OSTalpha Blocking Peptide
- Known as:
- OSTalpha Blocking Peptide
- Catalog number:
- 33r-5169
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- OSTalpha Blocking Peptide
Related genes to: OSTalpha Blocking Peptide
- Gene:
- SLC51A NIH gene
- Name:
- solute carrier family 51 alpha subunit
- Previous symbol:
- -
- Synonyms:
- OSTalpha
- Chromosome:
- 3q29
- Locus Type:
- gene with protein product
- Date approved:
- 2012-08-03
- Date modifiied:
- 2015-12-08
Related products to: OSTalpha Blocking Peptide
Related articles to: OSTalpha Blocking Peptide
- Obeticholic acid (OCA), a potent agonist of the bile salt-activated nuclear receptor farnesoid X receptor (FXR), accelerates liver hypertrophy after portal vein embolization (PVE), but the mechanisms underlying this effect are incompletely understood. In a rabbit model of PVE, New Zealand White rabbits received OCA (10 mg/kg/day) or vehicle by oral gavage before and after embolization. We quantified systemic and hepatic bile salt pools, profiled FXR-regulated genes in ileum and liver, and related these parameters to volumetric and histological indices of regeneration. OCA shifted bile salt composition towards a more hydrophobic profile and improved homeostasis, with earlier normalization of serum total bile salts, reduced bile salt content in the non-embolized (hypertrophic) lobe, and lower circulating levels of the hepatotoxic bile salt lithocholic acid. Serum lithocholic acid strongly and inversely correlated with both caudal liver volume gain and hepatocyte proliferation. In the hypertrophic lobe, OCA markedly suppressed expression of CYP7A1, reduced circulating levels of the bile salt synthesis marker 7-alpha-hydroxy-4-cholesten-3-one, and increased expression of the basolateral bile salt exporter SLC51A/B, consistent with reduced bile salt synthesis and enhanced sinusoidal efflux. OCA also induced the mitotic entry regulator CDC25B. RNA sequencing identified ileal and hepatic signaling candidates, including C1q subunits, bone morphogenetic protein 3 (BMP3), and Indian hedgehog (IHH), which correlated with liver growth. These data indicate that FXR agonism by OCA promotes PVE-induced liver regeneration by improving bile salt homeostasis and modulating gut-liver growth signaling, supporting further evaluation of FXR agonists to enhance future liver remnant hypertrophy before major hepatectomy. - Source: PubMed
Publication date: 2026/04/18
Chang XinweiOlthof Pim BJin HanChau StevenSoons Zitavan Eijk Hansvan Golen Rowanvan Gulik Thomas MJansen Peter LDamink Steven W M OldeHeger MichalSchaap Frank G - We aimed to investigate the relative efficacy of feeding different bile acids in preventing PNALD in neonatal pigs. Newborn pigs given total parenteral nutrition (TPN) combined with minimal enteral feeding of chenodeoxycholic acid (CDCA) or increasing doses of obeticholic acid (OCA) for 19 days. Enteral OCA (5 and 15 mg/kg), but not CDCA (30 mg/kg) reduced blood cholestasis markers compared to TPN controls and increased bile acids in the gallbladder and intestine. Major bile acids in the liver and distal intestine were CDCA, HCA, HDCA, and OCA, and their relative proportions were increased by the type of bile acid (CDCA or OCA) given enterally. High doses of OCA increased the total NR1H4-agonistic bile acid profile in the liver and intestine above 50% total bile acids. Both CDCA and OCA treatments suppressed hepatic CYP7A1 expression, but only OCA increased hepatobiliary transporters, ABCB11, ABCC4, and ABCB1. Plasma phytosterol levels were reduced and biliary levels were increased by CDCA and OCA and hepatic sterol transporters, abcg5/8, expression were increased by OCA. Both CDCA and OCA increased plasma FGF19 and OCA increased intestinal FGF19, FABP6, and SLC51A. Both CDCA and OCA increased intestinal mucosal growth, whereas CDCA increased the plasma GLP-2, GLP-1 and GIP. Enteral OCA prevented cholestasis and phytosterolemia by increased hepatic bile acid and sterol transport via induction of hepatobiliary transporter NR1H4 target genes and not by suppression of bile acid synthesis genes. We also showed an intestinal trophic action of OCA that demonstrates a dual clinical benefit of NR1H4 agonism in the prevention of PNALD in pigs. - Source: PubMed
