Ask about this productRelated genes to: RAB3IL1 antibody
- Gene:
- RAB3IL1 NIH gene
- Name:
- RAB3A interacting protein like 1
- Previous symbol:
- -
- Synonyms:
- GRAB
- Chromosome:
- 11q12.2-q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-07-30
- Date modifiied:
- 2018-02-13
Related products to: RAB3IL1 antibody
Related articles to: RAB3IL1 antibody
- Acetylcholine (ACh) plays important roles in memory encoding and attention in the hippocampus. However, changes in ACh signaling patterns during different neural and behavioral states remain poorly understood. Here, we used a genetically encoded ACh sensor and multi-plane, dual-color two-photon microscopy to establish the ACh signaling patterns in hippocampal CA1 of mice performing spatial behaviors. We observed spatially homogeneous signaling across volumes spanning hundreds of microns, which was positively correlated with locomotion speed. In novel environments, there was an increase in release persisting for dozens of laps while maintaining a positive speed correlation. When mice voluntarily disengaged, the magnitude of the speed-correlated release decreased, and this was accompanied by reduced place cell numbers and less precise place maps. Administration of scopolamine mimicked the effects of voluntary disengagement in terms of behavior and place cell metrics. These findings establish behaviorally correlated ACh signaling patterns in the hippocampus. - Source: PubMed
Publication date: 2025/10/16
Xuan FengLi GuochuanLi YulongDombeck Daniel A - Breast ductal carcinoma in situ (DCIS), a common precursor of breast cancer, has poorly understood susceptible driver genes. This study aimed to identify genes influencing DCIS progression by integrating Mendelian randomization (MR) and Gene Expression Omnibus (GEO) datasets. - Source: PubMed
Publication date: 2025/09/11
Mo Cai-QinXie Rui-WangLi Wei-WeiZhong Min-JieLi Yu-YangLin Jun-YuZhang Juan-SiZheng Sheng-KaiLin WeiKong Ling-JunXu Sun-WangChen Xiang-Jin - Ferroptosis, an iron-dependent form of regulated cell death characterized by phospholipid peroxidation, plays a pivotal role in various diseases. However, its involvement in male infertility, particularly in idiopathic non-obstructive azoospermia (iNOA), remains largely unexplored. Idiopathic non-obstructive azoospermia accounts for 10-15% of male infertility cases, presenting a significant clinical challenge due to its unknown origins. This study investigated the potential link between ferroptosis and iNOA, revealing excessive activation of both ferroptosis and autophagy in the testes of iNOA patients, along with severe disruption of the blood-testis barrier (BTB). The BTB, formed by tight junctions between Sertoli cells, is essential for maintaining the spermatogenesis microenvironment. Using the ferroptosis inducer erastin, an antagonist of the cystine antiporter Solute Carrier Family 7 Member 11 (SLC7A11), we established a ferroptosis model in mouse Sertoli cells, demonstrating that ferroptosis activation led to cytoskeletal disarray and BTB disruption, accompanied by excessive autophagy activation. Notably, inhibition of autophagy using 3-methyladenine significantly rescued erastin-induced ferroptosis and restored BTB integrity, highlighting a crucial cross-talk between ferroptosis and autophagy in maintaining the spermatogenic microenvironment. Furthermore, through combined transcriptome analysis of iNOA testes and Sertoli cells, we identified RAB3IL1 as a novel regulator of ferroptosis. Mechanistically, Rab3il1 knockdown induced ferroptosis via translocation of SLC7A11, resulting in cytoskeletal defects and BTB damage. Our findings underscore the critical role of the ferroptosis-autophagy axis, regulated by RAB3IL1, in preserving the spermatogenic microenvironment, offering a potential therapeutic target for restoring spermatogenesis in iNOA patients. - Source: PubMed
Ma BinyuHong ZhidanGao YingWan YingjingHe XuanyiWang MeiZhang Yuanzhen - Autism spectrum disorder (ASD) presents a wide range of cognitive and language impairments. In this study, we investigated the genetic basis of non-verbal status in ASD using a comprehensive genomic approach. We identified a novel common variant, rs1944180 in CNTN5, significantly associated with non-verbal status through family-based Transmission Disequilibrium Testing. Polygenic risk score (PRS) analysis further showed that higher ASD PRS was significantly linked to non-verbal status (p = 0.034), specific to ASD and not related to other conditions such as bipolar disorder, schizophrenia and three language-related traits. Using structural equation modeling (SEM), we found two causal SNPs, rs1247761 located in KCNMA1 and rs2524290 in RAB3IL1, linking ASD with language traits. The model indicated a unidirectional effect, with ASD driving language impairments. Additionally, de novo mutations (DNMs) were found to be related with ASD and interaction between common variants and DNMs significantly impacted non-verbal status (p = 0.038). Our findings also identified 5 high-risk ASD genes, and DNMs were enriched in glycosylation-related pathways. These results offer new insights into the genetic mechanisms underlying language deficits in ASD. - Source: PubMed
Publication date: 2025/06/07
Liu HuanWang ShenghanCao BinbinZhu JijunHuang ZhifangLi PanZhang ShunjieLiu XianYu JingHuang ZhongtingLv LinzhuoCai FuqiangLiu WeixinSong ZhijianLiu YuxinPang TaoChang SuhuaChen YingChen JunfangChen Wen-Xiong - Developing erythroblasts acquire massive amounts of iron through the transferrin (Tf) cycle, which involves endocytosis, sorting, and recycling of the Tf-Tf receptor (Tfrc) complex. Previous studies on the hemoglobin-deficit (hbd) mouse have shown that the exocyst complex is indispensable for the Tfrc recycling; however, the precise mechanism underlying the efficient exocytosis and recycling of Tfrc in erythroblasts remains unclear. Here, we identify the guanine nucleotide exchange factor Grab as a critical regulator of the Tf cycle and iron metabolism during erythropoiesis. Grab is highly expressed in differentiating erythroblasts. Loss of Grab diminishes the Tfrc recycling and iron uptake, leading to hemoglobinization defects in mouse primary erythroblasts, mammalian erythroleukemia cells, and zebrafish embryos. These defects can be alleviated by supplementing iron together with hinokitiol, a small-molecule natural compound that can mediate iron transport independent of the Tf cycle. Mechanistically, Grab regulates the exocytosis of Tfrc-associated vesicles by activating the GTPase Rab8, which subsequently promotes the recruitment of the exocyst complex and vesicle exocytosis. Our results reveal a critical role for Grab in regulating the Tf cycle and provide new insights into iron homeostasis and erythropoiesis. - Source: PubMed
Chen MengyingZhang YuhanJiang KailunWang WeixiFeng HeZhen RuMoo ChingyeeZhang ZhuonanShi JiahaiChen Caiyong