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The protein encoded by SAT1 belongs to the acetyltransferase family, and is a rate-limiting enzyme in the catabolic pathway of polyamine metabolism. Zusätzlich bieten wir Ihnen SAT1 Kits (20) und SAT1 Proteine (20) und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 54 products:
Cow (Bovine) Polyclonal SAT1 Primary Antibody für IHC, IHC (p) - ABIN258375
Liao, Lasbury, Wang, Zhang, Durant, Murakami, Matsufuji, Lee: Pneumocystis mediates overexpression of antizyme inhibitor resulting in increased polyamine levels and apoptosis in alveolar macrophages. in The Journal of biological chemistry 2009
Activation of SAT1 expression induces lipid peroxidation and sensitizes cells to undergo ferroptosis upon reactive oxygen species (ROS (zeige ROS1 Antikörper))-induced stress, which also leads to suppression of tumor growth in xenograft tumor models. Notably, SAT1 expression is down-regulated in human tumors, and CRISPR-cas9-mediated knockout of SAT1 expression partially abrogates p53 (zeige TP53 Antikörper)-mediated ferroptosis. Moreover, SAT1 induction is correlated
our results indicated depletion of polyamines by SSAT signi fi cantly inhibited cell proliferation, migration and invasion through AKT (zeige AKT1 Antikörper)/GSK3beta/beta-catenin (zeige CTNNB1 Antikörper) signaling pathway in hepatocellular carcinoma and colorectal cancer cells.
SLC26A1 L348P was associated with lower whole-body bone mineral density (BMD) and higher serum calcium, consistent with the osteochondrodysplasia exhibited by dogs and sheep with naturally occurring, homozygous, loss-of-function mutations in Slc13a1
Extracellular polyamines induced proliferation and cancer cell migration by inducing ODC (zeige ODC1 Antikörper) and SSAT expression, and the Akt1 (zeige AKT1 Antikörper)-mediated pathway.
Human SLC26A1 (zeige SLC26A1 Antikörper) resembles SLC26 paralogs in its inhibition.
Mutations in SLC26A1 (zeige SLC26A1 Antikörper) gene is associated with Nephrolithiasis.
we used siRNA on SSAT and compared the SSAT level in knockdown and normal cells. Results showed that the monoclonal antibody specifically recognized SSAT.
4H6 was also compared with the commercial antibody. The produced mAbs will be a useful tool for further investigation of SSAT functions in organisms.
Results show low SAT1 brain expression in depressed suicides and implicate low SAT1 brain expression in major depression independent of suicide
Data suggest that SAT1 plays role in apoptosis; overexpression of SAT1 in human embryonic kidney cell line leads to a rapid depletion of spermidine and spermine, arrest in cell growth, and mitochondria-mediated apoptosis.
the level of SSAT enzyme activity affected osteoblastogenesis and hence influenced bone remodeling and the bone phenotype in mice
Enhanced SSAT expression by proximal tubule epithelial cells leads to tubular damage, and its deficiency reduces the severity of renal I/R injury through reduction of cellular damage and modulation of the innate immune response
The SSAT overexpression and the concomitantly accelerated polyamine metabolism in hematopoietic cells and bone marrow microenvironment affect lineage commitment and lead to the development of a mouse myeloproliferative disease in SSAT mice.
the results indicate that transcriptional modulation of the SAT1 gene is not a significant component of the hyperoxaluria observed in these rat models
study suggests that SSAT overexpression obtained in SSAT mice enhances the anti-inflammatory actions in the acute phase of LPS (zeige TLR4 Antikörper)-induced immune response
Expression of SSAT increases in kidneys subjected to endotoxic acute kidney injury and that increased polyamine back conversion and oxidation contribute to tubular damage in endotoxin-induced AKI.
increased SSAT expression solely accompanies the proliferative response of mouse kidney, and suggest the importance of post-transcriptional regulation to the control of SSAT activity
Testosterone treatment enhanced AZ1 (zeige AZI1 Antikörper) and N1-SSAT mRNA levels in a time-dependent manner
antiproliferative and metabolic consequences of SSAT overexpression in a prostate cancer model
cutaneous changes of SSAT transgenic animals are due to disorders of the keratinocyte differentiation.
This gene is a member of a family of sulfate/anion transporter genes. Family members are well conserved in their genomic (number and size of exons) and protein (aa length among species) structures, but have markedly different tissue expression patterns. This gene is primarily expressed in the liver, pancreas, and brain. Three splice variants that encode different isoforms have been identified.
diamine N-acetyltransferase 1
, diamine acetyltransferase 1
, polyamine N-acetyltransferase 1
, putrescine acetyltransferase
, spermidine/spermine N(1)-acetyltransferase 1
, spermidine/spermine N1-acetyltransferase alpha
, solute carrier family 26 (sulfate transporter), member 1
, sulfate anion tranporter AT1
, sulfate anion transporter 1
, sulfate/anion transporter SAT-1 protein
, spermidine/spermine N-acetyltransferase
, diamine N-acetyltransferase 1 b
, spermidine/spermine N1-acetyltransferase 1 b
, spermidine/spermine N1-acetyltransferase 1
, Spermidine / spermine N1-acyltransferase (diamine acetyltransferase)
, Polyamine N-acetyltransferase 1
, Putrescine acetyltransferase
, Spermidine/spermine N(1)-acetyltransferase 1