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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 Proteins) 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 Proteins)) suggesting an association between ADD1 and CRC (show CALR Proteins) risk.
The T allele of ADD1 is associated with essential hypertension in Asians.
study of potential effects of interaction between DNA methylation (show HELLS Proteins) 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 Proteins) 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 Proteins) I/D (P<0.05) and AGT (show AGXT Proteins) 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 in astrocytes, non-cell autonomous neurodegeneration is triggered.
Results showed that Glrx (show GRX1 Proteins)(-/-) mice exhibited decreased SirT1 (show SIRT1 Proteins) activity that leads to hyperacetylation and activation of SREBP-1 (show SREBF1 Proteins) and upregulation of key hepatic enzymes involved in lipid synthesis.
Inhibition of NAMPT (show NAMPT Proteins) aggravates high fat diet-induced hepatic steatosis in mice through regulating Sirt1 (show SIRT1 Proteins)/AMPKalpha (show GRK4 Proteins)/SREBP1 (show SREBF1 Proteins) signaling pathway.
SREBP1 (show SREBF1 Proteins) is dramatically reduced in dysbindin-1 (show DTNBP1 Proteins) knockout mice; possibly related to cognitive deficits.
Epidermal growth factor receptor (EGFR (show EGFR Proteins)) signaling enhances miR (show MLXIP Proteins)-29 expression in glioblastoma cells via upregulation of Sterol regulatory element binding protein 1 (show SREBF1 Proteins)
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 (show TOM1L2 Proteins) as well as the main genes controlling the synthesis of fatty acids. Transgenic mice also exhibited more adiposity and an increased LPL (show LPL Proteins)-mediated FFA influx into the WAT without affecting glucose tolerance
Data show that miR (show MLXIP Proteins)-200b and miR (show MLXIP Proteins)-200c could directly bind the 3' UTR of JUN (show JUN Proteins), and JUN (show JUN Proteins) activated the transcription of srebp1 (show SREBF1 Proteins) to increase lipid accumulation.
a novel role for SREBP-1 (show SREBF1 Proteins) as a cell surface retention factor for TbetaRI (show TGFBR1 Proteins) in mesangial cells, is reported.
Srebp1c (show SREBF1 Proteins) 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 Proteins) in the insulin (show INS Proteins)-mediated induction of SREBP-1c (show SREBF1 Proteins) mRNA expression in rodent liver. Coupled with previous data showing that this induction requires LXRalpha (show NR1H3 Proteins), our data reported herein indicate a requirement for both transcription factors.
Sez6l2 (show SEZ6L2 Proteins) is one of the auxiliary subunits of the AMPA (show GRIA3 Proteins) receptor and acts as a scaffolding protein to link GluR1 (show GRIA1 Proteins) to ADD. Furthermore, Sez6l2 (show SEZ6L2 Proteins) overexpression upregulates ADD phosphorylation, whereas siRNA-mediated downregulation of Sez612 prevents ADD phosphorylation, suggesting that Sez6l2 (show SEZ6L2 Proteins) modulates AMPA (show GRIA3 Proteins)-ADD signal transduction.
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.
, erythrocyte adducin alpha subunit
, erythrocyte adducin subunit alpha
, adducin 1 (alpha)
, adducin 2 (beta)