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The ADD1 Gly460Trp gene polymorphism is significantly and independently associated with Essential Hypertension risk in a Caucasian population from Madeira Island.
ZNF322A (show ZNF322A ELISA Kits) overexpression transcriptionally dysregulates genes involved in cell growth and motility therefore contributes to lung tumorigenesis and poor prognosis
ADD1 rs4963 polymorphism showed an increased hypertension risk.
This indicates that ADD1 G460W polymorphism could be an important factor in the pathophysiology of tinnitus.
Study shows that ADD1-rs4963 conferred susceptibility to colorectal cancer (CRC (show CALR ELISA Kits)) suggesting an association between ADD1 and CRC (show CALR ELISA Kits) risk.
The T allele of ADD1 is associated with essential hypertension in Asians.
study of potential effects of interaction between DNA methylation (show HELLS ELISA Kits) of ADD1 promoter and ADD1 tagSNPs and environmental factors on essential hypertension (EH); results indicate ADD1 SNP rs4961 has a protective role in development of EH; interactions between alcohol consumption and DNA methylation (show HELLS ELISA Kits) of ADD1 gene promoter have a significant role in modifying EH susceptibility
There were significant differences between the control group and pediatric hypertensive group in terms of ACE (show ACE ELISA Kits) I/D (P<0.05) and AGT (show AGXT ELISA Kits) M235T (P<0.05) polymorphisms, but there were no differences in ADD Gly460Trp (P>0.05) polymorphism.
A significant association was found between ADD1 gene G614T polymorphism and essential hypertension in Chinese patients. Further studies need to be done to confirm these findings in a large sample.
When alpha-adducin complexes with sodium potassium ATPase (show DNAH8 ELISA Kits) in astrocytes, non-cell autonomous neurodegeneration is triggered.
The expression of hHL promoted hepatic triglyceride accumulation and de novo lipogenesis without affecting triglyceride secretion, and this was associated with an upregulation of Srebf1 as well as the main genes controlling the synthesis of fatty acids. Transgenic mice also exhibited more adiposity and an increased LPL (show LPL ELISA Kits)-mediated FFA influx into the WAT without affecting glucose tolerance
Data show that miR (show MLXIP ELISA Kits)-200b and miR (show MLXIP ELISA Kits)-200c could directly bind the 3' UTR (show UTS2R ELISA Kits) of JUN (show JUN ELISA Kits), and JUN (show JUN ELISA Kits) activated the transcription of srebp1 (show SREBF1 ELISA Kits) to increase lipid accumulation.
a novel role for SREBP-1 (show SREBF1 ELISA Kits) as a cell surface retention factor for TbetaRI (show TGFBR1 ELISA Kits) in mesangial cells, is reported.
Srebp1c (show SREBF1 ELISA Kits) is a key regulator of metabolic remodeling leading to the beneficial effects of caloric restriction.
The present study indicates a requirement for C/EBPbeta (show CEBPB ELISA Kits) in the insulin (show INS ELISA Kits)-mediated induction of SREBP-1c (show SREBF1 ELISA Kits) mRNA expression in rodent liver. Coupled with previous data showing that this induction requires LXRalpha (show NR1H3 ELISA Kits), our data reported herein indicate a requirement for both transcription factors.
Sez6l2 (show SEZ6L2 ELISA Kits) is one of the auxiliary subunits of the AMPA (show GRIA3 ELISA Kits) receptor and acts as a scaffolding protein to link GluR1 (show GRIA1 ELISA Kits) to ADD. Furthermore, Sez6l2 (show SEZ6L2 ELISA Kits) overexpression upregulates ADD phosphorylation, whereas siRNA-mediated downregulation of Sez612 prevents ADD phosphorylation, suggesting that Sez6l2 (show SEZ6L2 ELISA Kits) modulates AMPA (show GRIA3 ELISA Kits)-ADD signal transduction.
The deletion of Srebf-2 (show SREBF2 ELISA Kits) and subsequent lower sterol synthesis in hepatocytes eliminated the production of an endogenous sterol ligand required for LXR (show NR1H3 ELISA Kits) activity and SREBP-1c (show SREBF1 ELISA Kits) expression.
The fasting-induced (show C10orf10 ELISA Kits) transcription factor KLF15 (show KLF15 ELISA Kits), a key regulator of gluconeogenesis, forms a complex with LXR (show NR1H3 ELISA Kits)/RXR, specifically on the Srebf1 promoter.
Exposure to a xenobiotic during early development induced persistent fat accumulation via hypomethylation of lipogenic genes. Moreover, increased Nrf2 (show NFE2L2 ELISA Kits) recruitment to the Srebp-1c (show SREBF1 ELISA Kits) promoter in livers of BPA (show DST ELISA Kits)-exposed mice was observed.
Reduction in ADD1 protein in NEK1 (show NEK1 ELISA Kits) mutant mice is associated with hyperphosphorylation of ADD1, thereby preventing the interaction with MYO10 (show MYO10 ELISA Kits) during meiotic spindle formation
Adducins are a family of cytoskeleton proteins encoded by three genes (alpha, beta, gamma). Adducin is a heterodimeric protein that consists of related subunits, which are produced from distinct genes but share a similar structure. Alpha- and beta-adducin include a protease-resistant N-terminal region and a protease-sensitive, hydrophilic C-terminal region. Alpha- and gamma-adducins are ubiquitously expressed. In contrast, beta-adducin is expressed at high levels in brain and hematopoietic tissues. Adducin binds with high affinity to Ca(2+)/calmodulin and is a substrate for protein kinases A and C. Alternative splicing results in multiple variants encoding distinct isoforms\; however, not all variants have been fully described.
adducin 1 (alpha)
, adducin 2 (beta)
, erythrocyte adducin alpha subunit
, erythrocyte adducin subunit alpha
, adipocyte determination- and differentiation-dependent factor 1
, sterol regulatory element-binding protein 1