Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
Select your origin of interest
These findings highlight that ADD1 methylation may have a contributing role in the pathogenesis of EH with varying implications for both genders.
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.
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.
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 (show PKCd Proteins)(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 (show ADD3 Proteins), 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)