediterranean Fever.
Familial Mediterranean fever patients homozygous for E148Q variant may have milder disease.
MEFV gene polymorphism rs3743930 might be significantly associated with ankylosing spondylitis susceptibility in Chinese Han population
MEFV variants in exon 10 may affect clinical presentation of Henoch-Schonlein purpura in populations where Familial Mediterranean fever is common
Case Report: triple MEFV mutations in familial Mediterranean fever patients with no specific phenotype correlation.
A novel single base mutation in the coding region of the MEFV gene, named K447M (p.Lys447Met, c.1340 A>T) heterozygote resulting in mutated Pyrin/Marenostrin protein was detected.
Propose that a variant allele of the MEFV gene may be responsible for the severity of gout.
its single-nucleotide variant is genetic predictor of tumor reduction in glucocorticoid-treated patients with chronic myelomonocytic leukemia.
Carrying the pro-inflammatory M694V mutation in MEFV can be a potential cause of early coronary heart disease.
R202Q/M694V gene mutations related to chronic periodontitis
Carriage of mutations in the MEFV gene is not associated with development of Postpericardiotomy Syndrome; however, it may affect Postpericardiotomy Syndrome severity.
One third of our childhood MS patients had a heterozygous mutation in the TNFRSF1A and/or MEFV gene. This proportion by far exceeds the number of mutations expected and was higher than in adult MS patients, suggesting that these mutations might contribute to the pathogenesis of childhood MS.
The frequency of MEFV gene mutation was detected at a high rate of 35.9% in patients with biopsy-proven primary glomerulonephritis
Sequencing analysis found exon 2 mutations of the MEFV gene (c.329T>C [L110P], and c.442G>C [E148Q]). INTERVENTION: Her arthritis was well-controlled with colchicine treatment, but fever, and rashes were not. OUTCOMES: She eventually received tocilizumab, in addition to colchicine, and her symptoms completely disappeared. LESSONS: MEFV mutations may exist in AOSD patients, and treatment with colchicine might
Pyrin (MEFV) is required for inflammasome activation and IL18 maturation, which promote intestinal barrier integrity and prevent colon inflammation and tumorigenesis.
Mechanistically, Yersinia pseudotuberculosis YopM recruits and activates the mouse host kinases PRK1 and PRK2 to negatively regulate pyrin by phosphorylation.
These results are consistent with a model in which pyrin acts to limit the release of IL-1beta generated by activation and assembly of inflammasomes in response to subclinical immune challenges.
pyrin has a critical role in the innate immune response, possibly by acting on ASC, a known caspase-1 activator
This gene encodes a protein, also known as pyrin or marenostrin, that is an important modulator of innate immunity. Mutations in this gene are associated with Mediterranean fever, a hereditary periodic fever syndrome.
Mediterranean fever protein
, Mediterranean fever
, familial mediterranean fever