PUS3{pseudouridylate synthase 3}rabbit.pAb
- Known as:
- PUS3{pseudouridylate synthase 3}host: rabbit.pAb
- Catalog number:
- 201-20-4641
- Product Quantity:
- 0.2ml
- Category:
- -
- Supplier:
- Shanghai Sunred
- Gene target:
- PUS3{pseudouridylate synthase 3}rabbit.pAb
Related genes to: PUS3{pseudouridylate synthase 3}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
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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: PUS3{pseudouridylate synthase 3}rabbit.pAb
- 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 - Protein glycosylation is an essential post-translational modification. In evolutionarily conserved mucin-type -glycosylation, the most common -glycan, T antigen, is synthesized by core 1 β1,3-galactosyltransferase 1 (C1GalT1). Loss of leads to developmental defects across organisms. We previously found that mutants exhibit malformed legs, but the underlying mechanism was unclear. Here, we identify a glycan-mediated inter-tissue signaling mechanism wherein embryonic hemocytes regulate leg morphogenesis. We show that T antigen-modified Papilin (Ppn), an extracellular matrix (ECM) protein secreted by embryonic hemocytes, suppresses JAK/STAT signaling in the epidermis surrounding Keilin's organ. This repression is essential for proper tubulogenesis of the peripodial stalk anchoring the leg disc and ensuring its correct positioning during development. Disrupted mucin-type -glycosylation impairs Ppn secretion and causes mislocalized leg discs and morphogenetic defects. These findings identify Ppn carrying mucin-type -glycan as long-range modulators of epithelial signaling and underscore the role of immune-like cells in coordinating organogenesis via ECM. - Source: PubMed
Publication date: 2026/02/18
Fuwa Takashi JItoh KazuyoshiIchimiya TomomiAkimoto YoshihiroNishihara Shoko - Colorectal cancer (CRC) progression is fuelled by immune evasion, yet the underlying molecular mechanisms remain to be fully characterized. CD276 (B7-H3), an immune checkpoint glycoprotein frequently overexpressed in aggressive tumors, is extensively modified by glycosylation, a process known to regulate protein stability, localization, and immune interactions. However, its glycosylation-dependent functions in CRC remain unclear. - Source: PubMed
Publication date: 2026/01/20
Soares JanineFerreira DylanMiranda AndreiaGonçalves MartinaRelvas-Santos MartaBrandão AndreiaPaulo PaulaCotton SofiaFreitas RuiMagalhães MarianaFerreira EduardoMarinho-Santos BeatrizAfonso Luís PedroSilva André M NPalmeira CarlosAmado FranciscoPeixoto AndreiaSantos Lúcio LaraFerreira José Alexandre