TULP3 antigen

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636.35 €

Known as:: TULP3 antigenic
Catalog number:: 'H00007289-P01-10
Product Quantity:: 10
Category:: -
Supplier:: ACR
Gene target:: TULP3 antigen

Related genes to: TULP3 antigen

Gene:: TULP3 ^{NIH gene}
Name:: TUB like protein 3
Previous symbol:: -
Synonyms:: TUBL3
Chromosome:: 12p13.33
Locus Type:: gene with protein product
Date approved:: 1998-05-11
Date modifiied:: 2019-04-11

Related products to: TULP3 antigen

Related articles to: TULP3 antigen

Multi-Level Genomic and Computational Analyses Identify a Novel IFT122 Variant Associated With Cranioectodermal Dysplasia 1 in a Consanguineous Saudi Family.
Cranioectodermal dysplasia (CED) is a rare autosomal recessive ciliopathy characterized by craniofacial, skeletal, and ectodermal anomalies. Significant phenotypic heterogeneity often results in clinical overlap with other skeletal dysplasias, including Robinow syndrome. In consanguineous populations, the presence of multiple rare variants can further complicate the molecular diagnosis. This study aimed to clarify the genetic basis of a complex syndromic presentation in a consanguineous Saudi family exhibiting features suggestive of both disorders using an integrated phenotypic, genomic, and computational approach. - Source: PubMed
Aljeaid DeemaAlmadiny AbdulrahmanNasser Khalidah KAlmutadares MahmoudIssa Noha M
Primary cilia regulate GLP-1 signaling in pancreatic β cells.
Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are mainstay therapies for diabetes and obesity, acting in part by enhancing glucose-dependent insulin secretion. While the primary cilium is a known signaling compartment for certain G-protein coupled receptors (GPCRs), its role in the β-cell response to incretins remains undefined. Here, we show that primary cilia are essential for full GLP-1R signaling. Loss of β-cell cilia in mouse and human islets severely impaired GLP-1-potentiated insulin secretion, an effect preceded by blunted whole-cell cAMP and Ca responses. Immunofluorescence and immunogold scanning electron microscopy revealed endogenous GLP-1R localized to the primary cilium. Adenylyl cyclase immunostaining was also enriched within cilia, and targeted inhibition of ciliary PKA reduced insulin secretion. Critically, disrupting ciliary GPCR trafficking via Tulp3 knockdown - while preserving cilia structure - recapitulated the signaling and secretory deficits, demonstrating a specific requirement for the ciliary receptor pool. These findings establish the primary cilium as a non-redundant signaling compartment for GLP-1R and uncover a new layer of subcellular organization in incretin action in β cells. - Source: PubMed
Publication date: 2026/03/25
Melena IsabellaJo Jeong HunTownsend Shannon EDiGruccio Samantha AdamsonDong XinhangZhu LifeiCampbell JonathanHughes Jing W
Primary cilia regulate GLP-1 signaling in pancreatic β cells.
Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are mainstay therapies for diabetes and obesity, acting in part by enhancing glucose-dependent insulin secretion. While the primary cilium is a known signaling compartment for certain G-protein coupled receptors (GPCRs), its role in the β-cell response to incretins remains undefined. Here, we show that primary cilia are essential for GLP-1R signaling. Loss of β-cell cilia in mouse and human islets severely impaired GLP-1-potentiated insulin secretion, an effect preceded by blunted whole-cell cAMP and Ca²⁺ responses. Immunofluorescence and immunogold scanning electron microscopy revealed endogenous GLP-1R localized to the primary cilium. Critically, disrupting ciliary GPCR trafficking via Tulp3 knockdown - while preserving cilia structure - recapitulated the signaling and secretory deficits, demonstrating a specific requirement for the ciliary receptor pool. These findings establish the primary cilium as a non-redundant signaling compartment for GLP-1R and uncover a new layer of subcellular organization in incretin action in β cells. - Source: PubMed
Publication date: 2026/02/22
Melena IsabellaJo Jeong HunTownsend Shannon EDiGruccio Samantha AdamsonDong XinhangZhu LifeiCampbell JonathanHughes Jing W
A HaloTag Knock-In Resource for In Vivo and In Vitro Analysis of Endogenous Polycystin-2 Localization, Turnover, and Transport.
A HaloTag knock-in resource allows direct visualization of endogenous polycystin-2 (PC2), enabling quantitative analysis of its localization, turnover, and transport dynamics. PC2-HaloTag labeling establishes PC1-dependent and Tulp3-dependent control of PC2 ciliary targeting in vivo and in cells. - Source: PubMed
Publication date: 2026/02/10
Li ZhangHaycraft Courtney JCroyle Mandy JHudson DanielYuan YuanSimanyi KristinVendrame Hanan ChweihWang JunKachwala Alfiya IbrahimbhaiMa YongjieParant John MChumley PhillipZhou JulingMrug MichalParnell Stephen CTran Pamela VGao HongjuanQian FengOuteda PatriciaWallace Darren PWatnick Terry JYoder Bradley K
Correction: Tulp3 deficiency results in ciliopathy phenotypes during zebrafish embryogenesis.
- Source: PubMed
Publication date: 2026/01/12
Epting DanielDevane JohnMertes RalfKayser SéverineHelmstädter MartinMetzger PatrickBoerries MelanieBergmann CarstenOtt Elisabeth

TULP3 antigen

Related genes to: TULP3 antigen

Related products to: TULP3 antigen

Related articles to: TULP3 antigen

Multi-Level Genomic and Computational Analyses Identify a Novel IFT122 Variant Associated With Cranioectodermal Dysplasia 1 in a Consanguineous Saudi Family.

Primary cilia regulate GLP-1 signaling in pancreatic β cells.

Primary cilia regulate GLP-1 signaling in pancreatic β cells.

A HaloTag Knock-In Resource for In Vivo and In Vitro Analysis of Endogenous Polycystin-2 Localization, Turnover, and Transport.

Correction: Tulp3 deficiency results in ciliopathy phenotypes during zebrafish embryogenesis.