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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 (zeige ZNF322A Proteine) 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 Proteine)) suggesting an association between ADD1 and CRC (zeige CALR Proteine) risk.
The T allele of ADD1 is associated with essential hypertension in Asians.
study of potential effects of interaction between DNA methylation (zeige HELLS Proteine) 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 Proteine) 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 Proteine) I/D (P<0.05) and AGT (zeige AGXT Proteine) 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.
Sez6l2 (zeige SEZ6L2 Proteine) is one of the auxiliary subunits of the AMPA (zeige GRIA3 Proteine) receptor and acts as a scaffolding protein to link GluR1 (zeige GRIA1 Proteine) to ADD. Furthermore, Sez6l2 (zeige SEZ6L2 Proteine) overexpression upregulates ADD phosphorylation, whereas siRNA-mediated downregulation of Sez612 prevents ADD phosphorylation, suggesting that Sez6l2 (zeige SEZ6L2 Proteine) modulates AMPA (zeige GRIA3 Proteine)-ADD signal transduction.
Reduction in ADD1 protein in NEK1 mutant mice is associated with hyperphosphorylation of ADD1, thereby preventing the interaction with MYO10 during meiotic spindle formation
adducin activity is not essential for actin ring assembly and periodicity but is necessary to control the diameter of both actin rings and axons and actin filament growth within rings.
Targeted deletion of Add1 reveals strain-dependent hyperkyphosis and megaesophagus in c57bl, 129s1 and B6 mice.
organization of a spectrin-like cytoskeleton is associated with keratinocyte differentiation, and cytoskeleton disruption is mediated by either PKCdelta (zeige PKCd Proteine)(Thr505) phosphorylation associated with phosphorylated adducin or due to reduction of endogenous adducin
Reorganization of the unique cytoskeletal network defining a primary quiescent T cell is mediated thru the TCR-dependent modification & downregulation of alpha-adducin, resulting in a cytoskeletal shape compatible with T cell effector & memory functions.
Targeted deletion of alpha-adducin results in absent beta- and gamma-adducin (zeige ADD3 Proteine), compensated hemolytic anemia, and lethal hydrocephalus in mice
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)