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Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
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...
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...
Phosphoinositides and PIPs01:42

Phosphoinositides and PIPs

Phosphoinositides are a group of phospholipids containing a glycerol backbone with two fatty acid chains and a phosphate attached to a myoinositol sugar ring. The inositol head group extends into the cytoplasm, where it is modified by adding phosphate groups to form phosphatidylinositol phosphates or PIPs.
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Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
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Related Experiment Video

Updated: May 10, 2026

A Mass Spectrometry-Based Approach to Identify Phosphoprotein Phosphatases and their Interactors
10:17

A Mass Spectrometry-Based Approach to Identify Phosphoprotein Phosphatases and their Interactors

Published on: April 29, 2022

PPM1A is a RelA phosphatase with tumor suppressor-like activity.

X Lu1, H An2, R Jin3

  • 1Department of Cancer Biology, Vanderbilt University, Nashville, TN, USA.

Oncogene
|July 2, 2013
PubMed
Summary

Protein phosphatase PPM1A dephosphorylates RelA, inhibiting NF-κB signaling and tumor growth. PPM1A suppresses prostate cancer metastasis, offering a potential therapeutic strategy for cancer treatment.

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Assessing Cellular Target Engagement by SHP2 (PTPN11) Phosphatase Inhibitors
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Assessing Cellular Target Engagement by SHP2 (PTPN11) Phosphatase Inhibitors

Published on: July 17, 2020

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Last Updated: May 10, 2026

A Mass Spectrometry-Based Approach to Identify Phosphoprotein Phosphatases and their Interactors
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A Mass Spectrometry-Based Approach to Identify Phosphoprotein Phosphatases and their Interactors

Published on: April 29, 2022

Assessing Cellular Target Engagement by SHP2 (PTPN11) Phosphatase Inhibitors
08:45

Assessing Cellular Target Engagement by SHP2 (PTPN11) Phosphatase Inhibitors

Published on: July 17, 2020

Area of Science:

  • Molecular Biology
  • Oncology
  • Biochemistry

Background:

  • Nuclear factor-κB (NF-κB) signaling is implicated in cancer and inflammation.
  • RelA phosphorylation at serine residues S536 and S276 is crucial for NF-κB function and oncogenesis.
  • Identifying phosphatases that target RelA is key to understanding tumor suppression.

Purpose of the Study:

  • To identify and characterize novel RelA phosphatases with tumor-inhibiting activities.
  • To investigate the role of PPM1A as a RelA phosphatase and its impact on NF-κB signaling.
  • To evaluate PPM1A's potential as a therapeutic target for inhibiting cancer metastasis.

Main Methods:

  • Biochemical assays to demonstrate PPM1A's direct dephosphorylation of RelA at S536 and S276.
  • Assessment of NF-κB transcriptional activity and downstream cytokine expression (MCP-1, IL-6).
  • In vitro cell invasion assays and in vivo mouse models of prostate cancer metastasis.

Main Results:

  • PPM1A directly dephosphorylates RelA at S536 and S276, inhibiting NF-κB activity.
  • PPM1A expression reduces pro-metastatic cytokine expression and inhibits cancer cell invasion.
  • Lower PPM1A expression correlates with metastatic prostate cancer; PPM1A inhibits bone metastasis in mice.

Conclusions:

  • PPM1A acts as a RelA phosphatase, suppressing NF-κB signaling and exhibiting tumor suppressor-like activity.
  • PPM1A inhibits prostate cancer metastasis, suggesting its therapeutic potential.
  • Enhancing PPM1A activity represents a promising strategy to combat NF-κB-driven cancers and bone metastases.