IGFBP-1 ELISA
- Known as:
- IGFBP-1 Enzyme-linked immunosorbent assay test
- Catalog number:
- kapme01
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Diasource
- Gene target:
- IGFBP-1 ELISA
Related genes to: IGFBP-1 ELISA
- 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: IGFBP-1 ELISA
Related articles to: IGFBP-1 ELISA
- - Source: PubMed
Publication date: 2026/08/22
Riaz AminaKaisrani AneetaKumar Naresh - Recurrent spontaneous abortion (RSA) is a distressing disorder affecting numerous women of reproductive age. N6-methyladenosine (m6A) RNA modification is a crucial epigenetic regulator, but its role in RSA remains elusive. ALKBH5 (AlkB homolog 5) is a pivotal m6A demethylase that erases m6A marks to positively regulate target gene expression. This research examines the role of the m6A demethylase ALKBH5 in the decidualization process associated with RSA. Decidual tissues from RSA patients and healthy controls were collected. ALKBH5 was knocked down or overexpressed in primary human endometrial stromal cells (ESCs). Decidualization was induced using medroxyprogesterone acetate and 8-Br-cAMP. Phenotypes were assessed via morphology, qPCR, ELISA (for IGFBP1/PRL), and Western blotting. RNA-seq, MeRIP-qPCR, dual luciferase reporter assay, and bioinformatics were applied to determine targets and mechanisms, and immunohistochemistry was used to assess protein expression in decidual tissues. ALKBH5 was downregulated in RSA decidual tissues but upregulated during in vitro decidualization. ALKBH5 knockdown inhibited the morphological transformation and reduced the expression and secretion of decidual markers IGFBP1 and PRL. RNA-seq and intersection analysis identified BMP2 as a key candidate target. Mechanistically, ALKBH5 knockdown increased m6A methylation on BMP2 mRNA, leading to decreased BMP2 expression. Conversely, ALKBH5 overexpression reduced BMP2 m6A levels and enhanced BMP2 expression, which further potentiated decidualization. Importantly, BMP2 knockdown reversed the pro-decidualization effects of ALKBH5 overexpression. Clinically, a strong positive correlation was observed between ALKBH5 and BMP2 expression levels in both the HC group and the RSA group. Furthermore, the ROC curve results indicate that either ALKBH5 or BMP2 could serve as a better diagnostic factor for patients with RSA. ALKBH5 promotes endometrial decidualization by demethylating BMP2 mRNA and enhancing its expression. The downregulation of the ALKBH5-BMP2 axis contributes to decidualization deficiency and may represent a novel epigenetic mechanism underlying RSA. - Source: PubMed
Li LipingChen JinZhou ShanshanZou YiLi ZengmingYang BichengLuo Yong - To investigate the effects of Shaofu Zhuyu Decoction on decidualization and the expression of progesterone receptor-β (PR-β) and heterogeneous nuclear ribonucleoprotein L (HNRNPL) in a mouse model of endometriosis. - Source: PubMed
Publication date: 2026/08/13
Zhang ChenSun XinhuiSui CongluCao Ying - Successful implantation requires coordinated decidual differentiation of endometrial stromal cells. This study shows that anandamide treatment of decidualising cells is associated with reduced NOTCH1 activation and selective alterations in decidual, inflammatory and structural programs. - Source: PubMed
Publication date: 2026/08/17
Carriero IleniaLacconi ValentinaBianco ClaudiaBertani NicoleStamme CamillaGasperi ValeriaMassimiani MicolTicconi CarloMaccarrone MauroLa Sala GinaCampagnolo Luisa - Abnormal endometrial decidualization is a critical contributor to implantation failure and pregnancy loss, with exposure to environmental pollutants increasingly recognized as a potential risk factor. N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine quinone (6PPD-Q), an ozonation byproduct of the tire antioxidant 6PPD, is widely detected in environmental matrices. Despite growing concern over its reproductive toxicity, the effects of peri-implantation exposure on endometrial decidualization remain unclear. In this study, peri-implantation 6PPD-Q exposure (4 mg/kg) in mice significantly reduced implantation site weight at embryonic day 7.5 (E7.5), increased embryo resorption rate at E13.5, decreased placental and fetal weights in viable embryos, and further reduced litter size and offspring birth weight. 6PPD-Q markedly reduced polyploid decidual cells at E7.5 in both pregnant and pseudopregnant mouse models. In pregnant mice, it also disrupted the expression of decidualization markers and steroid hormone receptors, accompanied by defective decidual angiogenesis. Transcriptomic analysis further revealed dysregulation of biological processes associated with decidualization, angiogenesis, immune regulation, cytoskeletal and matrix remodeling, and metabolism. In vitro, telomerase-immortalized human endometrial stromal cells (T-hESCs) exhibited dose-dependent (0.01-10 μM) reductions in viability and decidual markers IGFBP1, PRL, BMP2, and WNT4 upon 6PPD-Q exposure. This study provides new mechanistic insights into the reproductive toxicity of this emerging contaminant during early pregnancy. - Source: PubMed
Publication date: 2026/08/09
Fu WantingYang ZiyaoLi YiChen TianxiaoYang QinglingHu Linli