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Related Concept Videos

MAPK Signaling Cascades01:07

MAPK Signaling Cascades

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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...
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Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
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Small interfering RNAs, or siRNAs, are short regulatory RNA molecules that can silence genes post-transcriptionally, as well as the transcriptional level in some cases. siRNAs are important for protecting cells against viral infections and silencing transposable genetic elements.
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Identification of Alternative Splicing and Polyadenylation in RNA-seq Data
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Multispecies transcriptomics identifies SIKE as a MAPK repressor that prevents NASH progression.

Lan Bai1,2,3, Weiyi Qu3,4, Xu Cheng1,2

  • 1Key Laboratory of Prevention and Treatment of Cardiovascular and Cerebrovascular Diseases, Ministry of Education, Gannan Medical University, Ganzhou 341000, China.

Science Translational Medicine
|February 14, 2024
PubMed
Summary

Suppressor of IKKε (SIKE) inhibits MAP kinase (MAPK) activation, a key driver in nonalcoholic fatty liver (NAFL) progression to nonalcoholic steatohepatitis (NASH). Upregulating SIKE shows promise for preventing and treating NASH.

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Area of Science:

  • Hepatology
  • Molecular Biology
  • Biochemistry

Background:

  • Nonalcoholic fatty liver (NAFL) is a spectrum of liver conditions, often benign, but can progress to nonalcoholic steatohepatitis (NASH), a severe, progressive liver disease.
  • The molecular mechanisms driving the progression from NAFL to NASH are not fully understood, hindering effective therapeutic strategies.

Purpose of the Study:

  • To identify key molecular signatures associated with NASH progression.
  • To investigate the role of suppressor of IKKε (SIKE) as a regulator of NASH pathogenesis.
  • To explore the therapeutic potential of targeting the SIKE-TAK1 axis for NASH treatment.

Main Methods:

  • Comparative analysis of molecular signatures across species to identify NASH progression markers.
  • Utilizing diet- and toxin-induced mouse models of NASH.
  • Investigating the interaction of SIKE with TAK1 and TAB2 using biochemical assays.
  • Evaluating the therapeutic efficacy of indobufen in preclinical NASH models.

Main Results:

  • MAP kinase (MAPK) activation was identified as a critical molecular signature in NASH progression across multiple species.
  • Suppressor of IKKε (SIKE) was identified as a potent negative regulator of MAPK activation.
  • Hepatocyte-specific overexpression of SIKE ameliorated NASH in mouse models.
  • SIKE directly inhibits the TAK1-MAPK signaling pathway by disrupting TAK1-TAB2 binding.
  • Indobufen treatment upregulated SIKE expression and improved NASH features in mice and macaques.

Conclusions:

  • SIKE acts as a crucial suppressor of MAPK signaling, preventing the progression of NAFL to NASH.
  • Targeting the SIKE-TAK1 axis represents a novel therapeutic strategy for managing NASH.
  • Indobufen demonstrates potential as a therapeutic agent for NASH by modulating SIKE expression.