INSL5 Over-expression Lysate Product
- Known as:
- INSL5 Over-expression Lysate Product
- Catalog number:
- GWB-64FD6D
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- INSL5 Over-expression Lysate Product
Ask about this productRelated genes to: INSL5 Over-expression Lysate Product
- Gene:
- INSL5 NIH gene
- Name:
- insulin like 5
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1p31.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-01-08
- Date modifiied:
- 2015-11-23
Related products to: INSL5 Over-expression Lysate Product
(META) Human Metapneumovirus Type 16 (A1) Lysate(META) Human Metapneumovirus Type 18 (B2) Lysate(META) Human Metapneumovirus Type 20 (A2) Lysate(META) Human Metapneumovirus Type 27 (A2) Lysate(META) Human Metapneumovirus Type 3 (B1) Lysate(META) Human Metapneumovirus Type 4 (B2) Lysate(META) Human Metapneumovirus Type 5 (B1) Lysate(META) Human Metapneumovirus Type 8 (B2) Lysate(META) Human Metapneumovirus Type 9 (A1) Lysate0 day neonate eyeball cDNA. RIKEN full-length enriched library. clone E130107M17 product hypothetical protein. full insert seque - N_A Polyclonal0 day neonate head cDNA. RIKEN full-length enriched library. clone 4831434J02 product nuclear factor of activated T-cells. cytop - N_A Polyclonal0 day neonate head cDNA. RIKEN full-length enriched library. clone 4832421E02 product myocyte enhancer factor 2C. full insert se - N_A Polyclonal1,2,3,4-Tetrahydro-1,2-dimethyl-4,6-isoquinolinediol
(Major Product) CAS: 102830-16-0 Formula: C11H15NO21,2,3,4-tetrahydro-1,2-dimethyl-4,8-isoquinolinediol
(Minor Product) CAS: 102830-20-6 Formula: C11H15NO210 days embryo whole body cDNA. RIKEN full-length enriched library. clone 2610510L15 product poly(A)-specific ribonuclease (dead - N_A Polyclonal Related articles to: INSL5 Over-expression Lysate Product
- Immune dysregulation is increasingly recognized as an important contributor to the pathophysiology of irritable bowel syndrome (IBS). This study aimed to identify immune-related core genes in IBS and predict potential regulatory traditional Chinese medicines (TCMs). Two IBS-related Gene Expression Omnibus datasets were integrated and analyzed to identify differentially expressed genes (DEGs). Functional enrichment, immune cell infiltration profiling, and intersection with ImmPort immune-related genes were performed. Core genes were selected through 3 machine-learning algorithms, and potential TCMs were predicted using the Coremine Medical database. A total of 95 DEGs were identified, including 56 upregulated and 39 downregulated genes. Enrichment analyses indicated involvement in muscle system processes, membrane-associated structures, and peptidase inhibitor activity, with significant enrichment in the neuroactive ligand-receptor interaction pathway. Immune infiltration analysis showed increased M2 macrophages, resting natural killer cells, resting dendritic cells, and activated mast cells in IBS samples. Seven immune-related DEGs were obtained, among which LEFTY1, SLPI, and INSL5 were consistently recognized as core genes across all machine-learning approaches. These genes exhibited distinct immune regulatory relevance. Five TCMs: Drynaria fortunei, Crataegus pinnatifida, Houttuynia cordata, Poria cocos, and Bubalus bubalis horn were predicted as potential therapeutic agents targeting the core genes. LEFTY1, SLPI, and INSL5 represent key immune-related genes in IBS and may contribute to its immune regulatory mechanisms. The predicted TCMs provide potential candidates for further validation in IBS management. - Source: PubMed
Bai WeiQian ZixingYang YangHuang GuodongRao XianjunLi HaoZhou TingtingWei Wei - - Source: PubMed
Publication date: 2026/01/05
Di Vincenzo AngeloGranzotto MarnieMoreni LauraTrevellin ElisabettaCapone FedericoRossato Marco - - Source: PubMed
Publication date: 2026/01/08
Donowitz MarkSingh Varsha - Insulin-like peptide 5 (INSL5) is an enteroendocrine hormone expressed in distal colonic 'L cells'. Bile acid receptor agonists are known to stimulate INSL5 secretion in primary cell culture, and administration of an INSL5 analogue in animals promotes colonic motility. - Source: PubMed
Publication date: 2026/01/08
Bannon Christopher AWalters Julian R FWu TongzhiKay Richard GPunnoose AustinSpiller Robin CWilson JonathanVerdino PetraBarker PeterBurling KeithHorowitz MichaelRayner Christopher KFord Alexander CReimann FrankGribble Fiona M - Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder with diverse metabolic and hormonal manifestations. Insulin-like peptide 5 (INSL5), a gut-derived hormone of the relaxin/insulin family, is expressed in the central nervous system, colonic and reproductive tissues, but its clinical significance in PCOS remains unclear. This study aimed to evaluate circulating INSL5 levels in PCOS and explore their associations with key hormonal and metabolic parameters. In this prospective cross-sectional study, 45 women with newly diagnosed PCOS and 35 age-matched healthy controls (18-35 years) were evaluated. Clinical characteristics, hormonal profiles, and metabolic markers - including serum anti-Müllerian hormone (AMH) and INSL5 - were assessed. INSL5 levels were measured using enzyme-linked immunosorbent assay (ELISA). Median serum INSL5 levels did not differ significantly between PCOS and control groups (12.5 vs. 15.5 ng/ml; p=0.103). However, within the PCOS group, INSL5 was inversely correlated with body mass index, insulin, HOMA-IR, total and LDL cholesterol, triglycerides, fat mass, and free androgen index, and positively correlated with sex hormone-binding globulin (p<0.05 for all). AMH was significantly higher in the PCOS group and demonstrated a diagnostic cut-off of 5.04 ng/ml (AUC: 0.808; sensitivity: 75.6%; specificity: 74.3%). Although INSL5 did not show diagnostic utility for PCOS, its consistent associations with insulin resistance, androgenic activity, and lipid metabolism suggest a potential role in metabolic regulation. These findings support its relevance as a candidate marker for metabolic phenotyping and warrant further investigation into its physiological role within the PCOS spectrum. - Source: PubMed
Publication date: 2025/07/01
Cengiz DenizAdemoğlu Dilekçi Esra NurAlbayrak ÖmürYis Özgür Mehmet