Publication date: 2025/10/01
Jiang YanjunFang ZhengfengGuthrie GregoryStoll BarbaraChacko ShajiLin SenHartmann BoletteHolst Jens JDawson HarryPastor Jose JIpharraguerre Ignacio RBurrin Douglas G - We aimed to investigate the relative efficacy of feeding different bile acids in preventing PNALD in neonatal pigs. - Source: PubMed
Publication date: 2024/09/07
Jiang YanjunFang ZhengfengGuthrie GregoryStoll BarbaraChacko ShajiLin SenHartmann BoletteHolst Jens JDawson HarryPastor Jose JIpharraguerre Ignacio RBurrin Douglas G - Progressive familial intrahepatic cholestasis (PFIC) is a rare childhood manifested disease associated with impaired bile secretion with severe pruritus yellow stool, and sometimes hepatosplenomegaly. PFIC is caused by mutations in ATP8B1, ABCB11, ABCB4, TJP2, NR1H4, SLC51A, USP53, KIF12, ZFYVE19, and MYO5B genes depending on its type. ABCB11 mutations lead to PFIC2 that encodes the bile salt export pump (BSEP). Different mutations of ABCB11 have been reported in different population groups but no data available in Pakistani population being a consanguineous one. We sequenced coding exons of the ABCB11 gene along with its flanking regions in 66 unrelated Pakistani children along with parents with PFIC2 phenotype. We identified 20 variations of ABCB11: 12 in homozygous form, one compound heterozygous, and seven heterozygous. These variants include 11 missenses, two frameshifts, two nonsense mutations, and five splicing variants. Seven variants are novel candidate variants and are not detected in any of the 120 chromosomes from normal ethnically matched individuals. Insilico analysis revealed that four homozygous missense variations have high pathogenic scores. Minigene analysis of splicing variants showed exon skipping and the addition of exon. This data is a useful addition to the disease variants genomic database and would be used in the future to build a diagnostic algorithm. - Source: PubMed
Publication date: 2024/08/14
Riaz HafsaZheng BixiaZheng YucanLiu ZhifengGu Hong-MeiImran MuhammadYaqoob TahirBhinder Munir AhmadZhang Da-WeiZahoor Muhammad Yasir - Rheumatoid arthritis (RA) is a complex autoimmune disease that leads to joint destruction. A number of immune cells that affect joint tissues are involved in the pathogenesis of this disease. This leads to the synthesis of many pro-inflammatory mediators. The transport of drugs, as well as many cytokines involved in the development of inflammation in RA patients, is mediated by membrane transporters. Membrane transporters are proteins that mediate the transfer of substrates across biological membranes. But to date there are no studies examining the expression of solute carrier (SLC) transporters in joint tissues. The aim of the study was to evaluate the expression of individual SLC family transporters in the synovial membranes (SMs) and infrapatellar fat pad (Hoffa's pad) of RA patients. The study included 20 patients with rheumatoid arthritis and 20 with osteoarthritis as the control group who were undergoing joint replacement surgery as a normal part of clinical care. In the SM and Hoffa's pad of RA patients the following 17 membrane transporters were defined at relevant expression levels for SLC transporter superfamily: . The confirmed expression of these transporters in the SMs as well as Hoffa's pad of patients with RA and OA, and the differences in their expression between these groups, suggests the involvement of SLC transporters in both the maintenance of homeostasis under physiological conditions in the tissues of the joints, as well as in the inflammatory process in RA. - Source: PubMed
Publication date: 2024/06/27
Malinowski DamianPiotrowska KatarzynaDroździk MarekPawlik Andrzej