Mouse IGFBP-1 ELISA kit
- Known as:
- Mouse IGFBP-1 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- lf-ek50101
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Abfrontier
- Gene target:
- Mouse IGFBP-1 ELISA kit
Related genes to: Mouse IGFBP-1 ELISA kit
- Gene:
- CCN1 NIH gene
- Name:
- cellular communication network factor 1
- Previous symbol:
- IGFBP10, CYR61
- Synonyms:
- GIG1
- Chromosome:
- 1p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-02
- Date modifiied:
- 2018-10-11
- Gene:
- IGFBP1 NIH gene
- Name:
- insulin like growth factor binding protein 1
- Previous symbol:
- IBP1
- Synonyms:
- IGF-BP25, AFBP, hIGFBP-1, PP12
- Chromosome:
- 7p12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1988-11-30
- Date modifiied:
- 2015-11-12
Related products to: Mouse IGFBP-1 ELISA kit
Related articles to: Mouse IGFBP-1 ELISA kit
- Insulin-like growth factor binding protein 1 (IGFBP1) is documented as a pro- tumorigenic gene in various cancers; nevertheless, its specific function in esophageal carcinoma (ESCA) is unclear. This study used data obtained from The Cancer Genome Atlas (TCGA) to assess IGFBP1 expression, investigating its clinical outcome-related relevance, and explore its correlation in the context of ESCA tumor microenvironment. The Wilcoxon rank-sum test indicated a notable overexpression of IGFBP1 in ESCA compared to normal tissues, which was further validated via immunohistochemistry. Functional enrichment analysis identified tumor-related pathways, while ssGSEA/CIBERSORT methods linked IGFBP1 expression to altered immune infiltration. Furthermore, an investigation of single-cell data sourced from the GSE196756 data uncovered unique immune cell subsets linked to the expression of IGFBP1. The application of Cox regression alongside Kaplan-Meier survival analyses indicated that elevated levels of IGFBP1 were correlated with unfavorable outcomes in overall survival (OS), and disease-specific survival (DSS). Functional validation utilizing CCK-8 and transwell assays revealed that IGFBP1 silencing significantly suppressed the proliferative, invasive, and migratory capabilities of ESCA cell lines. Furthermore, analyses also presented similar results. Collectively, these results position IGFBP1 as a prognostic biomarker in ESCA, highlighting its functional involvement in tumor progression. - Source: PubMed
Publication date: 2026/09/16
Jiang HuijuanZhu JunlingLei ZhangYimamu TuxunayiChen HailinLi QiannanMuhetaer AishanjiangAbudourousuli Ainiwaerjiang - Metabolic dysfunction associated steatotic liver disease (MASLD) is the most prevalent liver disease, yet accurate early detection remains challenging. A particular diagnostic obstacle is distinguishing MASLD from metabolic dysfunction and alcohol-related liver disease (MetALD), currently defined using clinically informed moderate alcohol consumption thresholds without biological validation. This study aimed to identify and externally validate plasma proteomic signatures associated with MASLD and assess whether proteomic profiles support a molecular distinction between MASLD and MetALD as currently defined. - Source: PubMed
Jakhar NiharikaSeibel TobiasMironova MariaMeeßen CorinnaClusmann JanChen YazhouRaju Thriveni BKoop Paul-HenryPearce Juliette ECosta Ivan GStiehl ThomasSchuppert AndreasSchneider Kai MarkusRotman YaronSchneider Carolin V - A higher ratio of IGF-1:IGF binding protein 1 (IGFBP1) was associated with improved prognosis in the CHAARTED trial of docetaxel in participants with metastatic hormone-sensitive prostate cancer (mHSPC). The ENZAMET trial demonstrated the survival benefit of adding enzalutamide to androgen deprivation therapy (ADT) in mHSPC, and included participants who also received docetaxel as standard of care. The aim of this study was to validate the association between levels of circulating IGF-1 and IGFBP1 and survival of ENZAMET participants. - Source: PubMed
Publication date: 2026/09/27
Cilento Michael ALin Hui-MingYeung NicoleKim Rachel M NPortman NeilStockler Martin RMartin Andrew JSubhash VinodYip SoniaButler Lisa MMarschner Ian CMeikle Peter JAzad Arun ADavis Ian DHorvath Lisa GSweeney Christopher J - In eutherians, Insulin-like Growth Factor-I (IGF-I) and IGF-II exert insulin-like activity by interacting with type-I receptor. IGF bioavailability is finely regulated by six IGF-Binding Proteins (IGFBPs), IGFBP-1 to -6, which bind IGF-I and -II with high affinity but not insulin. Moreover, the Pregnancy-Asssociated Plasma Protein-A protease in able to specifically degrade IGFB-2, -4, -5. In the present work, we were interested in the evolution of this regulation of bioavailability in vertebrates, in particular in the question of the different nodes of appearance of IGFs, IGFBPs and PAPP-A in the tree of life. We confirmed that insulin-like/IGF peptides and their receptors appeared in non-vertebrate species, whereas IGFBPs first appeared in the vertebrate ancestor. More precisely, the first IGFBP that appeared was IGFBP-5 in amphioxus, whereas IGFBP-1, -2 and -3 apperaed in lamprey, IGFBP-4 in jawed fishes, and IGFBP-6 in teleost with a loss in birds. We also showed that the pregnancy-associated plasma protein A (PAPP-A) and PAPP-A2 metzincin proteases, which degrade several IGFBPs, might have appeared in non-vertebrates and that their two inhibitors, proMBP and STC, probably appeared before both proteases. Interestingly, the cleavage sites of IGFBP were restricted to some species : for IGFBP-2 and -5, it was present in mammals, birds and reptiles, but not in amphibians and fishes; for IGFBP-4 in Mammals only. Another important point is that another insulin-like peptide-binding protein found in the fruit fly, IMPL2, has probably disappeared in vertebrates. - Source: PubMed
Publication date: 2026/09/22
Fouchécourt SophieCallebaut IsabelleMonget Philippe - is a major human pathogen that can elicit immune-inflammatory responses and infections, largely driven by its broad repertoire of antigenic proteins. Understanding these factors is valuable for elucidating mechanisms of infection. - Source: PubMed
Publication date: 2026/09/02
Dalloul Rajaa S DSohail Muhammad UChennakkandathil SareenaSawarth HinaAl-Noubi MunaChoi SunkyuSchmidt Frank