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Human Polyclonal STS Primary Antibody für 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 Pubmed References
Human Polyclonal STS Primary Antibody für IHC, ELISA - ABIN1850088
Xu, Wang, Wen, Sang, Wang, Zeng: Inhibition of NLRP3 inflammasome: a new protective mechanism of cinnamaldehyde in endotoxin poisoning of mice. in Immunopharmacology and immunotoxicology 2018
High ASC expression is associated with Gastric Cancer.
ASC has a role in the regulation of renal fibrosis and endoplasmic reticulum stress after unilateral ureter obstruction, strongly indicating that ASC could serve as an attractive target in the treatment of chronic kidney disease
both Nlrp3(-/-) and Asc(-/-) mice showed a strongly improved host defense, as reflected by a markedly reduced mortality rate accompanied by diminished bacterial growth and dissemination.
Cl(-) channel-dependent formation of dynamic ASC oligomers and inflammasome specks that remain inactive in the absence of K(+) efflux. Formed after Cl(-) efflux exclusively, ASC specks are NLRP3 dependent, reversible, and inactive, although they further prime inflammatory responses.
we found that butyrate significantly decreased Nlrp3 inflammasome formation and activation in the carotid arterial wall of wild type mice (Asc(+/+)), which was comparable to the effect of gene deletion of the adaptor protein apoptosis-associated speck-like protein gene (Asc(-/-)).
oligomerization of ASC creates a multitude of potential caspase-1 activation sites, thus serving as a signal amplification mechanism for inflammasome-mediated cytokine production
Collectively, these results are consistent with a model whereby the type III secretion system apparatus of Pseudomonas aeruginosa activates the caspase-1-dependent inflammasome and caspase-3/7 through an ASC-dependent mechanism.
ASC specks released by microglia bind to amyloid-beta and increase amyloid-beta oligomer and aggregate formation, acting as an inflammation-driven cross-seed for amyloid-beta pathology
results suggest that although Pyk2 and FAK are involved in inflammasome activation, only Pyk2 directly phosphorylates ASC and brings ASC into an oligomerization-competent state by allowing Tyr146 phosphorylation to participate ASC speck formation and subsequent NLRP3 inflammation.
Alendronate (ALN)-augmented IL-1beta production and cell death require Smad3 and ASC activation, and SIS3 and anti-ASC antibodies may serve as palliative agents for necrotizing inflammatory diseases caused by ALN
These data provide evidence that the inflammasome components ASC, NLRP3 and AIM2 play a role in regulating macrophage adhesion and activation in response to surface nanotopography and chemistry.
SGLT-2 inhibition with dapagliflozin reduces the activation of the Nlrp3/ASC inflammasome and attenuates the development of diabetic cardiomyopathy in mice with type 2 diabetes. Effects are augmentated of the by DPP4 inhibitor Saxagliptin.
Elevations of CO2 cause oligomerization of the inflammasome components ASC, NLRP3, caspase 1, thioredoxin interacting protein, and calreticulin - a protein from endoplasmic reticulum, leading to IL-1beta synthesis. An increased production rate of MPs containing elevated amounts of IL-1beta persists for hours after short-term exposures to elevated CO2
Our cumulative findings indicate that ASC suppresses cancer metastasis and progression via the modulation of cytoskeletal remodeling and the Src-caspase-8 signaling pathway.
these findings suggest that p205 controls expression of Asc mRNA to regulate inflammasome responses. These findings expand on our understanding of immune-regulatory roles for the PYHIN protein family.
this study shows that ASC-dependent Inflammasomes do not shape the commensal gut microbiota composition
Our data identify RIPK3 and the ASC inflammasome as key tumor suppressors in AML.
Data show that T cell-intrinsic PYD and CARD domain containing protein ASC is required for TH17-mediated experimental autoimmune encephalomyelitis (EAE).
Data suggest that interleukin 22 (IL-22) plays a pro-inflammatory/pathogenic role in the onset of antigen-induced arthritis (AIA) through apoptosis-associated speck-like Pycard protein (ASC)-dependent stimulation of interleukin-1 beta (IL-1beta) 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 comparable with C57BL/6 mice
Polymorphisms of STS gene is associated with attention-deficit/hyperactivity disorder.
STS is increased in preeclamptic placentas and maternal whole blood. Our data suggests that STS may affect sFlt1 secretion by regulating sFlt1-i13 transcription, and not via alterations in syncytialisation.
This study reveals that STS is a key player of steroid biosynthesis regulating the availability of circulating cholesterol.
In contrast to the situation in boys with ADHD, in healthy men, the G-allele at rs17268988 of STS is associated with enhanced cognition.
miR-661 overexpression sensitized tumors to TRAIL or STS induced apoptosis in a xenograft mouse model, and these effects were attenuated by co-expression of CYC1.
Collectively, STS point mutations demonstrate restricted localization, causing efficient impairment of the corresponding enzyme activity, and are more unlikely to be responsible for the phenotypic heterogeneity in XLRI subjects
STS expression was not significantly associated with DFS 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-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.
Data show that both estrogen sulfatase (STS) and estrogen sulfotransferase (EST) were highly expressed in the human umbilical vein endothelial cells (HUVECs).
Effects of steroid hormone on estrogen sulfotransferase and on steroid sulfatase expression in endometriosis tissue and stromal cells
represents one of the major pathways in regenerating biologically active steroids in both steroidogenic and nonsteroidogenic tissues [review]
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
complete deletion in Pakistani families with x-linked ichthyosis
results suggest that steroid sulfatase expression can be decreased in the process of large intestinal carcinogenesis
Data suggest that expression of STS and 17beta-hydroxysteroid dehydrogenase isoenzymes is up-regulated in subcutaneous abdominal fat of morbidly obese women as compared with morbidly obese men.
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