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Human Polyclonal STS Primary Antibody for Func, ICC - ABIN1169071
Dashdorj, Jyothi, Lim, Jo, Nguyen, Ha, Yoon, Kim, Park, Murphy, Kim: Mitochondria-targeted antioxidant MitoQ ameliorates experimental mouse colitis by suppressing NLRP3 inflammasome-mediated inflammatory cytokines. in BMC medicine 2013
Show all 10 references for ABIN1169071
Human Monoclonal STS Primary Antibody for FACS - ABIN2662386
Masumoto, Taniguchi, Ayukawa, Sarvotham, Kishino, Niikawa, Hidaka, Katsuyama, Higuchi, Sagara: ASC, a novel 22-kDa protein, aggregates during apoptosis of human promyelocytic leukemia HL-60 cells. in The Journal of biological chemistry 1999
Show all 8 references for ABIN2662386
Human Monoclonal STS Primary Antibody for FACS - ABIN2666298
Conway, McConnell, Bowring, Donald, Warren, Vertino: TMS1, a novel proapoptotic caspase recruitment domain protein, is a target of methylation-induced gene silencing in human breast cancers. in Cancer research 2000
Show all 8 references for ABIN2666298
Our data identify RIPK3 (show RIPK3 Antibodies) and the ASC inflammasome as key tumor suppressors in AML (show RUNX1 Antibodies).
Data show that T cell-intrinsic PYD and CARD domain containing protein ASC (show PYCARD Antibodies) is required for TH17-mediated experimental autoimmune encephalomyelitis (EAE).
Data suggest that interleukin 22 (IL-22 (show IL22 Antibodies)) plays a pro-inflammatory/pathogenic role in the onset of antigen-induced arthritis (AIA) through apoptosis-associated speck-like Pycard (show PYCARD Antibodies) protein (ASC)-dependent stimulation of interleukin-1 beta (IL-1beta (show IL1B Antibodies)) production.
report herein that lack of ASC does not confer preferential protection in response to P. aeruginosa acute infection and that ASC(-/-) mice are capable of producing robust amounts of IL-1beta (show IL1B Antibodies) comparable with C57BL/6 mice
These data identify a novel non-canonical immunoregulatory function of NLRP3 (show NLRP3 Antibodies) and ASC in autoimmunity.
a significant role for NLRP3 (show NLRP3 Antibodies) and ASC in prion (show PRNP Antibodies) pathogenesis
ASC-driven caspase-1 (show CASP1 Antibodies) autoprocessing and speck formation are dispensable for the activation of caspase-1 (show CASP1 Antibodies) and the NLRP1b inflammasome.
IKKalpha (show CHUK Antibodies) controls the inflammasome at the level of the adaptor molecule ASC, which interacts with IKKalpha (show CHUK Antibodies) in the nucleus of resting macrophages in an IKKalpha (show CHUK Antibodies) kinase-dependent manner.
Hypoxia-induced elevated right ventricular pressure and remodeling were attenuated in mice lacking the inflammasome adaptor protein ASC, suggesting that inflammasomes play an important role in the pathogenesis of pulmonary hypertension.
gene deficiency results in absence of IL-1beta (show IL1B Antibodies) maturation in the middle ear response to non-typeable Haemophilus influenza, and in reduction of both leukocyte infiltration and macrophage phagocytosis
STS expression was not significantly associated with DFS (show FST Antibodies) and OS, despite positive STS expression in 27% of endometrial cancer patients. Therefore, the role of STS as a prognostic factor in patients with endometrial cancer remains unclear and requires further research.
The induced STS facilitates the conversion of inactive estrogen sulfates to active estrogens, which in return attenuates the NF-kappaB (show NFKB1 Antibodies)-mediated inflammation.
The antagonistic actions of glucocorticoids and NFkB on STS expression are similar to the regulation of inflammatory response proteins
Letter/Case Report: novel nonsense mutation in the STS gene in X-linked ichthyosis (show LBR Antibodies).
Data show that both estrogen sulfatase (show ARSH Antibodies) (STS) and estrogen sulfotransferase (EST (show SULT1E1 Antibodies)) were highly expressed in the human umbilical vein endothelial cells (HUVECs).
Effects of steroid hormone on estrogen sulfotransferase (show SULT1E1 Antibodies) and on steroid sulfatase expression in endometriosis tissue and stromal cells
Our analyses show that the two phenotypes in our patient are due to independent genetic defects: a genomic rearrangement involving the Kallmann syndrome 1 gene and a point mutation of the steryl-sulfatase gene.
In both arm and subumbilical skin biopsy of patients with idiopathic hirsutism, there was an up-regulation of STS mRNA expression.
Genetic variation in ARSC may be associated with change in mammographic density after women stop using estrogen-progestin therapy.
STS is present in human pre-osteoblastic bone cells and that it can influence bone cell growth
The protein encoded by this gene catalyzes the conversion of sulfated steroid precursors to estrogens during pregnancy. The encoded protein is found in the endoplasmic reticulum, where it acts as a homodimer. Mutations in this gene are known to cause X-linked ichthyosis (XLI).
PYD and CARD domain-containing protein
, apoptosis-associated speck-like protein containing a CARD
, arylsulfatase C
, estrone sulfatase
, steryl-sulfate sulfohydrolase