SLITRK1 Protein
- Known as:
- SLITRK1 Protein
- Catalog number:
- 10340-H03H
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- SLITRK1 Protein
Related genes to: SLITRK1 Protein
- Gene:
- SLITRK1 NIH gene
- Name:
- SLIT and NTRK like family member 1
- Previous symbol:
- LRRC12
- Synonyms:
- KIAA1910
- Chromosome:
- 13q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-08
- Date modifiied:
- 2015-11-18
Related products to: SLITRK1 Protein
Related articles to: SLITRK1 Protein
- Most pregnancies are affected by nausea and vomiting, but the most severe form-hyperemesis gravidarum-can be life threatening. Here we performed a multi-ancestry genome-wide association study of hyperemesis gravidarum in 10,974 cases and 461,461 controls across European, Asian, African and Latino ancestries. We identified ten associations: four identified previously (GDF15, IGFBP7, PGR and GFRAL) and six additional loci (SLITRK1, SYN3, IGSF11, FSHB, TCF7L2 and CDH9). Downstream analyses revealed GDF15 and TCF7L2 expression primarily in extravillous trophoblasts, with opposing effects for GDF15 between maternal and fetal genotype. Conversely, IGFBP7 and PGR were expressed primarily in maternal spiral arteries, with effects limited to the maternal genome. Selected loci were associated with abnormal pregnancy weight gain, duration, birth weight and pre-eclampsia. Functional studies identified additional associations including antisense IGFBP7-AS1 and protein ACP1. Potential roles for candidate genes in appetite, insulin signaling and brain plasticity provide pathways to explore etiological mechanisms and therapeutic avenues. - Source: PubMed
Publication date: 2026/04/14
Fejzo MarlenaWang XinranTan QingZöllner JuliaPujol-Gualdo NatàliaLaisk Triin Finer Sarahvan Heel David A Brumpton BenBhatta LaxmiHveem KristianJasper Elizabeth AVelez Edwards Digna RHellwege Jacklyn NEdwards ToddJarvik Gail PLuo YuanKhan AtlasMacGibbon KimberGao YuanGe GaoxiangAverbukh InnaSoon ErinAngelo MichaelMagnus PerJohansson StefanNjølstad Pål RKim ArtemGazal StevenVaudel MarcShu Chang AprilMancuso Nicholas - Vertebrate neural circuit properties are shaped by synaptic cell adhesion molecules (CAMs). CAMs often have multiple paralogs but the possible redundancy of such paralogs remains underexplored. Using circuit-specific conditional knockout (cKO) mice deficient for Slitrk1 and Slitrk2, we show that these paralogs lack specific laminar expression in mature hippocampal neurons but divergently guide the specificity of neural circuits in distinct hippocampal subfields. Slitrk1 and Slitrk2 regulate distinct facets of excitatory synaptic properties in a microcircuit-dependent manner through binding to LAR-RPTPs, and additionally in the case of Slitrk2, through binding to PDZ domain-containing proteins and TrkB. Analyses of Slitrk2 V89M knock-in mice revealed that this schizophrenia-associated substitution acts uniquely as a loss-of-function mutation in some microcircuits to impair excitatory synaptic transmission, asynchronous release, and spatial reference memory. These findings demonstrate that even structurally and biochemically similar synaptic CAMs can play distinct roles in specifying neural circuit architecture. - Source: PubMed
Publication date: 2025/12/18
Kim DongwookKim ByeongchanKim JinhuSeo Na-YoungKim HyeonhoHan Kyung AhYoon JubeenMacks Christian Pde Wit JorisSohn Chang HoLee Kea JooUm Ji WonKo Jaewon - This preliminary study explores the feasibility of identifying novel site-specific biomarkers in keloid disease to enhance understanding of its pathobiology. Keloid scars are clinically and morphologically heterogeneous, showing variable response to therapy. They also differ at the cellular and molecular levels between their actively growing margins and their dormant centers. In addition, keloids behave differently to other fibrous skin tumors, including DSFP and FS. Thus, we performed a high-throughput RNA sequencing and gene/protein analysis on keloid tissue, primary keloid fibroblasts, and keloid-derived immortalized fibroblast cell lines from different sites of the keloid tissue (Extralesional, Peripheral, Middle, and Top). These were compared with normal skin, DFSP, and FS. We identified MTCO1P12 as a common gene transcript exhibiting significantly high expression across all three keloid sites (Peripheral, Middle, and Top), FS, and DFSP compared to the extralesional keloid. Furthermore, three site-specific biomarkers were identified. SLITRK1 was uniquely expressed in the peripheral keloid tissue site and its corresponding fibroblasts. FOXS1 was localized to the middle keloid tissue site and its corresponding fibroblasts. KCNJ6 was exclusively expressed in the top keloid tissue site and its corresponding fibroblasts. It was not found in FS and DFSP. In conclusion, for the first time, we identified and validated three novel site-specific biomarkers within keloid, two of which (SLITRK1 and FOXS1) overlap with more aggressive tumors, while KCNJ6 is unique to keloids. In conclusion, for the first time, we identified and validated three novel site-specific biomarkers in keloids, two of which (SLITRK1 and FOXS1) overlap with more aggressive tumors, while KCNJ6 is unique to keloids. These findings demonstrate the feasibility of identifying spatially distinct molecular signatures in keloids, providing a foundation for future research into targeted therapies. - Source: PubMed
