Browse our anti-alpha Adducin (ADD1) Antibodies

Human Adducin 1 (Alpha) (ADD1) interaction partners

1. These findings unveil a novel function of ADD1 in maintaining spindle pole integrity through its interaction with TPX2.

2. alpha-adducing SNPs were not associated with bone density among lead workers.

3. These findings highlight that ADD1 methylation may have a contributing role in the pathogenesis of EH with varying implications for both genders.

4. The ADD1 Gly460Trp gene polymorphism is significantly and independently associated with Essential Hypertension risk in a Caucasian population from Madeira Island.

5. ZNF322A overexpression transcriptionally dysregulates genes involved in cell growth and motility therefore contributes to lung tumorigenesis and poor prognosis

6. ADD1 rs4963 polymorphism showed an increased hypertension risk.

7. This indicates that ADD1 G460W polymorphism could be an important factor in the pathophysiology of tinnitus.

8. study shows that the a-adducin G460T polymorphism is associated with essential hypertension

9. Study shows that ADD1-rs4963 conferred susceptibility to colorectal cancer (CRC) suggesting an association between ADD1 and CRC risk.

10. The T allele of ADD1 is associated with essential hypertension in Asians.

11. study of potential effects of interaction between DNA methylation 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 of ADD1 gene promoter have a significant role in modifying EH susceptibility

12. There were significant differences between the control group and pediatric hypertensive group in terms of ACE I/D (P<0.05) and AGT M235T (P<0.05) polymorphisms, but there were no differences in ADD Gly460Trp (P>0.05) polymorphism.

13. 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.

14. When alpha-adducin complexes with sodium potassium ATPase in astrocytes, non-cell autonomous neurodegeneration is triggered.

15. Data indicate that adducin promotes adhesion by regulating desmosomes and is part of a protective pathway in pemphigus.

16. Phosphorylation of ADD1 at Ser12 and Ser355 by cyclin-dependent kinase 1 enables ADD1 to bind to myosin-X (Myo10).

17. Fnnctional polymorphism in the phosphorylation site of ADD1 (rs4963) may influence the susceptibility of non-cardia gastric cancer.

18. concentration of AST was inversely correlated with ADD1 CpG2-5 methylation levels in female controls. These observations may bring new hints to elaborate the pathogenesis of essential hypertension

19. study is the first meta-analysis to evaluate the influences of ACE and ADD1 polymorphisms on blood pressure responses to hydrochlorothiazide to combine the inconsistent results of previous studies

20. the rs4963 polymorphism within ADD1 gene is associated with essential hypertension in the Chinese population

Mouse (Murine) Adducin 1 (Alpha) (ADD1) interaction partners

1. 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.

2. Reduction in ADD1 protein in NEK1 mutant mice is associated with hyperphosphorylation of ADD1, thereby preventing the interaction with MYO10 during meiotic spindle formation

3. 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.

4. Targeted deletion of Add1 reveals strain-dependent hyperkyphosis and megaesophagus in c57bl, 129s1 and B6 mice.

5. organization of a spectrin-like cytoskeleton is associated with keratinocyte differentiation, and cytoskeleton disruption is mediated by either PKCdelta(Thr505) phosphorylation associated with phosphorylated adducin or due to reduction of endogenous adducin

6. These results strongly suggest coordinated expression and phosphorylation of alpha-, beta-, and gamma-adducins as key mechanism underlying synaptic plasticity, motor coordination performance and learning behaviors.

7. 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.

8. Targeted deletion of alpha-adducin results in absent beta- and gamma-adducin, compensated hemolytic anemia, and lethal hydrocephalus in mice