PGS1{phosphatidylglycerophosphate synthase 1}rabbit.pAb
- Known as:
- PGS1{phosphatidylglycerophosphate synthase 1}host: rabbit.pAb
- Catalog number:
- 201-20-4189
- Product Quantity:
- 0.2ml
- Category:
- -
- Supplier:
- Shanghai Sunred
- Gene target:
- PGS1{phosphatidylglycerophosphate synthase 1}rabbit.pAb
Related genes to: PGS1{phosphatidylglycerophosphate synthase 1}rabbit.pAb
- Gene:
- C1GALT1 NIH gene
- Name:
- core 1 synthase, glycoprotein-N-acetylgalactosamine 3-beta-galactosyltransferase 1
- Previous symbol:
- -
- Synonyms:
- C1GALT, T-synthase
- Chromosome:
- 7p22.1-p21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-01-26
- Date modifiied:
- 2018-02-13
Related products to: PGS1{phosphatidylglycerophosphate synthase 1}rabbit.pAb
guanine nucleotide binding protein alpha inhibiting activity polypeptide 1 (GNAI1) polyclonal antibody kinase suppressor of ras (KSR) polyclonal antibody(2-5')oligo(A) synthase 1B,2-5A synthase 1B,2'-5'-oligoadenylate synthase 1B,2'-5'-oligoadenylate synthase-like protein 1,Mouse,Mus musculus,Oas1b,Oias2(2-5')oligo(A) synthase 2,2-5A synthase 2,2'-5'-oligoadenylate synthase 2,Homo sapiens,Human,OAS2,p69 OAS _ p71 OAS,p69OAS _ p71OAS(Alpha)_ 1 _ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_1_ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,β-cyclohexyl-Ala8,D-Tic16,Arg17,Cys18)-Atrial Natriuretic Factor (6-18) amide (mouse, rabbit, rat)
A71915 98% C69H116N26O15S2 CAS:(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host Rabbit(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Rabbit(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Rabbit(Arg8)-Vasopressin - EIA Kit (H - sr, pl), Host Rabbit, Extraction-free, CE-marked Related articles to: PGS1{phosphatidylglycerophosphate synthase 1}rabbit.pAb
- Black soldier fly larvae (Hermetia illucens L., BSFL) efficiently degrade lignocellulosic waste despite lacking endogenous lignocellulolytic enzymes, indicating a critical dependence on gut-associated microbiota. However, how BSFL are associated with the enrichment and spatial organization of lignocellulose-degrading symbionts within the gut remains poorly understood. - Source: PubMed
Publication date: 2026/06/09
Xiang Fang MingTang Xiao TianBrandón María GómezHenawy Ahmed RJiang ShuoYunXu XinHuaChen XueXinZhang ZhiJian - IgA nephropathy (IgAN) is a common primary glomerulonephritis characterized by glomerular immune-complex deposits with (co)dominant IgA. These deposits are enriched for IgA1 glycoforms with some -glycans deficient in galactose (Gd-IgA1). Circulating Gd-IgA1 is bound by IgG autoantibodies to form immune complexes, some of which deposit in glomeruli. Genomic and immunologic studies indicate involvement of pro-inflammatory signaling pathways in the production of Gd-IgA1 in IgAN. Genomic studies identified multiple genetic loci associated with IgAN and suggested a convergence on the NF-κB pathway, including , the gene encoding the NF-κB subunit p65. However, the mechanisms by which NF-κB pathways may affect -glycosylation in IgA1-producing cells are unknown. Using EBV-immortalized B cells derived from peripheral-blood mononuclear cells of IgAN patients and healthy controls that have constitutively activated NF-κB, we report that inhibition of NF-κB/p65 by a selective IKKβ inhibitor TPCA-1 reduced phosphorylation of NF-κB/p65 at S536 and decreased production of IgA1 and, conversely, increased Gd-IgA1 production. This was likely related to reduced expression of gene that encodes the enzyme responsible for galactosylation of IgA1 -glycans. Flow-cytometry imaging revealed changes in nuclear translocation and co-localization of the NF-κB/p65 with co-transcriptional factor SP1, a transcriptional activator of , suggesting that NF-κB pathway affects IgA1 -glycosylation via SP1 transcriptional control of expression. Furthermore, prolonged IKKβ inhibition altered B cell subpopulations, enhancing generation of cells with a plasmablast-like phenotype, characterized by high SSC MFI and CD138 expression. Together, these findings provide functional evidence for involvement of NF-κB/p65 and its transcriptional partners in IgA1 -glycosylation. - Source: PubMed
Publication date: 2026/05/05
Person TaylorPhillips MaggieRice TerriHall StacyJulian Bruce ARizk Dana VNovak JanReily Colin - Aberrant O-linked glycosylation of the IgA hinge segment resulting in galactose-deficient IgA1 (Gd-IgA1) is frequently observed in patients with IgA nephropathy (IgAN), and it is hypothesized to be pathogenic. Here, we genetically disrupted the expression of galactosyltransferase 1 (C1galt1) to elevate Gd-IgA1 levels in mice and examine its role in glomerular deposition. - Source: PubMed
Publication date: 2026/03/27
Wu JingyiXie TongZhang ZhaoLiu XingziZhou XujieZhang YongTian WenminGale Daniel PZhu ShuBarratt JonathanJin JingZhang YuemiaoZhang HongLv Jicheng - Premature ovarian insufficiency (POI) is a major cause of infertility, yet its underlying mechanisms remain poorly understood. The double-mutant (DM) mouse, featuring oocyte-specific deletion of mannosyl (α-1,3-)-glycoprotein β-1,2-N-acetylglucosaminyltransferase (Mgat1) and core 1 β-1,3-galactosyltransferase (C1galt1), develops early-onset POI and offers a valuable system to investigate causes. This study explored whether autoimmunity leads to POI in DM mice. We transplanted control and DM neonatal ovaries into immunocompromised hosts. Three months post-transplantation, follicular development was assessed. While both DM and control ovarian grafts contained follicles, only control ovaries showed healthy progression through to the antral stage. In contrast, DM ovaries exhibited a marked developmental block at the primary stage. In DM follicles, oocytes were smaller, and granulosa cell (GC) number and area were reduced at all follicular stages present. There was a strong correlation between oocyte growth and GC proliferation in controls, but was weaker in DM, suggesting disrupted oocyte-somatic cell communication. Analyses showed strong anti-Müllerian hormone (AMH) in Control GCs, whilst DM levels were less than half of the control, indicating compromised GC function in DM ovaries. Forkhead box L2 (FOXL2) was also reduced in DM follicles compared to control GCs. The persistence of follicular defects, including reduced AMH and FOXL2 levels, in DM ovaries even in severe combined immunodeficient mice reveals that POI is not due to autoimmunity and the phenotype results from intrinsic defects in follicular development caused by the oocyte-specific mutation. These findings underscore the role of oocyte-GC interactions in follicle development and contribute to our understanding of POI pathogenesis. - Source: PubMed
Publication date: 2026/03/18
Kuscu NilayAppeltant RuthPetrovic SergejWilliams Suzannah A - Blunt abdominal trauma (AT) can cause significant intestinal injury and act as a trigger for remote posttraumatic organ dysfunction, including the development of multi-organ dysfunction syndrome (MODS). A deeper understanding of its impact on intestinal barrier integrity and immune regulation is essential for developing therapeutic strategies that support posttraumatic recovery. - Source: PubMed
Publication date: 2026/03/17
Meisen SophieRayatdoost FarahnazOßwald KatharinaPalmer AnnetteBreunig MarkusHuber-Lang MarkusHalbgebauer Rebecca