Ask about this productRelated genes to: SLIT3 antibody
- Gene:
- SLIT1 NIH gene
- Name:
- slit guidance ligand 1
- Previous symbol:
- SLIL1
- Synonyms:
- slit1, MEGF4, Slit-1, SLIT3
- Chromosome:
- 10q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-25
- Date modifiied:
- 2016-07-12
- Gene:
- SLIT3 NIH gene
- Name:
- slit guidance ligand 3
- Previous symbol:
- SLIL2
- Synonyms:
- slit2, MEGF5, SLIT1, Slit-3
- Chromosome:
- 5q34-q35.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-25
- Date modifiied:
- 2018-02-13
Related products to: SLIT3 antibody
Related articles to: SLIT3 antibody
- Drug-induced liver injury accounts for approximately 10% of acute hepatitis and up to 50% of acute liver failure. Despite its clinical significance, treatment remains largely limited to cessation of the offending agent. SLIT/ROBO signaling, known for roles in organ development, angiogenesis, leukocyte migration, and cancer metastasis, has demonstrated protective effects against various organ damage. In mouse models of liver injury induced by acetaminophen (APAP), thioacetamide, bile duct ligation, and serum from patients with toxic liver disease, Slit2 expression significantly increases, while Slit1 and Slit3 remain unchanged. Liver-specific Slit2 knockdown exacerbates liver injury, whereas recombinant SLIT2 alleviates liver damage by reducing oxidative stress via CYP2E1 downregulation and suppressing inflammation through nuclear factor κB inhibition. Notably, among ROBO receptors, only ROBO4 was induced in hepatocytes after APAP exposure. ROBO4 knockdown eliminates the hepatoprotective effects of SLIT2, highlighting the importance of SLIT2/BOBO4 signaling in toxic liver injury. Furthermore, the novel Slit2-derived peptide 5 (SP5), designed from the ROBO4-binding LRR2 domain, significantly reduces liver damage and inflammation. Notably, both recombinant SLIT2 and SP5 confer hepatoprotection even when administered 24 h after APAP challenge. These findings suggest that SLIT2/ROBO4-targeted therapies may offer a promising approach for preventing fulminant hepatitis in the context of toxic liver injury. - Source: PubMed
Publication date: 2026/01/10
Choi Yong WonChoi Jae HoLee Young-SamJeong JinjuKang EunhoPark So HyunLee Young-KyoungPark Soon SangKang Hee YoungKim Young HwaPark Tae Jun - SLIT1 has recently been shown to regulate ovarian follicle development and female fertility. In this study, we elucidate SLIT1's intracellular signaling mechanisms and transcriptional targets and further show that it acts in a redundant manner with SLIT2 in granulosa cells. - Source: PubMed
Publication date: 2025/09/25
Grudet FlorineGusscott SamuelGodin PhilippeMartinot EmmanuelleChédotal AlainBrind'Amour JulieBoerboom Derek - The SLIT family (SLIT1-3) of highly conserved glycoproteins was originally identified as ligands for the Roundabout (ROBO) family of single-pass transmembrane receptors, serving to provide repulsive axon guidance cues in the nervous system. Intriguingly, studies involving SLIT3 mutant mice suggest that SLIT3 might have crucial biological functions outside the neural context. Although these mutant mice display no noticeable neurological abnormalities, they present pronounced connective tissue defects, including congenital central diaphragmatic hernia, membranous ventricular septal defect, and osteopenia. We recently hypothesized that the phenotype observed in SLIT3-deficient mice may be tied to abnormalities in fibrillar collagen-rich connective tissue. Further research by our group indicates that both SLIT3 and its primary receptor, ROBO1, are expressed in fibrillar collagen-producing cells across various nonneural tissues. Global and constitutive SLIT3 deficiency not only reduces the synthesis and content of fibrillar collagen in various organs but also alleviates pressure overload-induced fibrosis in both the left and right ventricles. This review delves into the known phenotypes of SLIT3 mutants and the debated role of SLIT3 in vasculature and bone. Present evidence hints at SLIT3 acting as an autocrine regulator of fibrillar collagen synthesis, suggesting it as a potential antifibrotic treatment. However, the precise pathway and mechanisms through which SLIT3 regulates fibrillar collagen synthesis remain uncertain, presenting an intriguing avenue for future research. - Source: PubMed
Publication date: 2023/10/13
Gong LianghuiSi Ming-Sing - Liver fibrosis is a common outcome of most chronic liver insults/injuries that can develop into an irreversible process of cirrhosis and, eventually, liver cancer. In recent years, there has been significant progress in basic and clinical research on liver cancer, leading to the identification of various signaling pathways involved in tumorigenesis and disease progression. Slit glycoprotein (SLIT)1, SLIT2, and SLIT3 are secreted members of a protein family that accelerate positional interactions between cells and their environment during development. These proteins signal through Roundabout receptor (ROBO) receptors (ROBO1, ROBO2, ROBO3, and ROBO4) to achieve their cellular effects. The SLIT and ROBO signaling pathway acts as a neural targeting factor regulating axon guidance, neuronal migration, and axonal remnants in the nervous system. Recent findings suggest that various tumor cells differ in SLIT/ROBO signaling levels and show varying degrees of expression patterns during tumor angiogenesis, cell invasion, metastasis, and infiltration. Emerging roles of the SLIT and ROBO axon-guidance molecules have been discovered in liver fibrosis and cancer development. Herein, we examined the expression patterns of SLIT and ROBO proteins in normal adult livers and two types of liver cancers: hepatocellular carcinoma and cholangiocarcinoma. This review also summarizes the potential therapeutics of this pathway for anti-fibrosis and anti-cancer drug development. - Source: PubMed
Publication date: 2023/05/01
Basha SreenivasuluJin-Smith BradySun ChunbaoPi Liya - This study aimed to understand aberrant methylation of genes as a biomarker for the early detection and prognosis prediction of non-small cell lung cancer (NSCLC). Methylation levels of were determined using the Infinium HumanMethylation450 BeadChip or pyrosequencing. Five CpGs at the CpG island of , or genes were significantly (Bonferroni corrected < 0.05) hypermethylated in tumor tissues obtained from 42 NSCLC patients than in matched normal tissues. Methylation levels of these CpGs did not differ significantly between bronchial washings obtained from 76 NSCLC patients and 60 cancer-free patients. However, methylation levels of gene were significantly higher in plasma cell-free DNA of 72 NSCLC patients than in that of 61 cancer-free patients ( = 0.001, Wilcoxon rank sum test). Prediction of NSCLC using methylation was achieved with a sensitivity of 73.7% and a specificity of 61.9% in a plasma test dataset ( = 40). A Cox proportional hazards model showed that hypermethylation in plasma cell-free DNA was significantly associated with poor recurrence-free survival (hazards ratio = 2.19, 95% confidence interval = 1.21-4.36, = 0.01). The present study suggests that aberrant methylation of in plasma cell-free DNA is a valuable biomarker for the early detection of NSCLC and prediction of recurrence-free survival. However, further research is needed with larger sample size to confirm results. - Source: PubMed
Publication date: 2022/01/07
Kim YujinLee Bo BinKim DonghoUm Sang-WonHan JounghoShim Young MogKim Duk-Hwan