Ask about this productRelated genes to: RRAD antibody
- Gene:
- RRAD NIH gene
- Name:
- RRAD, Ras related glycolysis inhibitor and calcium channel regulator
- Previous symbol:
- -
- Synonyms:
- REM3, RAD
- Chromosome:
- 16q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-12-11
- Date modifiied:
- 2016-10-05
Related products to: RRAD antibody
Related articles to: RRAD antibody
- Plasma phosphorylated tau (p-tau)217 levels and apolipoprotein E () ε4 genotype are used for prodromal identification of individuals at high risk for dementia. We used baseline samples from cognitively normal subjects in the Risk Reduction for Alzheimer's Disease (rrAD) clinical trial (NCT02913664) to investigate the relationship between these two markers in older adults with additional vascular risk factors. - Source: PubMed
Publication date: 2026/03/09
Stowe Ann MKahn BilalBallesteros AliCortez MoniqueHynan Linda SCantrell VictoriaRaman InduChen GuangchunVidoni Eric DBinder EllenBurns JeffreyKeller Jeffrey NKerwin Diana RHall TristynYanev PavelVongapatanasin WanpenZhu David CScheel NormanCullum C MunroZhang RongGerman Dwight C - The (rrAD) trial included 513 cognitively normal, sedentary, hypertensive older adults (aged 60 to 85 years) with dementia risk factors. We utilized 420 high-quality baseline resting-state functional MRI (rs-fMRI) scans from this cohort to develop a functional atlas tailored for aging populations. Typical rs-fMRI atlases derived from healthy young adults do not account for age-related changes, such as cortical atrophy, enlarged ventricles, and altered connectivity. To address this gap, we created a cohort-specific MNI-adjacent anatomical template, rrAD420, using SPM12's DARTEL registration. In this space, we derived a comprehensive functional atlas using both group independent component analysis (GICA) and probabilistic functional mode decomposition (PROFUMO). The rrAD420 atlas offers detailed representations of Resting-State Network (RSN) connectivity, encompassing unique configurations and overlapping interactions. It features two Default-Mode Network (DMN)-specific seed-based maps (DMN24 with cerebellum, DMN18 without) and data-driven components resembling the major RSNs. Furthermore, PROFUMO allowed for the identification of multimodal and combinatory networks, capturing connections within and between RSNs. While optimized for hypertensive older adults, the rrAD420 atlas serves as a versatile tool for broader aging populations, aiding in the study of neurodegenerative processes and biomarker discovery. - Source: PubMed
Publication date: 2025/12/01
Scheel NormanFernandez ZacBaker JoshYanev PavelKeller Jeffrey NBinder Ellen FVidoni Eric DBurns Jeffrey MStowe Ann MKerwin Diana RCullum C MunroHynan Linda SVongpatanasin WanpenZhang RongZhu David C - The ionic mechanism by which catecholamines increase the heart rate is incompletely understood. In this study, we have assessed the roles of sinoatrial node L-type Ca1.3 (α) Ca channels, phosphorylation of L-type channel regulatory partner protein Rad (Ras-related RGK GTP-binding protein), and cAMP-dependent regulation of hyperpolarization-activated HCN (hyperpolarization-activated cyclic nucleotide-gated) channels. - Source: PubMed
Publication date: 2025/12/04
Torre EleonoraFaure MélanieBidaud IsabelleBaudot MatthiasGaillardon MarvinPereira de Vasconcelos WalmaLaarioui SihameTalssi LeïlaEngeland BirgitReiken StevenSaponaro AndreaChen Bi-XingMoroni AnnaD'Souza AliciaIsbrandt DirkMarks Andrew RMarx Steven OMesirca PietroMangoni Matteo E - Heart failure with reduced ejection fraction (HFrEF) is a major health problem. Increasing L-type calcium channel (LTCC) activity deteriorates heart function; however, myocardial RRAD knockout (cRADΔ/Δ) instills tonic modulated LTCC current (ICa,L) that preserves healthy myocardium. Thus, we chose to challenge the dogma that enhanced trigger Ca2+ is maladaptive. The study objective was to test the hypothesis that modulated ICa,L in cRADΔ/Δ mice rescues dilated cardiomyopathy by providing tonic modulated trigger Ca2+. - Source: PubMed
Elmore GarrettLohano Sarisha SMcVay Nicholas MLevitan Bryana MSebastian AndreaBarker Kyle WDupont AlecLeung Steven WAbouleisa Riham R EMathew Pretty RWellette-Hunsucker AustinMinton Austin TCampbell Kenneth SHarrar Solomon WMehri MohammadWenk Jonathan FMohamed Tamer M AAndres Douglas ASatin Jonathan - Pancreatic β-cells undergo senescence and loss during aging; however, the underlying mechanisms remain incompletely understood. This study aimed to investigate what sirtuin 6 (SIRT6) does during β-cell aging. Pancreatic β-cell-specific Sirt6 transgenic (TgSIRT6) mice were generated for this study. DNA damage, cell death, and cell proliferation were analyzed in cell and mouse models. SIRT6 protein levels were decreased in pancreatic β-cells during aging. TgSIRT6 mice exhibited less DNA damage and cell death, including apoptosis, necroptosis, and pyroptosis, in β-cells than control mice. TgSIRT6 mice had increased total islet area and mass in pancreas compared with control mice. As a result, TgSIRT6 mice showed better glucose tolerance and glucose-stimulated insulin secretion than control mice. RRAD and GEM-like GTPase 2 (REM2), an endogenouse inhibitor of high-voltage-activated calcium channels, was negatively regulated by SIRT6. Knockdown of Rem2 in INS-1 cells partially rescued the SIRT6 deficiency- and palmitic acid-induced DNA damage, lipid peroxidation, and cell death. Rem2 β-cell-specific knockout mice had less DNA damage and cell death in β-cells than control mice. Our data suggest that SIRT6 is a critical antiaging factor in pancreatic β-cells and is a potential therapeutic target. - Source: PubMed
Park JiminLokuge Sandali DHuang MenghaoWang ShenLiu ShengLiang JingruKatturajan RamkumarMarakovits CorinnYang ZhihongWan JunDong X Charlie