Publication date: 2025/11/13
Sadiq AliaKhumalo Nonhlanhla PZiemann MarkBayat Ardeshir - Global population aging highlights frailty as a critical health concern, yet its genetic basis remains poorly understood. We employed Mendelian randomization (MR) and National Health and Nutrition Examination Survey (NHANES) to examine causal relationships between frailty index (FI) and 36 urological diseases, investigating shared genetic mechanisms. The FI was calculated using genome-wide association data, and bidirectional MR analysis with multiple statistical methods was applied to investigate causal links between FI and 36 urological diseases. Complementary observational analyses using NHANES and generalized summary MR validation were conducted, followed by genetic correlation assessments, genome annotation, and metabolomic explorations to identify mediating pathways. MR analysis identified a significant causal association between FI and renal tubule-interstitial disease, chronic kidney diseases (CKDs), diabetes with renal complications, renal failure, and acute kidney injury. Reverse MR analysis indicated a bidirectional causal relationship between FI and acute renal failure, as well as CKD and type 1 diabetic kidney disease. NHANES data confirmed FI as an independent risk factor for CKD and renal failure. Genetic linkage analyses identified strong regional correlations between FI and CKD/renal failure within the chromosome 6 locus (31,571,218-32,682,664). Genome-wide analyses uncovered 103 novel single-nucleotide polymorphism with pleiotropic effects on the frailty-urinary disease relationship. Mediation analyses implicated the complement pathway (C2), SLITRK1, and 4-methylhexanoylglutamine as putative mediators of FI effects on CKD and kidney failure. This study elucidates the bidirectional causal relationship between frailty and CKD, while identifying novel genetic variants and metabolic pathways. These findings provide a molecular basis for developing personalized therapeutic strategies targeting both frailty and urological disorders. - Source: PubMed
Publication date: 2025/11/11
Chen YidingWang KunZhang XiangyuYang FeixiangLiu TianruiCheng AndongGuan YuZhong JinbiaoMeng JialinZhang XianshengLiao Guiyi - Developing cost-effective, noninvasive biomarker-based tests could transform moyamoya disease (MMD) management. This study aimed to identify clinically relevant cerebrospinal fluid (CSF) biomarkers through comprehensive proteomic screening in a large MMD cohort. CSF protein profiles from 104 MMD patients and 14 non-tumorous hydrocephalus patients were analyzed via liquid chromatography-tandem mass spectrometry. Enrichment analysis was conducted on canonical pathways and differentially expressed proteins (DEPs). The protein-protein interaction network data included all proteins involved in canonical pathways. Potential markers were validated via ELISA. Weighted gene coexpression network analysis (WGCNA) revealed clinical factor-related modules. We identified 2463 proteins, and 2307 were quantified in at least one sample. A total of 321 significant DEPs were identified, with 8 proteins upregulated and 11 proteins downregulated in MMD samples. ELISA confirmed the increased expression of ALB and SLITRK1. WGCNA revealed seven modules correlated with clinical factors, linking preoperative cerebral infarction to the module eigengene (ME) red module and favorable modified Rankin scale scores to the MEblack module. BASP1 and LDHA were significantly upregulated in MEred, whereas CD9 and EMILIN1 were upregulated in MEblack. Our findings shed light on the proteomics of CSF from MMD patients, identifying potential novel biomarkers such as SLITRK1 and markers of preoperative cerebral infarction (BASP1, LDHA) and clinical outcome (CD9, EMILIN1). These markers have potential as new diagnostic and therapeutic targets for MMD. - Source: PubMed
Publication date: 2025/10/01
Shim YoungboChoi Seung AhDan KisoonKoh Eun JungHa SaehimPhi Ji HoonKim Joo WhanHan DohyunKim Seung-Ki