Related Experiment Video

Updated: May 11, 2026

Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes
15:43

Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes

Published on: January 7, 2013

PTPN4 negatively regulates CrkI in human cell lines

Juan Zhou1, Bingbing Wan, Jingxuan Shan

  • 1State Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University, Shanghai, China.

Cellular & Molecular Biology Letters
|May 14, 2013
PubMed

Insights

Protein tyrosine phosphatase non-receptor type 4 (PTPN4) inhibits cell growth by interacting with CrkI. PTPN4 dephosphorylates CrkI, negatively regulating cell proliferation and motility.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • Protein tyrosine phosphatase non-receptor type 4 (PTPN4) is widely expressed.
  • PTPN4 overexpression inhibits cell growth, but its interacting partners are unknown.

Purpose of the Study:

  • To identify proteins interacting with PTPN4.
  • To elucidate the role of PTPN4-CrkI interaction in cell growth regulation.

Main Methods:

  • Yeast two-hybrid screening to identify interacting proteins.
  • GST pull-down, co-immunoprecipitation, and co-localization assays to confirm interactions.
  • siRNA-mediated knockdown and ectopic expression studies in HEK293T and Hep3B cells.

Main Results:

  • CrkI was identified as a PTPN4-interacting protein.
  • The SH3 domain of CrkI and a proline-rich region of PTPN4 mediate the interaction.
  • PTPN4 inhibits CrkI-mediated proliferation and wound healing, while PTPN4 knockdown enhances CrkI-mediated cell growth and motility.
  • PTPN4 reduces CrkI phosphorylation levels.

Conclusions:

  • PTPN4 negatively regulates cell proliferation and motility.
  • PTPN4 exerts its function through the dephosphorylation of CrkI.

More Related Videos

Electroporation-Based CRISPR-Cas9-Mediated Gene Knockout in THP-1 Cells and Single-Cell Clone Isolation09:29

Electroporation-Based CRISPR-Cas9-Mediated Gene Knockout in THP-1 Cells and Single-Cell Clone Isolation

Published on: February 28, 2025

Related Concept Videos

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...
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.
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...