IGFBP_1 (pp12)
- Known as:
- IGFBP_1 (pp12)
- Catalog number:
- 4I52
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- Hytest
- Gene target:
- IGFBP_1 (pp12)
Related genes to: IGFBP_1 (pp12)
- 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
- Gene:
- NEK4 NIH gene
- Name:
- NIMA related kinase 4
- Previous symbol:
- STK2
- Synonyms:
- NRK2, pp12301
- Chromosome:
- 3p21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-05-10
- Date modifiied:
- 2016-01-13
Related products to: IGFBP_1 (pp12)
3CH61,CCN family member 1,Ccn1,Cyr61,Cysteine-rich angiogenic inducer 61,IBP-10,IGF-binding protein 10,Igfbp10,IGFBP-10,Insulin-like growth factor-binding protein 10,Mouse,Mus musculus,Protein CYR61Anti-bovine Insulin Like Growth Factor Binding Protein-2 (IGFBP-2) antiserumAnti-Human Insulin Like Growth Factor Binding Protein-1 (IGFBP-1) protein antiserumAnti-Human Insulin Like Growth Factor Binding Protein-3 (IGFBP-3) antiserumAnti-Human Insulin Like Growth Factor Binding Protein-4 (IGFBP-4) protein antiserumAnti-Human Insulin Like Growth Factor Binding Protein-5 (IGFBP-5) protein antiserumAnti-Human Insulin Like Growth Factor Binding Protein-7 (IGFBP-7) protein IgG, aff pureAnti-Insulin-like Growth Factor Binding Protein-1 (IGFBP-1 (pp12)) AntibodyAnti-Insulin-like Growth Factor Binding Protein-1 IGFBP-1 pp12 antibodyAntigens IGFBP-4Antigens Insulin like growth factor binding protein-1 (IGFBP-1)Anti_Insulin_like Growth Factor Binding Protein_1 (IGFBP_1 (pp12))Biochemical: IGFBP-3, human recombinantBovine IGFBP-2Bovine IGFBP-2 Related articles to: IGFBP_1 (pp12)
- 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 - 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