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Interactions Between Signaling Pathways

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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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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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When a ligand binds to a cell-surface receptor, the receptor's intracellular domain changes shape, which may either activate its enzyme function or allow its binding to other molecules. The initial signal is amplified by most signal transduction pathways. This means that a single ligand molecule can activate multiple molecules of a downstream target. Proteins that relay a signal are most commonly phosphorylated at one or more sites, activating or inactivating the protein. Kinases catalyze...
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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
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Crosstalk between p38 MAPK and GR Signaling.

Lisa Zeyen1, Ole Morten Seternes1, Ingvild Mikkola1

  • 1Department of Pharmacy, UiT-The Arctic University of Norway, 9037 Tromsø, Norway.

International Journal of Molecular Sciences
|March 25, 2022
PubMed
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The p38 MAPK pathway and glucocorticoid receptor (GR) signaling are crucial for cellular stress responses. Their crosstalk influences gene expression, offering potential for treating inflammatory diseases and cancer.

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Area of Science:

  • Cellular biology
  • Molecular signaling
  • Endocrinology

Background:

  • The p38 mitogen-activated protein kinase (MAPK) pathway regulates cellular responses to stress, inflammation, proliferation, apoptosis, and differentiation.
  • Glucocorticoids (GCs) are key stress hormones that exert effects via the glucocorticoid receptor (GR), influencing metabolism and immune responses.
  • Dysregulation of p38 MAPK and GR signaling is implicated in inflammatory diseases and cancer.

Purpose of the Study:

  • To review the intricate crosstalk between the p38 MAPK pathway and the glucocorticoid receptor (GR).
  • To elucidate how this interplay regulates gene expression in response to steroid hormones.
  • To explore the clinical potential of targeting the p38-GR axis for therapeutic applications.

Main Methods:

  • Literature review focusing on studies investigating the p38 MAPK pathway.
  • Analysis of research on glucocorticoid receptor (GR) signaling and its downstream effects.
  • Synthesis of findings on the interaction and crosstalk between p38 MAPK and GR.

Main Results:

  • The GR is a downstream target of p38 MAPK.
  • Glucocorticoids can modulate p38 MAPK signaling.
  • The crosstalk between p38 and GR significantly impacts gene expression regulation.

Conclusions:

  • The interplay between p38 MAPK and GR is vital for cellular responses to steroids and stress.
  • Understanding this crosstalk is essential for developing novel therapeutic strategies.
  • Targeting the p38-GR axis holds promise for treating inflammatory conditions and cancers.