Ask about this productRelated genes to: SLIT2 antibody
- Gene:
- SLIT2 NIH gene
- Name:
- slit guidance ligand 2
- Previous symbol:
- SLIL3
- Synonyms:
- Slit-2
- Chromosome:
- 4p15.31
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-11
- Date modifiied:
- 2016-10-05
Related products to: SLIT2 antibody
Related articles to: SLIT2 antibody
- Diabetes mellitus-induced erectile dysfunction (DMED) is a common and debilitating vascular-neurogenic complication of diabetes. The poor responsiveness of DMED patients to phosphodiesterase type-5 inhibitors underscores the need for therapies capable of restoring both endothelial integrity and cavernous nerve function. The Slit2/Roundabout (Robo) pathway, a conserved regulator of axon guidance and vascular remodeling, is well positioned to coordinate neurovascular repair; however, its involvement in DMED remains largely undefined. - Source: PubMed
Publication date: 2026/06/18
Fu SenHu PengYang ZizhongJin ZhenghuiZhu XiaoyuWang TaoLiu JihongCui Kai - The SLIT2-ROBO signaling axis plays a context-dependent role in cancer, functioning as either a tumor suppressor or oncogenic driver. This bidirectionality creates both therapeutic opportunity and significant challenges for drug development and patent strategy. - Source: PubMed
Publication date: 2026/06/18
Al-Ruweidi Mahmoud KhatibGabr Moustafa T - Chronic obstructive pulmonary disease (COPD) is a leading cause of global morbidity and mortality, with smoking being its primary etiological factor. The Slit2-roundabout (Robo) signaling axis is recognized for its pivotal roles in guiding cell migration and regulating immune responses. Recently, its involvement in smoking-related lung inflammation and tissue remodeling has garnered increasing attention. The objective of this narrative review is to synthesize current evidence on the immune regulatory functions of the Slit2-Robo axis in the pathogenesis of COPD, and to explore its translational potential. - Source: PubMed
Publication date: 2026/05/22
An WeiweiLiang Dejin - Contactin-6 (CNTN6) is a membrane protein that belongs to the contactin subgroup of the immunoglobulin (Ig) superfamily. Substantial evidence supports a significant role of its encoding gene, CNTN6, in neurodevelopment and psychiatric disorders, including autism spectrum disorders and schizophrenia. Further studies are required to clarify the role of CNTN6 in the etiology of these disorders. Here, we show that the first three Ig domains of the extracellular region of CNTN6 compete with Robo2 for binding to the leucine-rich repeat (LRR) domain of Slit2 and inhibit Slit-Robo signaling, thereby regulating neurite outgrowth in cortical neurons. The repulsive effect of Slit2 on the migration of GABAergic neurons was attenuated by the interaction between CNTN6 and Slit2, both in vitro and ex vivo. Male mice deficient in Cntn6 exhibited a significant reduction in the number of calbindin-positive GABAergic neurons in the motor cortex. Cntn6-null male mice also exhibited impaired social recognition and disrupted self-grooming behavior. These findings suggest that CNTN6 inhibits Slit-Robo signaling and modulates the migration of a subset of GABAergic neurons, thereby contributing to the development of autism-related behaviors associated with CNTN6 dysfunction. - Source: PubMed
Publication date: 2026/06/13
Xu YiliangZhao TianZhao DanZhang WeiMu DiGui AilingGuo JunzhiWatanabe KazutadaXiao Zhi-ChengYe Haihong - Pancreatic islets regulate blood glucose homeostasis. Although islet architecture is stable under homeostatic conditions, increased metabolic demand drives compensatory islet expansion. In mice, islets are organized as a β cell core surrounded by a mantle of α and δ cells. The formation of islet architecture during development requires expression of Roundabout receptors 1 and 2 (Robo1/2) in endocrine cells and of Slits 2 and 3 (Slit2/3) from islet-extrinsic sources. Furthermore, expression of Robo2 in endocrine cells is required to maintain islet architecture in the adult mouse. However, the cellular sources of Slit2/3 in the adult pancreas and their expression dynamics during islet expansion remain unknown. Here, we identify distinct stromal populations, including fibroblasts and pericytes, as well as neurons within intrapancreatic ganglia, as the sources of Slit2/3. We further show that Slit3 expression is increased in Ob/Ob mice, and that SLIT2 expression is elevated in stromal cell populations of humans with type 2 diabetes. The expression of neither Slit2 nor Slit3 was affected by deletion of Robo2 in β cells. Together, these findings define the cellular origins of Slit2/3 and their expression dynamics in the adult pancreas, supporting a potential role for Slit signaling in the diabetic islet microenvironment. - Source: PubMed
Publication date: 2026/05/18
Wagner Matthew RPintozzi Nicolas GSchoff Bjorn MGold Marissa IKasper Rachel HSteele Nina GBlum Barak