INHBB & ACVR1C Protein Protein Interaction Antibody Pair
- Known as:
- INHBB & ACVR1C Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0042
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- INHBB & ACVR1C Protein Interaction Antibody Pair
Related genes to: INHBB & ACVR1C Protein Protein Interaction Antibody Pair
- Gene:
- ACVR1C NIH gene
- Name:
- activin A receptor type 1C
- Previous symbol:
- -
- Synonyms:
- ALK7, ACVRLK7
- Chromosome:
- 2q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-07-21
- Date modifiied:
- 2019-03-21
- Gene:
- INHBB NIH gene
- Name:
- inhibin subunit beta B
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 2q14.2
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2018-04-23
Related products to: INHBB & ACVR1C Protein Protein Interaction Antibody Pair
Related articles to: INHBB & ACVR1C Protein Protein Interaction Antibody Pair
- Preeclampsia (PE) is a serious hypertensive pregnancy disorder with a significant genetic component. Numerous genetic studies, including our own, have yielded many susceptibility genes from distinct functional groups. Additionally, transcriptome profiling of tissues at the maternal-fetal interface has likewise yielded many differentially expressed genes. Often there is little overlap between these two approaches, although genes identified in both approaches are significantly associated with PE. We have thus taken a novel integrative bioinformatics approach of analysing pathways common to the susceptibility genes and the PE transcriptome. - Source: PubMed
Publication date: 2015/05/26
Yong Hannah E JMelton Phillip EJohnson Matthew PFreed Katy AKalionis BillMurthi PadmaBrennecke Shaun PKeogh Rosemary JMoses Eric K - A link between elevated luteinizing hormone (LH) levels, GATA-4 and LH receptor (LHCGR) expression and gonadotropin-dependent adrenocortical tumorigenesis in humans and mice has been shown. To assess the mechanistic tumorigenic interrelationships between these factors, we transgenically expressed Gata4 under the 21-hydroxylase promoter (Cyp21a1, 21-OH) in C57Bl/6N mice. There was a gradual age-dependent increase of GATA-4 expression only in 21-OH-GATA-4 (TG) female adrenals, in association with slowly progressing neoplasia of non-steroidogenic spindle-shaped A cells in the subcapsular cortex. Gonadectomy (GDX), apparently through direct action of elevated serum LH, markedly enhanced the adrenocortical neoplasia, which now also appeared in GDX TG males. The neoplastic areas of the post-GDX TG adrenals contained, besides A cells, larger lipid-laden, steroidogenically active and LHCGR-positive B cells. Prolonged (>10 months) exposure to elevated post-GDX LH levels resulted in formation of adrenocortical adenomas in the TG mice. Intact and GDX TG mouse adrenals displayed elevated FOG-2 and decreased GATA-6 expression. Additionally, increased expression/activation of components of the Inhbb-Acvr2a-Acvr1c-Smad2/3 signaling system was observed in 12-month-old GDX TG adrenals. Our findings show that two distinct GATA-4-dependent populations of neoplastic adrenocortical cells form: non-steroidogenic LH-independent A cells and steroidogenic LH-dependent B cells. - Source: PubMed
Publication date: 2013/02/26
Chrusciel MarcinVuorenoja SusannaMohanty BidutRivero-Müller AdolfoLi XiangdongToppari JormaHuhtaniemi IlpoRahman Nafis A - Human adipose tissue is a major site of expression of inhibin beta B (INHBB) which homodimerizes to form the novel adipokine activin B. Our aim was to determine if molecules needed for a local action of activin B are expressed in adipose tissue. Microarray analysis showed that adipose tissue expressed activin type I and II receptors and that the expression of activin receptor-like kinase 7 (ALK7) was adipose tissue specific. In obesity discordant siblings from the SOS Sib Pair study, adipose tissue ALK7 expression was higher in lean (n=90) compared to obese (n=90) subjects (p=4 x 10(-31)). Adipose tissue ALK7 expression correlated with several measures of body fat, carbohydrate metabolism and lipids. In addition, ALK7 and INHBB expression correlated but only in lean subjects and in subjects with normal glucose tolerance. We conclude that activin B may have local effects in adipose tissue and thereby influence obesity and its comorbidities. - Source: PubMed
Publication date: 2009/03/09
Carlsson Lena M SJacobson PeterWalley AndrewFroguel PhilippeSjöström LarsSvensson Per-ArneSjöholm Kajsa - Activins play a fundamental role in cell differentiation and development. Activin A signaling is mediated through a combination of activin type II receptors (ActRIIs) and the activin type IB receptor, ALK4. Signaling receptors of other activin isoforms remain to be elucidated. Here, we found that activin AB and activin B are ligands for ALK7. ALK7 is an orphan receptor serine/threonine kinase expressed in neuroendocrine tissues including pancreatic islets. The combination of ActRIIA and ALK7, preferred by activin AB and activin B but not by activin A, is responsible for activin-mediated secretion of insulin from pancreatic beta cell line, MIN6. In contrast, all activins activate a combination of ActRIIA and ALK4 with various levels of potency. Thus, variation in activin signaling through type I receptors is dependent upon homo- and heterodimeric assembly of activin isoforms. Thus, the differential combination of receptor heterodimers mediates variation in activin isoform signaling. - Source: PubMed
Tsuchida KunihiroNakatani MasashiYamakawa NorioHashimoto OsamuHasegawa YoshihisaSugino Hiromu