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betaadducin was demonstrated to have a critical role in neutrophil migration.
Aberrant DNA methylation of ADD2 could be potential screening markers of colorectal cancer.
Study evaluated effects of ADD genetic variability on cognitive functions in a sample of patients with schizophrenia, known to show a wide and heterogeneous neuropsychological deficit and found that ADD2 C1797T polymorphism showed diffuse effects on almost every cognitive domain.
ADD2 and NCX1 variants influence the risk and the clinical features of systemic lupus erythematosus and lupus nephritis.
Taken together, these results show that beta-adducin is a pivotal lipid raft-associated protein in PSGL-1-mediated neutrophil rolling on P-selectin.
chorein interacts with beta-adducin and beta-actin.
phosphorylation of beta-adducin by GSK3 promotes efficient neurite outgrowth in neurons.
ALPHA AND BETA ADDUCIN POLYMORPHISMS AFFECT DECLINE OF RENAL FUNCTION IN HUMAN IGA NEPHROPATHY.
there was significant heterogeneity between Slavic and Italian subjects in the phenotype-genotype relationships with beta-adducin
Expression of the hypertensive rat or human variant of adducin into normal renal epithelial cells recreates the hypertensive phenotype with higher Na+,K+-ATPase activity, mu2-subunit hyperphosphorylation, and impaired Na+,K+-ATPase endocytosis.
Polymorphisms in the ADD2 and ADD3 genes taken alone were not associated with blood pressure and renin activity
The very high levels of expression of ADD2 suggest that its promoter may be useful for directing erythroid-specific gene expression.
beta-adducin is a downstream target of and regulated by the PTN/RPTPbeta/zeta signaling pathway
Changes in intra-erythrocyte cations in ADD2 1797CC homozygous men might lead to osmotic fragility of erythrocytes, but to what extent they reflect systemic changes or are possibly involved in blood pressure regulation remains unknown.
hypertension candidate gene variation may influence BP responses to specific antihypertensive drug therapies and measurement of genetic variation may assist in identifying subgroups of hypertensive patients benefiting from antihypertensive drug therapies
Study shows that a single injection of 3 pharmacologically distinct psychoactive drugs can modify spines in the nucleus accumbens within a day. beta-adducin is necessary for these effects. Study suggests that fine regulation of DARPP-32 phosphorylation is a major factor in mediating common effects on beta-adducin of various drugs with distinct or even opposite modes of action.
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.
Darpp32 interaction with beta-adducin may be the molecular pathway by which environmental changes may rapidly alter responsiveness of striatal neurons involved in the reward system.
Calcium plays a role in regulating the expression and function of beta-adducin to sustain normal organization of the spectrin-based cytoskeleton and the differentiation properties in keratinocytes through the calmodulin/EGFR/cadherin signaling pathway.
study identified novel long-distance upstream non-canonical polyadenylation-regulatory elements that enhance or silence 3'end processing of the Add2 PAS4
betaAdd-knockout mice show increased dendritic spine density in nucleus accumbens and elevated locomotor activity in response to cocaine.
mice lacking beta-Adducin fail to assemble new synapses upon enhanced plasticity and exhibit diminished long-term hippocampal memory upon environmental enrichment.
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.
Analysis of 3 new alleles reveals previously unknown consequences of red blood cell (RBC) spectrin deficiency, resulting in markedly reduced RBC membrane spectrin content, decreased band 3, and absent beta-adducin.
Further analysis based on antibody staining of central and peripheral nerves revealed beta-adducin, septin 2, and sh3p8 as putative paranodal proteins.
beta-Adducin may play an important role in the cellular mechanisms underlying activity-dependent synaptic plasticity associated with learning and memory.
Beta-adducin plays an essential role in the maintenance of erythrocyte shape and membrane stability.
Targeted deletion of alpha-adducin results in absent beta- and gamma-adducin, compensated hemolytic anemia, and lethal hydrocephalus in mice
Adducins are heteromeric proteins composed of different subunits referred to as adducin alpha, beta and gamma. The three subunits are encoded by distinct genes and belong to a family of membrane skeletal proteins involved in the assembly of spectrin-actin network in erythrocytes and at sites of cell-cell contact in epithelial tissues. While adducins alpha and gamma are ubiquitously expressed, the expression of adducin beta is restricted to brain and hematopoietic tissues. Adducin, originally purified from human erythrocytes, was found to be a heterodimer of adducins alpha and beta. Polymorphisms resulting in amino acid substitutions in these two subunits have been associated with the regulation of blood pressure in an animal model of hypertension. Heterodimers consisting of alpha and gamma subunits have also been described. Structurally, each subunit is comprised of two distinct domains. The amino-terminal region is protease resistant and globular in shape, while the carboxy-terminal region is protease sensitive. The latter contains multiple phosphorylation sites for protein kinase C, the binding site for calmodulin, and is required for association with spectrin and actin. Alternatively spliced transcript variants have been described.
adducin 2 (beta)
, erythrocyte adducin subunit beta
, snoRNA MBII-396
, adducin beta