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brucellosis/tyrosine

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9 結果

PTPN22 C1858T polymorphism and human brucellosis.

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The PTPN22 gene encodes for an intracellular lymphoid-specific phosphatase (Lyp) that has a negative regulatory effect on T-cell activation. The minor allele of the single nucleotide polymorphism (SNP) in the PTPN22 gene encoding the Lyp-tyrosine phosphatase has been associated with multiple

Lack of the Association of the PTPN22 C1858T Gene Polymorphism With Susceptibility to Familial Mediterranean Fever.

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UNASSIGNED This study aims to investigate whether the protein tyrosine phosphatase non-receptor type 22 (PTPN22) C1858T gene polymorphism plays a role in the pathogenesis of familial Mediterranean fever (FMF) through T-lymphocyte activation. UNASSIGNED We conducted a case-control study with 180 FMF

Pyrin binds the PSTPIP1/CD2BP1 protein, defining familial Mediterranean fever and PAPA syndrome as disorders in the same pathway.

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Pyrin, the familial Mediterranean fever protein, is found in association with the cytoskeleton in myeloid/monocytic cells and modulates IL-1beta processing, NF-kappaB activation, and apoptosis. These effects are mediated in part through cognate interactions with the adaptor protein ASC, which shares

GTPases of the Rho subfamily are required for Brucella abortus internalization in nonprofessional phagocytes: direct activation of Cdc42.

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Members of the genus Brucella are intracellular alpha-Proteobacteria responsible for brucellosis, a chronic disease of humans and animals. Little is known about Brucella virulence mechanisms, but the abilities of these bacteria to invade and to survive within cells are decisive factors for causing

A dual-targeting approach to inhibit Brucella abortus replication in human cells.

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Brucella abortus is an intracellular bacterial pathogen and an etiological agent of the zoonotic disease known as brucellosis. Brucellosis can be challenging to treat with conventional antibiotic therapies and, in some cases, may develop into a debilitating and life-threatening chronic illness. We

Colchicine toxicity precipitated by interaction with sunitinib.

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OBJECTIVE Colchicine is an anti-inflammatory agent used primarily in treatment of gout and familial Mediterranean fever. Toxicity is uncommon, and depends on dose, hepatic or renal impairment, co-administration with P-glycoprotein or CYP3A4 inhibitors and route of administration. In patients taking

The IFNgamma-induced STAT1-CBP/P300 association, required for a normal response to the cytokine, is disrupted in Brucella-infected macrophages.

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To develop intracellularly within phagocytes and cause chronic infection, Brucella must overcome different steps of the host immune responses. IFNgamma is a key mediator of the innate and adaptive responses produced during Brucella infection. Therefore, Brucella would control host defenses by

Comparative Transcriptome Analysis of Artificially Induced Rough-Mutant Brucella Strain RM57 and Its Parent Strain Brucella melitensis M1981.

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Brucellosis is one of the most common zoonotic epidemics with a serious threat to public health and livestock development in many countries across the world. Vaccination is a key control strategy toward preventing brucellosis in high-prevalence regions. Recently, a rough-type Brucella

The systemic autoinflammatory diseases: inborn errors of the innate immune system.

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The autoinflammatory syndromes are a newly recognized group of immune disorders that lack the high titers of self-reactive antibodies and T cells characteristic of classic autoimmune disease. Nevertheless, patients with these illnesses experience unprovoked inflammatory disease in the absence of
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