Human IGFBP-1 ELISA kit
- Known as:
- Human IGFBP-1 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- lf-ek50097
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Abfrontier
- Gene target:
- Human IGFBP-1 ELISA kit
Related genes to: Human 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: Human IGFBP-1 ELISA kit
Related articles to: Human IGFBP-1 ELISA kit
- 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 - Patients with chronic liver disease (CLD) frequently develop reduced bone mass and an increased risk of fragility fractures, making osteoporosis a major extrahepatic complication that affects long-term prognosis and quality of life. Although the association between CLD and osteoporosis is well recognized, epidemiological risk factors and the shared versus etiology-specific mechanisms remain incompletely integrated. Current clinical risk assessment relies largely on bone mineral density, which fails to capture microarchitectural deterioration and may underestimate true fracture risk. This review aimed to integrate current epidemiological and mechanistic evidence and examine emerging approaches to precision prevention and management of CLD-related osteoporosis. - Source: PubMed
Publication date: 2026/09/15
Wang WenjingLiu GuangyuYokus BurhanYan TaiqiangSun HaolinPacher PalWang Yan - Embryo implantation critically depends on the establishment of endometrial receptivity, which is governed by progesterone-driven stromal decidualization during the mid-secretory phase. In recurrent implantation failure (RIF), this process is frequently disrupted, yet the molecular mechanisms remain unclear. Here, through integrative analysis of bulk and single-cell transcriptomic datasets, we identified nicotinamide N-methyltransferase (NNMT) as one of the most significantly downregulated genes in the endometrium of RIF patients. Temporal profiling of human endometrial samples across the menstrual cycle revealed progressive upregulation of NNMT from proliferative to secretory phase, while in hormonally induced stromal cell differentiation, NNMT expression rose sharply from day 4 onward. Functional assays demonstrated that NNMT knockdown impaired decidualization, as evidenced by reduced expression of PRL and IGFBP1 and attenuated cytoskeletal reorganization. Mechanistically, NNMT deficiency increased intracellular S-adenosylmethionine levels, enhanced the expression of core PRC2 components, and promoted H3K27me3 enrichment at the promoters of decidual genes, consistent with their transcriptional repression. Pharmacologic inhibition of histone methylation by 3-deazaneplanocin A or selective EZH2 inhibition by GSK126 partially rescued both molecular and morphological defects in NNMT-deficient stromal cells. In vivo, uterine NNMT silencing in pregnant mice also increased H3K27me3 level, reduced the expression of decidualization-related genes, and decreased the number of implantation sites. Collectively, our findings identify NNMT as a metabolic-epigenetic regulator of endometrial receptivity, and support its potential as a candidate biomarker for RIF. - Source: PubMed
Publication date: 2026/09/07
Yang BinPeng LinZhao ChenxiZeng YuqiDeng YanqingTian LifengZhao YanFan HanchengLin JiayingHuang Jialyu - Chronic endometritis (CE) is a persistent inflammatory disorder of the endometrium that is increasingly recognized as an important cause of reproductive failure. However, the molecular mechanisms by which CE impairs endometrial receptivity remain incompletely understood. Here, we found that decidualization markers IGFBP1 and PRL were significantly decreased in CE patients, accompanied by abnormal glandular architecture. Transcriptomic analysis revealed sphingolipid metabolism as a dysregulated pathway, with SphK1 markedly downregulated. S1P levels were reduced in both CE tissues and LPS-treated stromal cells during decidualization. Functional experiments confirmed that SphK1 is essential for this process, and its deficiency impairs decidualization. Mechanistically, transcription factor C/EBPδ directly bound and activated the SphK1 promoter. CE endometrium showed reduced C/EBPδ and SphK1, alongside increased LC3B, indicating autophagic dysregulation. Furthermore, S1P was demonstrated to act extracellularly through the G protein-coupled receptor S1PR3 to maintain autophagic homeostasis, thereby regulating endometrial decidualization. In conclusion, suppression of the C/EBPδ-SphK1 axis impairs decidualization with excessive autophagy, revealing a mechanistic link between chronic inflammation, sphingolipid dysregulation, and reproductive failure. - Source: PubMed
