Last update 01 Nov 2024

MUC13

Last update 01 Nov 2024

Basic Info

Synonyms

Down-regulated in colon cancer 1, DRCC1, MUC-13

+ [4]

Introduction

Epithelial and hemopoietic transmembrane mucin that may play a role in cell signaling.

Drugs associated with MUC13

TB-ADC-01

Target

MUC13

Mechanism

MUC13 inhibitors

Active Org.

Theragen Bio Co., Ltd.Startup

Originator Org.

Theragen Bio Co., Ltd.Startup

Active Indication

Rectal Cancer

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Cucurbitacin D

Target

MUC13

Mechanism

MUC13 inhibitors

Active Org.

The University of Tennessee Health Science Center

Originator Org.

The University of Tennessee Health Science Center

Active Indication

Pancreatic Ductal Adenocarcinoma

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

MUC13-SPIONS

Target

MUC13

Mechanism

MUC13 inhibitors

Active Org.

University of Connecticut

Originator Org.

University of Connecticut

Active Indication

Pancreatic Cancer

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with MUC13

100 Translational Medicine associated with MUC13

0 Patents (Medical) associated with MUC13

512

Literatures (Medical) associated with MUC13

01 Nov 2024·International Journal of Biological Macromolecules

Deficiency of SLC26A3 promotes jejunal barrier damage in metabolic disease-susceptible transgenic pigs

Article

Author: Wu, Tianwen ; Wang, Yanfang ; Xu, Shuang ; Fang, Meiying ; Zhang, Kaiyi ; Yang, Shulin ; Yang, Yu ; Du, Juan ; Miao, Jiakun ; Tao, Cong

Intestinal disorders are common in metabolic syndrome. However, their pathogenesis is still not fully understood. Pig and human intestines are highly similar in terms of associated metabolic processes. Here, we successfully constructed a metabolic disease-susceptible transgenic (TG) Bama pig model by knocking in three humanized disease risk genes with the CRISPR/Cas9 technique to assess its potential as a model for human intestinal diseases and explore the possible pathological mechanisms involved. We found that jejunal barrier integrity was disrupted and that the infiltration of inflammatory cells increased in TG pigs after high-fat and high-sucrose diet (HFHSD) treatment. We revealed significant differences in the transcriptome, associated microbiome profiles and microbial metabolite short-chain fatty acid (SCFA) content of the jejunum of TG pigs. Notably, we found that SLC26A3 was significantly downregulated in TG pigs. Knockdown or overexpression of the SLC26A3 gene in IPEC-J2 cells significantly affected the expression of MUC2, MUC13 and occludin. Furthermore, in vitro experiments further verified that CDX2 directly regulated the expression of SLC26A3. Mechanistically, CDX2 mediated intestinal barrier function by enhancing the expression of SLC26A3 by binding to its promoter region between -1120 and - 1070 bp. TG pigs represent a promising model that provides new insights into preclinical research on human intestinal metabolic diseases associated with metabolic disorders and revealed that SLC26A3 may be a potential therapeutic target for intestinal metabolic diseases.

09 Sep 2024·Nucleic Acids Research

RESC14 and RESC8 cooperate to mediate RESC function and dynamics during trypanosome RNA editing

Article

Author: Zhang, Ming ; Qu, Jun ; Wackowski, Katherine ; Read, Laurie K ; Zhu, Xiaoyu ; Shen, Shichen

AbstractMitochondrial transcripts in Trypanosoma brucei require extensive uridine insertion/deletion RNA editing to generate translatable open reading frames. The RNA editing substrate binding complex (RESC) serves as the scaffold that coordinates the protein–protein and protein–RNA interactions during editing. RESC broadly contains two modules termed the guide RNA binding complex (GRBC) and the RNA editing mediator complex (REMC), as well as organizer proteins. How the protein and RNA components of RESC dynamically interact to facilitate editing is not well understood. Here, we examine the roles of organizer proteins, RESC8 and RESC14, in facilitating RESC dynamics. High-throughput sequencing of editing intermediates reveals an overlapping RESC8 and RESC14 function during editing progression across multiple transcripts. Blue native PAGE analysis demonstrates that RESC14 is essential for incorporation of RESC8 into a large RNA-containing complex, while RESC8 is important in recruiting a smaller ribonucleoprotein complex (RNP) to this large complex. Proximity labeling shows that RESC14 is important for stable RESC protein–protein interactions, as well as RESC–RECC associations. Together, our data support a model in which RESC14 is necessary for assembly of editing competent RESC through recruitment of an RNP containing RESC8, GRBC and gRNA to REMC and mRNA.

01 Sep 2024·Digestive and Liver Disease

GCNT3 regulated MUC13 to promote the development of hepatocellular carcinoma through the GSK3β/β-catenin pathway

Article

Author: Kang, Qiu ; Bingzi, Dong ; Tingting, Wu ; Yuwei, Xie ; Chengzhan, Zhu ; Hao, Zou ; Chuandong, Sun

BACKGROUNDHepatocellular carcinoma (HCC) is a leading cause of cancer-related deaths worldwide. Extensive research is currently directed at identifying novel targets for its diagnosis and treatment.AIMSWe investigated the biological functions and clinical significance of mucin-type N-acetylglucosaminyltransferase 3 (GCNT3) in HCC.METHODSVariations in the mRNA expression of GCNT3 were examined in normal and HCC tissues. Cell function assays and animal models characterized the effects of GCNT3 on the proliferation, invasion, and migration abilities of HCC cells. Western blot and immunofluorescence analyses were performed to explore further the specific mechanisms whereby GCNT3 affects HCC progression.RESULTSThere is a strong correlation between GCNT3 overexpression and tumor formation and metastasis in vivo and in vitro. GCNT3 acted as a regulator of the synthesis of mucin-type O-glycans by interacting with mucin 13 (MUC13) to regulate its expression levels, activating the GSK3β/β-catenin signaling pathway. The activation of GSK3β/β-catenin signaling by GCNT3 was mitigated by MUC13 knockdown. In clinical HCC specimens, GCNT3 expression was upregulated in HCC tissues compared to non-tumor tissues. Further, there was a significant correlation between high GCNT3 expression and poor patient survival.CONCLUSIONSGCNT3 regulated tumor progression in HCC through the MUC13/GSK3-β/β-catenin signaling pathway.

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MUC13

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