Ask about this productRelated genes to: ROBO2 Blocking Peptide
- Gene:
- ROBO2 NIH gene
- Name:
- roundabout guidance receptor 2
- Previous symbol:
- -
- Synonyms:
- KIAA1568
- Chromosome:
- 3p12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-26
- Date modifiied:
- 2018-11-19
Related products to: ROBO2 Blocking Peptide
Related articles to: ROBO2 Blocking Peptide
- Alzheimer's disease (AD) is associated with dysregulation of membrane proteins controlling amyloid processing, synaptic signaling, and neuronal communication, yet most proteomic studies focus on soluble fractions, limiting insight into membrane-centered pathology. Here, we apply a membrane-mimetic, data-independent acquisition workflow to define disease- and drug-induced remodeling of the cortical membrane proteome in an APP mouse model of AD. Female wildtype B6C3F1/J and APP/PS1 mice were aged to 9 months, treated ± the M1 positive allosteric modulator VU0486846, and validated by enrichment of APP in cortical membranes of APP/PS1 mice. This confirmed pathological context enabled direct interrogation of membrane remodeling, revealing pronounced, genotype-specific changes characterized by selective enrichment of AD-linked membrane proteins including RyR2, PLD3, ITM2C, and CNTNAP2, alongside broader shifts in pathways related to calcium signaling, synaptic organization, and membrane trafficking. In contrast, wildtype membranes were enriched in proteins associated with axon guidance and synaptic structure, such as EPHA5 and ROBO2. M1 activation produced minimal changes in wildtype mice but selectively enhanced proteins linked to neuronal trafficking and synaptic plasticity in APP/PS1 mice, including SORCS2, PLXND1, and CADM1, indicating preferential engagement of disease-altered pathways. These findings demonstrate that AD-associated remodeling is concentrated at the membrane level and highlight Peptidisc-enabled membrane proteomics as a powerful approach to resolve disease mechanisms and therapeutic target engagement. - Source: PubMed
Publication date: 2026/05/01
Bhattacharya AshimAntony FrankAoki HiroyukiBabu MohanFerguson Stephen S GAbd-Elrahman Khaled SDuong van Hoa Franck - Congenital anomalies of the kidney and urinary tract (CAKUT) constitute the most common underlying cause of chronic kidney disease in pediatric populations. Maternal hypovitaminosis D links to mesoderm-related birth defects, leading to our hypothesis that maternal vitamin D deficiency (VDD) impairs renal development (a mesoderm-derived process) and induces offspring CAKUT. To investigate whether a low-vitamin D level can cause CAKUT, we used vitamin D-free diets to induce a maternal vitamin D deficiency mice model. The maternal vitamin D deficiency (VDD) mice models and normal vitamin D status (CON) were successfully established by administering a vitamin D-free or vitamin D-sufficient diet for 4 weeks prior to pregnancy. The overall incidence of CAKUT was significantly increased in VDD neonatal mice (19.4% vs. 2.44%; = 0.0006), with a higher incidence of early duplicated budding in E11.5. E11.5 ureteric bud tissue revealed significantly increased activity of Gdnf-Ret-p-Erk1/2 signaling in the VDD group. In vivo intervention with the p-Erk1/2 antagonist U0126 in the pregnant VDD mice model at E10.5 improved CAKUT occurrence in offspring with p-Erk1/2 expression decreasing toward normal levels. Early metanephric ureteric bud H3K4me3 CUT&TAG analysis at E12.5 revealed chromatin activation patterns, which revealed that the downregulation of Hnf1β promoter region peaks was accompanied by reduced Hnf1β expression, and Robo2 promoter region peak was upregulated with increased Robo2 expression in the VDD group. Maternal vitamin D deficiency in mice significantly increased offspring CAKUT incidence. This phenotype was mediated by enhanced Gdnf-Ret-p-Erk1/2 signaling and reversed by p-Erk1/2 inhibition, with VDD inducing epigenetic remodeling of Hnf1β and Robo2 promoters. - Source: PubMed
Publication date: 2026/03/27
Yu MinghuiYe NingliJu HaixinMiao QianfanWang ChunyanDai RufengChen JingZhai YihuiSun LeiWu XiaohuiXu HongShen Qian - Alcohol use disorder (AUD) is known to have a significant genetic component, yet there remains a gap between its heritability and findings from genome-wide association studies. One potential explanation for this could be genetic interactions, or epistasis, which remain largely unexplored in the context of AUD. We investigated the role of epistasis in AUD susceptibility among 742 American Indians. By analyzing 467 K variants in 3,736 genes and regulatory elements linked to AUD, we identified 97 interacting gene pairs significantly associated with AUD severity in an American Indian cohort. Five of these gene pairs: CNTNAP2-GRM8, CSMD1-DLGAP1, CSMD1-ERBB4, CSMD1-MAML2, and KCNQ5-ROBO2 - were replicated in All of Us research American Indian cohort (N = 5,037). These genes were enriched for immune system, cell adhesion, neuronal, and disease pathways. Their expressions were particularly enriched in midbrain GABAergic neurons. This large-scale epistasis study of AUD suggests that epistasis may contribute to the development of AUD. - Source: PubMed
Publication date: 2026/04/06
Listopad StanislavPeng Qian - Olfactory sensory neurons (OSNs) project a single axon from the olfactory epithelium to the olfactory bulb. OSNs initially target large, distinct, individually identifiable neuropils called protoglomeruli in the zebrafish embryo. Here we examine the contributions Robo axonal guidance receptors make to OSN axon targeting of protoglomeruli. We show that OSNs that project to the DZ protoglomerulus express higher levels of than those that project to the CZ protoglomerulus, and concordant with this observation, DZ-projecting axons are more often misrouted by loss of than are CZ-projecting axons. Further, we demonstrate that in the absence of , contributes to DZ-targeting but not to CZ-targeting. The loss of either or by themselves do not affect targeting to either the CZ or DZ protoglomeruli. These findings identify OSN subtype-dependent contributions of Robo receptors to vertebrate olfactory circuit assembly. In the absence of repellent Slit/Robo signaling, we propose that Netrin1b steers OSN axons to ectopic ventral midline locations where Slit1a and Netrin1b are both expressed. - Source: PubMed
Publication date: 2026/03/20
Herr Jessica BDevereaux Emily SCurran Matthew JSeligman Carly DCheng Ryan PBarnes Daniel TRaper Jonathan A - To explore associations between circulating proteomic pathways and structural, functional, and symptomatic measures of small- and large-fiber neuropathy and corneal immune activation in people with Type 2 diabetes (T2D). - Source: PubMed
Publication date: 2026/03/18
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