Publication date: 2026/09/07
Xiao JiahuiYu ShuyiXu ShiruYou GuanyingMo MeilanLian RuochunChen CongZhang XuelingLi Yuye - : The growth hormone (GH)-insulin-like growth factor (IGF) axis is profoundly dysregulated in critical illness. GDF-15 and individual IGF-binding proteins (IGFBPs) have separately been proposed as prognostic biomarkers, but to our knowledge, no prior study has simultaneously characterized all major GH-IGF axis components and GDF-15 in the same critically ill cohort, precluding assessment of their joint intercorrelation structure. : To provide the first simultaneous characterization of the intercorrelation structure among ten GH-IGF axis components and GDF-15 in a single ICU cohort, testing whether this structure is robust to adjustment for illness severity; and, secondarily, to describe admission discriminatory performance relative to APACHE II and SOFA. : This was a prospective observational pilot study of 43 critically ill adults with admission (T01) measurement of ten GH-IGF axis biomarkers and longitudinal follow-up to day 15. Spearman correlations and hierarchical clustering characterized the admission intercorrelation structure; partial correlations adjusting for APACHE II and SOFA, and bootstrap confidence intervals, assessed robustness. Secondary analyses included the examination of admission discrimination (ROC/AUC), a leave-one-out cross-validated combined model, and longitudinal trajectories. All analyses were exploratory, hypothesis-generating, and unadjusted for multiple comparisons unless stated. : Hierarchical clustering identified a coherent cluster comprising GDF-15, IGFBP-1, IGFBP-2, and growth hormone-binding protein (GHBP), distinct from classical GH-resistance markers (GHR vs. healthy controls, GHR vs. admission) and from GH, IGF-1, acid-labile subunit (ALS), and IGFBP-3. Within this cluster, GDF-15 correlated with IGFBP-1 (ρ = 0.65, 95% bootstrap CI 0.44-0.78), IGFBP-2 (ρ = 0.50, CI 0.19-0.71), and GHBP (ρ = 0.47, CI 0.20-0.68); GDF-15 showed no correlation with classical GH-resistance markers. These correlations were essentially unchanged after adjusting for APACHE II or SOFA (partial ρ within 0.03-0.16 of unadjusted values), indicating the structure is not attributable to shared confounding by illness severity. This robustness extended to further adjustment for IL-6, age, BMI, and mechanical-ventilation duration, and results from all 45 pairwise T01 correlations were re-examined with Benjamini-Hochberg false-discovery-rate correction (9 of 11 nominally significant pairs retained q < 0.05). However, the GDF-15-GHBP correlation, unlike the GDF-15-IGFBP-1/IGFBP-2 correlations, attenuated substantially after adjustment for IL-6 and was not consistent across a brain-injury/non-brain-injury subgroup sensitivity analysis, indicating this specific link is less specific than the others. In secondary exploratory analyses, GDF-15 had the highest individual admission AUC (0.74) among biomarkers but was substantially outperformed by APACHE II (AUC 0.90) and SOFA (AUC 0.81); a combined GDF-15 + IGFBP-2 model did not improve on GDF-15 alone. : This study identifies a severity-independent intercorrelation structure linking GDF-15 to inhibitory IGFBPs, distinct from classical GH-resistance signaling, in critically ill patients. Although the findings do not support any clinical application at this stage, further study in adequately powered, multicenter cohorts can be contemplated. - Source: PubMed
Publication date: 2026/07/27
Ilias IoannisKeskinidou ChrysiPoupouzas GeorgiosIssaris VasileiosLotsios Nikolaos SBotoula EfthymiaTzanela MarinellaVassiliadi Dimitra AKokkoris SteliosVrettou Charikleia SVassiliou Alice GDimopoulou Ioanna