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SAT1 is a member of a family of sulfate/anion transporter genes. 再加上，我们可以发SAT1 抗体 (59) 和 SAT1 蛋白 (20)和数多这个蛋白质的别的产品。
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our results indicated depletion of polyamines by SSAT signi fi cantly inhibited cell proliferation, migration and invasion through AKT (显示 AKT1 ELISA试剂盒)/GSK3beta/beta-catenin (显示 CTNNB1 ELISA试剂盒) signaling pathway in hepatocellular carcinoma and colorectal cancer cells.
Extracellular polyamines induced proliferation and cancer cell migration by inducing ODC (显示 ODC1 ELISA试剂盒) and SSAT expression, and the Akt1 (显示 AKT1 ELISA试剂盒)-mediated pathway.
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.
Analysis shows a significant direct correlation between SSAT expression in Prostatic Cancer tissues and disease progression.
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
A role for SAT1 in homologous recombination.
The Catabolic enzyme SSAT expression levels was up-regulated in both cell lines; however, the specific SSAT siRNA treatments prevented the EBR-induced apoptosis only in LNCaP (AR+) cells.
the level of SSAT enzyme activity affected osteoblastogenesis and hence influenced bone remodeling and the bone phenotype in mice
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-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 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.
The protein encoded by this gene belongs to the acetyltransferase family, and is a rate-limiting enzyme in the catabolic pathway of polyamine metabolism. It catalyzes the acetylation of spermidine and spermine, and is involved in the regulation of the intracellular concentration of polyamines and their transport out of cells. Defects in this gene are associated with keratosis follicularis spinulosa decalvans (KFSD). Alternatively spliced transcripts have been found for this gene.
diamine N-acetyltransferase 1
, diamine acetyltransferase 1
, polyamine N-acetyltransferase 1
, putrescine acetyltransferase
, spermidine/spermine N(1)-acetyltransferase 1
, spermidine/spermine N1-acetyltransferase alpha
, 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