Slit2 Recombinant Protein
- Known as:
- Slit2 Recombinant Protein
- Catalog number:
- ZR-40-494
- Product Quantity:
- 0.005 mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- Slit2 Recombinant Protein
Related genes to: Slit2 Recombinant Protein
- 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 Recombinant Protein
Related articles to: Slit2 Recombinant Protein
- 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 - Colorectal cancer (CRC) presents complex challenges in treatment and prognosis. This study aims to elucidate the role and mechanism of FYN in colorectal cancer progression and its potential as a prognostic marker. - Source: PubMed
Publication date: 2026/06/02
Su QiangWang KaiyueLiao RuohanZhang HanyuWang Bochu - Chemotherapy-induced alopecia (CIA) is a frequent and distressing adverse effect of cytotoxic cancer therapy that significantly affects patients' quality of life, yet its cellular mechanisms remain incompletely understood and effective pharmacological interventions are limited. Here, we combined single-cell RNA sequencing with in vivo mouse models and ex vivo human hair follicle organ culture to systematically characterize the cellular ecosystem underlying CIA. Our results demonstrate that CIA is not solely caused by apoptosis of rapidly proliferating epithelial cells but represents a coordinated multicompartmental dysfunction within the hair follicle niche. Cyclophosphamide treatment induces profound suppression of ribosomal biogenesis, cytoplasmic translation, mitochondrial oxidative phosphorylation, and Wnt-associated regenerative programs in hair matrix cells, indicating a functional metabolic arrest preceding overt epithelial cell loss. In parallel, dermal fibroblasts undergo inflammatory and stress-associated reprogramming accompanied by activation of IL-1, TNF, IL-6, and epithelial-mesenchymal transition signaling pathways. Chemotherapy also disrupts epithelial-mesenchymal communication through reduced expression of critical niche factors including FGF7, FGF10, and Slit2. Topical venlafaxine and its active metabolite desvenlafaxine preserved follicular architecture, suppressed apoptosis, and restored hair shaft elongation in both mouse CIA models and human hair follicle organ culture. At single-cell resolution, venlafaxine reversed epithelial translational shutdown, reactivated differentiation and Wnt signaling programs, and attenuated fibroinflammatory remodeling, thereby restoring paracrine niche signaling and matrix cell proliferation. Collectively, these findings redefine CIA as a disorder characterized by coordinated epithelial functional arrest and dermal inflammatory remodeling and identify venlafaxine as a potential pharmacological strategy to mitigate chemotherapy-associated hair loss. - Source: PubMed
Publication date: 2026/05/26
Zheng MeiCho JayhyunSong LeeguPark In GukKim JinoSong Seung YongPi Long-QuanNoh MinsooSung Jong-Hyuk - [This retracts the article DOI: 10.3389/fonc.2021.743840.]. - Source: PubMed
Publication date: 2026/05/07
Office Frontiers Editorial - Roundabout homolog 2 (ROBO2) is a transmembrane receptor implicated in glioblastoma (GBM) progression through its interaction with Slit2-mediated signaling pathways. In GBM, increased ROBO2 expression is associated with enhanced Slit2-ROBO2 signaling, promoting tumor cell migration, invasion, and the establishment of an immunosuppressive tumor microenvironment. Despite its therapeutic relevance, no small-molecule modulators targeting ROBO2 have been reported. To address this gap, we performed a structure-based virtual screening campaign targeting ROBO2, followed by experimental validation with Dianthus TRIC platform and microscale thermophoresis (MST). Fifteen compounds were screened for ROBO2 binding, from which four candidates exhibited robust TRIC signals. Subsequent affinity measurements revealed that two small molecules, Z1334432986 and Z1692774161, bind ROBO2 in a reproducible concentration-dependent manner, with dissociation constants (K) of 41±5 μM and 26±17 μM, respectively. Molecular docking with validated hits revealed a shared ROBO2 binding pocket defined by conserved anchor residues (ASN354, SER366, ASP385) and accommodation of distinct ligand conformations within the ROBO2 binding pocket. This work establishes a screening pipeline for identifying ROBO2-targeted small molecules and lays the foundation for developing therapeutics aimed at disrupting Slit-ROBO2 signaling in GBM. - Source: PubMed
Publication date: 2026/05/19
Upmanyu KirtiNada HossamGabr Moustafa T