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Related Concept Videos

Nuclear Transmutation03:20

Nuclear Transmutation

Nuclear transmutation is the conversion of one nuclide into another. It can occur by the radioactive decay of a nucleus, or the reaction of a nucleus with another particle. The first manmade nucleus was produced in Ernest Rutherford’s laboratory in 1919 by a transmutation reaction, the bombardment of one type of nuclei with other nuclei or with neutrons. Rutherford bombarded nitrogen-14 atoms with high-speed α particles from a natural radioactive isotope of radium and observed protons being...
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
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Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
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PI3K/mTOR/AKT Signaling Pathway01:22

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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...
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

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Related Experiment Video

Updated: Jul 15, 2026

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

PTEN enters the nuclear age.

Suzanne J Baker1

  • 1Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA. suzanne.baker@stjude.org

Cell
|January 16, 2007
PubMed
Summary

Ubiquitination controls the stability and location of the PTEN tumor suppressor. A nuclear PTEN pool is crucial for maintaining chromosomal stability, offering new insights into cancer regulation.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cancer Research

Background:

  • The regulatory mechanisms governing the PTEN tumor suppressor protein remain largely unclear.
  • Understanding PTEN regulation is critical for developing targeted cancer therapies.

Discussion:

  • Ubiquitination emerges as a key post-translational modification controlling PTEN protein stability.
  • Ubiquitination influences both the degradation and nuclear import of PTEN.
  • A distinct nuclear pool of PTEN plays a significant role in genomic integrity.

Key Insights:

  • Wang et al. (2007) and Trotman et al. (2007) demonstrate ubiquitination's role in PTEN stability and nuclear localization.
  • Shen et al. (2007) reveal that nuclear PTEN is essential for maintaining chromosomal stability.

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Last Updated: Jul 15, 2026

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Efficient Gene Knockdown in the Liver via Intrasplenic Injection of Adeno-Associated Virus Serotype 8 (AAV8)-Delivered Small Hairpin RNA

Published on: November 1, 2024

Outlook:

  • Further research into PTEN ubiquitination could uncover novel therapeutic strategies.
  • Investigating the interplay between PTEN's cytoplasmic and nuclear functions may yield deeper insights into tumor suppression.