ANKS1B
- Known as:
- ANKS1B
- Catalog number:
- 001661A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ANKS1B
Related genes to: ANKS1B
- Gene:
- ANKS1B NIH gene
- Name:
- ankyrin repeat and sterile alpha motif domain containing 1B
- Previous symbol:
- -
- Synonyms:
- EB-1, AIDA-1, cajalin-2, ANKS2
- Chromosome:
- 12q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 2006-02-17
- Date modifiied:
- 2016-01-14
Related products to: ANKS1B
Related articles to: ANKS1B
- The transition from controlled to escalated drug intake is a core feature of cocaine use disorder (CUD), yet the molecular mechanisms underlying this behavioral escalation remain poorly defined. Our prior genome-wide association study (GWAS) identified ANKS1B as a significant shared genetic risk factor for heroin, methamphetamine, and alcohol dependence, suggesting a broad role in addiction vulnerability. However, the specific function of ANKS1B in cocaine addiction and its associated neural mechanisms were unknown. Here, we found that ANKS1B expression level in the Nucleus Accumbens (NAc) was downregulated after extended cocaine use, and manipulating ANKS1B could selectively influence the escalation of cocaine intake and the subsequent cocaine-seeking behavior in the long-access cocaine self-administration rat model. Molecular experiments reveal that ANKS1B interacts with the histone acetyltransferase CBP to control H3K27 acetylation and extended cocaine intake, via epigenetically repressing the transcription factor FoxO3. Overall, these findings suggest that ANKS1B is a crucial factor influencing the escalation of cocaine use. The ANKS1B-CBP-FoxO3 signaling pathway presents a promising target for potential therapeutic interventions for controlling extended cocaine use. - Source: PubMed
Publication date: 2026/06/02
Yang LipingWu XiaoxuanChen XuanPeng ChaoLi ZihangGao ShuminMeng ShiqiuDong JingWu DongLv LiyingHan YingXue YanxueLu LinShi JieLiu JianfengSun Yan - Ischemic stroke triggers a cascade of metabolic shifts and excitotoxicity, partially mediated by GluN2B-containing N-methyl-d-aspartate receptors (NMDARs). While protein lactylation has emerged as a key metabolic regulator, its role in modulating neurotoxicity remains underexplored. In this study, we integrated proteomics datasets from middle cerebral artery occlusion (MCAO) mouse models and identified ANKS1B as a unique protein that is both differentially lactylated and downregulated in ischemic tissue. Using an oxygen-glucose deprivation/reperfusion (OGD/R) model in SH-SY5Y cells, we demonstrated that ischemia induces ANKS1B lactylation at the conserved K1222 site. This modification targets ANKS1B for ubiquitin-proteasome-mediated degradation. Functionally, ANKS1B regulates the endoplasmic reticulum (ER) export of GluN2B. Lactylation-driven ANKS1B loss leads to GluN2B retention in the ER. Notably, expressing a lactylation-resistant mutant (ANKS1B-K1222R) prevented this degradation, resulting in restored GluN2B surface trafficking. However, this preservation of ANKS1B proved detrimental, as it exacerbated intracellular Ca overload and increased neuronal death following OGD/R. These results indicate that ischemia-induced ANKS1B lactylation acts as an adaptive, neuroprotective feedback mechanism to limit excitotoxicity by downregulating surface NMDARs. This study reveals a novel link between metabolic reprogramming and synaptic protein trafficking, providing new insights into stroke pathophysiology and potential therapeutic targets. - Source: PubMed
Publication date: 2026/01/17
Yang PingLiu JunzhaoRong XiaLi TongyaoHu WensiWang NaLiu ZizhongShi LinLuo LinnaTang Haibo - Alzheimer's disease (AD) has genetic and environmental risk factors, including cigarette smoking. Gene-environment interactions may explain AD missing heritability. - Source: PubMed
Dacey RyanHou LeiGurnani AshitaHan XudongPaller-Moore Mackenzie RChung JaeyoonDurape ShrutiRosenthaler MaxUretsky MadelineAbdolmohammadi BobakLee Annie JBrickman Adam MHohman Timothy JCuccaro Michael LBennett David ACrane Paul KKamboh M IlyasKukull Walter AJun GyungahStein Thor DMcKee Ann CHaines Jonathan LPericak-Vance Margaret AWang Li-SanSchellenberg Gerard DMayeux RichardLunetta Kathryn LFarrer Lindsay AMez Jesse - Sexual dimorphism in mouse gonads becomes evident at around embryonic day (E)12.5, followed by germ cell differentiation. While prior studies have concentrated on protein-coding genes, our research expands this by profiling the complete spectrum of stranded RNAs including long and short RNAs in one preparation. We identified 2419 differentially expressed genes (DEGs) in the comparison between E12.5 and E11.5 mouse gonads, along with 333 and 770 DEGs in E13.5 versus E12.5 and in E14.5 versus E13.5, respectively. A total of 22 RNA types were annotated, highlighting mRNA, tRNA, long non-coding RNA, antisense RNA, small nucleolar RNA, and microRNA as the most significantly varied types. Serial chromosomal ideographs revealed active chromatin hubs encompassing Hox, tRNA, and stefin gene clusters. Chromosomes 11 and 13 exhibited a higher density of DEGs. Notably, some unassigned reads were mapped to the TESCO (testis-specific enhancer core sequence enhancer), with quantitative PCR results confirming elevated expression of TESCO enhancer RNA at E12.5. By integrating data from public databases, we propose potential regulatory networks involving transcription factors, miR6236, Snord33, long intergenic non-coding RNA , , and . Our study provides the first complete stranded RNA profiling during early gonad development and serves as a reference for future functional genetic and epigenetic research in reproductive biology. - Source: PubMed
Publication date: 2025/05/02
Ou FanghongWang ZhangtingChan See-WingMiu Kai-KeiChan Wai-Yee - - Source: PubMed
Publication date: 2025/08/27
Prasun PankajPulvermacher Rebecca C