Interferon alpha decreases expression of human scavenger receptor class BI, a possible HCV receptor in hepatocytesmore suppliers
In Virology Journal, 2007
... MEK, ERK, STAT1, phospho-MEK (Ser217/221), phospho-ERK (Thr202/Tyr204), phospho-SAPK/JNK (Thr183/Tyr185), phospho-p38 MAPK (Thr180/Tyr182), phospho-ATF-2 (Thr71), or phospho-STAT1 (Tyr701) were purchased from Cell Signaling Technology (Beverly, MA) ...
Mendelian susceptibility to mycobacterial disease: genetic, immunological, and clinical features of inborn errors of IFN-γ immunity.
New York City, United States. In Semin Immunol, Dec 2014
Since 1996, nine MSMD-causing genes, including seven autosomal (IFNGR1, IFNGR2, STAT1, IL12B, IL12RB1, ISG15, and IRF8) and two X-linked (NEMO, and CYBB) genes have been discovered.
Apoptosis of beta cells in diabetes mellitus.
Hyderābād, India. In Dna Cell Biol, Nov 2014
Cytokines induce the expression of Fas and tumor necrosis factor-alpha (TNF-α) by activating the transcription factor, nuclear factor-κb, and signal transducer and activator of transcription 1 (STAT-1) in the β cells in the extrinsic pathway of apoptosis.
Activated STING in a vascular and pulmonary syndrome.
Bethesda, United States. In N Engl J Med, Sep 2014
Mutant STING leads to increased phosphorylation of signal transducer and activator of transcription 1 (STAT1), so we tested the effect of Janus kinase (JAK) inhibitors on STAT1 phosphorylation in lymphocytes from the affected children and controls.
Interferons and their stimulated genes in the tumor microenvironment.
Cleveland, United States. In Semin Oncol, Apr 2014
Induction of the gene products by both unphosphorylated and phosphorylated STAT1 after ligand binding results in alterations in tumor cell survival, inhibition of angiogenesis, and augmentation of actions of T, natural killer (NK), and dendritic cells.
Herpes in STAT1 gain-of-function mutation [corrected].
More papers using
Debrecen, Hungary. In Lancet, 2012
individuals carrying STAT1 mutations might also be susceptible to viral diseases. The mechanism underlying reactivation disease in patients with STAT1 mutations and chronic mucocutaneous candidosis could involve the impairment of memory T cells