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anti-Human alpha Adducin Antikörper:
anti-Mouse (Murine) alpha Adducin Antikörper:
anti-Rat (Rattus) alpha Adducin Antikörper:
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Human Polyclonal alpha Adducin Primary Antibody für 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 (zeige ZNF322A Antikörper) 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 (zeige CALR Antikörper)) suggesting an association between ADD1 and CRC (zeige CALR Antikörper) risk.
The T allele of ADD1 is associated with essential hypertension in Asians.
study of potential effects of interaction between DNA methylation (zeige HELLS Antikörper) 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 (zeige HELLS Antikörper) 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 (zeige ACE Antikörper) I/D (P<0.05) and AGT (zeige AGXT Antikörper) 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 (zeige DNAH8 Antikörper) in astrocytes, non-cell autonomous neurodegeneration is triggered.
Inhibition of NAMPT (zeige NAMPT Antikörper) aggravates high fat diet-induced hepatic steatosis in mice through regulating Sirt1 (zeige SIRT1 Antikörper)/AMPKalpha (zeige GRK4 Antikörper)/SREBP1 (zeige SREBF1 Antikörper) signaling pathway.
SREBP1 (zeige SREBF1 Antikörper) is dramatically reduced in dysbindin-1 (zeige DTNBP1 Antikörper) knockout mice; possibly related to cognitive deficits.
Epidermal growth factor receptor (EGFR (zeige EGFR Antikörper)) signaling enhances miR (zeige MLXIP Antikörper)-29 expression in glioblastoma cells via upregulation of Sterol regulatory element binding protein 1 (zeige SREBF1 Antikörper)
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 (zeige TOM1L2 Antikörper) as well as the main genes controlling the synthesis of fatty acids. Transgenic mice also exhibited more adiposity and an increased LPL (zeige LPL Antikörper)-mediated FFA influx into the WAT without affecting glucose tolerance
Data show that miR (zeige MLXIP Antikörper)-200b and miR (zeige MLXIP Antikörper)-200c could directly bind the 3' UTR (zeige UTS2R Antikörper) of JUN (zeige JUN Antikörper), and JUN (zeige JUN Antikörper) activated the transcription of srebp1 (zeige SREBF1 Antikörper) to increase lipid accumulation.
a novel role for SREBP-1 (zeige SREBF1 Antikörper) as a cell surface retention factor for TbetaRI (zeige TGFBR1 Antikörper) in mesangial cells, is reported.
Srebp1c (zeige SREBF1 Antikörper) is a key regulator of metabolic remodeling leading to the beneficial effects of caloric restriction.
The present study indicates a requirement for C/EBPbeta (zeige CEBPB Antikörper) in the insulin (zeige INS Antikörper)-mediated induction of SREBP-1c (zeige SREBF1 Antikörper) mRNA expression in rodent liver. Coupled with previous data showing that this induction requires LXRalpha (zeige NR1H3 Antikörper), 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 (zeige SREBF2 Antikörper) and subsequent lower sterol synthesis in hepatocytes eliminated the production of an endogenous sterol ligand required for LXR (zeige NR1H3 Antikörper) activity and SREBP-1c (zeige SREBF1 Antikörper) 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)