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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...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...

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Related Experiment Video

Updated: May 25, 2026

Inducing Apical Periodontitis in Mice
10:26

Inducing Apical Periodontitis in Mice

Published on: August 6, 2019

MAPK usage in periodontal disease progression.

Qiyan Li1, Michael S Valerio, Keith L Kirkwood

  • 1Department of Endodontics, Periodontics and Oral Medicine, The First People's Hospital of Yunnan Province, Kunming, Yunnan 650032, China.

Journal of Signal Transduction
|February 9, 2012
PubMed
Summary
This summary is machine-generated.

Targeting the p38 MAPK signaling pathway, crucial in periodontal disease, can reduce bone loss. Inhibiting p38 MAPK activation and related molecules effectively decreases inflammation and cytokine expression, offering a potential therapeutic strategy for periodontitis.

Related Experiment Videos

Last Updated: May 25, 2026

Inducing Apical Periodontitis in Mice
10:26

Inducing Apical Periodontitis in Mice

Published on: August 6, 2019

Area of Science:

  • Periodontology
  • Immunology
  • Molecular Biology

Background:

  • Periodontal disease involves bacterial recognition, leading to p38 MAPK activation and inflammatory cytokine release.
  • This process promotes osteoclastogenesis and bone resorption in the periodontal tissues.

Purpose of the Study:

  • To investigate the role of the p38/MAPK-activated protein kinase-2 (MK2) signaling axis in periodontal disease progression.
  • To evaluate the therapeutic potential of targeting this pathway for treating periodontal inflammation and bone loss.

Main Methods:

  • Utilized an orally administered p38α inhibitor in experimental models of periodontal disease.
  • Employed RNA interference to attenuate MK2 and studied the effects of MAPK phosphatase-1 (MKP-1) deficiency and overexpression.
  • Investigated the impact of tristetraprolin (TTP) on inflammatory cytokine mRNA stability.

Main Results:

  • Oral p38α inhibition significantly reduced periodontal bone loss by decreasing inflammation and cytokine levels.
  • MK2 attenuation and MKP-1 deficiency exacerbated LPS-induced alveolar bone loss, while MKP-1 overexpression offered protection.
  • Overexpression of TTP stabilized inflammatory cytokine mRNA, mitigating periodontal inflammation.

Conclusions:

  • The p38 MAPK signaling pathway, including MK2 and MKP-1, is critical for periodontal disease progression.
  • Targeting p38 MAPK signaling and its downstream effectors like TTP presents a promising therapeutic avenue for periodontal disease.