Use your antibodies-online credentials, if available.
抗Human alpha Adducin 抗体:
抗Mouse (Murine) alpha Adducin 抗体:
抗Rat (Rattus) alpha Adducin 抗体:
Human Polyclonal alpha Adducin Primary Antibody for WB - ABIN2801956
Joshi, Gilligan, Otto, McLaughlin, Bennett: Primary structure and domain organization of human alpha and beta adducin. in The Journal of cell biology 1991
Show all 4 Pubmed References
The ADD1 Gly460Trp gene polymorphism is significantly and independently associated with Essential Hypertension risk in a Caucasian population from Madeira Island.
ZNF322A (显示 ZNF322A 抗体) 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 (显示 CALR 抗体)) suggesting an association between ADD1 and CRC (显示 CALR 抗体) risk.
The T allele of ADD1 is associated with essential hypertension in Asians.
study of potential effects of interaction between DNA methylation (显示 HELLS 抗体) 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 (显示 HELLS 抗体) 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 (显示 ACE 抗体) I/D (P<0.05) and AGT (显示 AGXT 抗体) 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 (显示 DNAH8 抗体) in astrocytes, non-cell autonomous neurodegeneration is triggered.
Inhibition of NAMPT (显示 NAMPT 抗体) aggravates high fat diet-induced hepatic steatosis in mice through regulating Sirt1 (显示 SIRT1 抗体)/AMPKalpha (显示 GRK4 抗体)/SREBP1 (显示 SREBF1 抗体) signaling pathway.
SREBP1 (显示 SREBF1 抗体) is dramatically reduced in dysbindin-1 (显示 DTNBP1 抗体) knockout mice; possibly related to cognitive deficits.
Epidermal growth factor receptor (EGFR (显示 EGFR 抗体)) signaling enhances miR (显示 MLXIP 抗体)-29 expression in glioblastoma cells via upregulation of Sterol regulatory element binding protein 1 (显示 SREBF1 抗体)
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 (显示 TOM1L2 抗体) as well as the main genes controlling the synthesis of fatty acids. Transgenic mice also exhibited more adiposity and an increased LPL (显示 LPL 抗体)-mediated FFA influx into the WAT without affecting glucose tolerance
Data show that miR (显示 MLXIP 抗体)-200b and miR (显示 MLXIP 抗体)-200c could directly bind the 3' UTR (显示 UTS2R 抗体) of JUN (显示 JUN 抗体), and JUN (显示 JUN 抗体) activated the transcription of srebp1 (显示 SREBF1 抗体) to increase lipid accumulation.
a novel role for SREBP-1 (显示 SREBF1 抗体) as a cell surface retention factor for TbetaRI (显示 TGFBR1 抗体) in mesangial cells, is reported.
Srebp1c (显示 SREBF1 抗体) is a key regulator of metabolic remodeling leading to the beneficial effects of caloric restriction.
The present study indicates a requirement for C/EBPbeta (显示 CEBPB 抗体) in the insulin (显示 INS 抗体)-mediated induction of SREBP-1c (显示 SREBF1 抗体) mRNA expression in rodent liver. Coupled with previous data showing that this induction requires LXRalpha (显示 NR1H3 抗体), our data reported herein indicate a requirement for both transcription factors.
Sez6l2 is one of the auxiliary subunits of the AMPA receptor and acts as a scaffolding protein to link GluR1 to ADD. Furthermore, Sez6l2 overexpression upregulates ADD phosphorylation, whereas siRNA-mediated downregulation of Sez612 prevents ADD phosphorylation, suggesting that Sez6l2 modulates AMPA-ADD signal transduction.
The deletion of Srebf-2 (显示 SREBF2 抗体) and subsequent lower sterol synthesis in hepatocytes eliminated the production of an endogenous sterol ligand required for LXR (显示 NR1H3 抗体) activity and SREBP-1c (显示 SREBF1 抗体) expression.
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)