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Related Concept Videos

MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a superfamily...
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...

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Related Experiment Video

Updated: Jun 27, 2026

Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin
10:21

Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin

Published on: September 12, 2019

MBNL1 Promotes Intestinal Fibrosis via RAS-MAPK Pathway-Mediated Fibroblast Activation and Proliferation.

Liwen Zhang1,2, Tianqi Liu1,2, Na Yu1,2

  • 1The First Clinical College, China Medical University, Shenyang 110001, China.

Biomedicines
|June 26, 2026
PubMed
Summary
This summary is machine-generated.

Muscleblind-like protein 1 (MBNL1) drives intestinal fibrosis in Crohn's disease by activating the RAS-MAPK pathway. Targeting MBNL1 offers a potential therapeutic strategy for this debilitating condition.

Keywords:
Crohn’s diseaseMBNL1RAS-MAPK pathwayintestinal fibrosis

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Chronic Salmonella Infection Induced Intestinal Fibrosis
08:40

Chronic Salmonella Infection Induced Intestinal Fibrosis

Published on: September 22, 2019

Area of Science:

  • Gastroenterology
  • Molecular Biology
  • Fibrosis Research

Background:

  • Intestinal fibrosis is a severe complication of Crohn's disease (CD) with limited therapeutic options.
  • Muscleblind-like protein 1 (MBNL1) is implicated in fibrosis but its role in CD-associated intestinal fibrosis is unknown.

Purpose of the Study:

  • To investigate MBNL1 expression, function, and mechanism in intestinal fibrosis.
  • To explore MBNL1 as a potential therapeutic target for CD-related intestinal fibrosis.

Main Methods:

  • Examined MBNL1 expression in a mouse model and CD patient tissues.
  • Utilized in vitro models with human colonic fibroblasts stimulated by TGF-β1.
  • Assessed MBNL1's effects on fibroblast behavior and validated downstream signaling pathways.

Main Results:

  • MBNL1 was upregulated in fibrotic tissues and TGF-β1-stimulated fibroblasts.
  • MBNL1 knockdown inhibited fibroblast activation/proliferation and promoted apoptosis.
  • MBNL1 positively regulated the RAS-MAPK pathway, crucial for fibroblast activation.

Conclusions:

  • MBNL1 promotes colonic fibroblast activation and proliferation via the RAS-MAPK pathway.
  • MBNL1 represents a promising therapeutic target for intestinal fibrosis in Crohn's disease.