Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

4.1K
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...
4.1K
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

7.9K
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.
There are several types of targeted therapies against...
7.9K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

3.9K
The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
3.9K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Self-management for youth and young adults with childhood-onset chronic conditions: A scoping review of health care transition planning literature.

Health care transitions·2026
Same author

Human aminoacyl-tRNA synthetases as integrators of translation and cell signalling networks.

Nature reviews. Molecular cell biology·2026
Same author

Activatable smart contrast agents for photoacoustic imaging.

Smart molecules : open access·2026
Same author

Immigration Policies as Social Determinants of Health Among International Students in the United States.

Journal of immigrant and minority health·2026
Same author

Effects of a second iron injection and sire line on growth performance, hemoglobin levels, antioxidative status, and whole-body iron retention in piglets.

Journal of animal science·2026
Same author

MDA reduction in HPGe gamma-ray spectrometry using a digital-twin-based intrinsic background construction.

Applied radiation and isotopes : including data, instrumentation and methods for use in agriculture, industry and medicine·2026

Related Experiment Video

Updated: Sep 23, 2025

A Melanoma Patient-Derived Xenograft Model
07:07

A Melanoma Patient-Derived Xenograft Model

Published on: May 20, 2019

12.6K

AIMP2-DX2 provides therapeutic interface to control KRAS-driven tumorigenesis.

Dae Gyu Kim1, Yongseok Choi2, Yuno Lee3

  • 1Medicinal Bioconvergence Research Center, Institute for Artificial Intelligence and Biomedical Research, College of Pharmacy & College of Medicine, Gangnam Severance Hospital, Yonsei University, Incheon, Korea.

Nature Communications
|May 13, 2022
PubMed
Summary
This summary is machine-generated.

A tumor suppressor variant, AIMP2-DX2, enhances KRAS-driven cancers by stabilizing KRAS. Inhibiting the AIMP2-DX2 and KRAS interaction with a novel molecule suppresses tumor growth.

More Related Videos

Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies
09:29

Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies

Published on: September 30, 2016

13.9K
Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts
10:27

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts

Published on: July 25, 2020

7.4K

Related Experiment Videos

Last Updated: Sep 23, 2025

A Melanoma Patient-Derived Xenograft Model
07:07

A Melanoma Patient-Derived Xenograft Model

Published on: May 20, 2019

12.6K
Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies
09:29

Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies

Published on: September 30, 2016

13.9K
Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts
10:27

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts

Published on: July 25, 2020

7.4K

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Oncogenic KRAS mutations drive cancer, and targeted inhibitors are of significant interest.
  • AIMP2-DX2, a variant of the tumor suppressor AIMP2, influences cancer progression.

Purpose of the Study:

  • To investigate the role of AIMP2-DX2 in regulating KRAS stability and KRAS-driven tumorigenesis.
  • To identify therapeutic strategies targeting the AIMP2-DX2-KRAS interaction.

Main Methods:

  • Investigated AIMP2-DX2 binding to KRAS and its effect on KRAS stability.
  • Examined the competitive inhibition of Smurf2 access to KRAS by AIMP2-DX2.
  • Correlated AIMP2-DX2 and KRAS levels in cancer cell lines and tissues.
  • Identified and tested a small molecule inhibitor of the AIMP2-DX2-KRAS interaction in vitro and in vivo.

Main Results:

  • AIMP2-DX2 binds to KRAS, preventing Smurf2-mediated degradation and enhancing KRAS stability.
  • AIMP2-DX2 levels positively correlate with KRAS levels in colon and lung cancers.
  • A novel small molecule inhibitor targeting the AIMP2-DX2-KRAS interface reduced KRAS levels and suppressed cancer cell growth.

Conclusions:

  • AIMP2-DX2 acts as a cancer-specific regulator, augmenting KRAS-driven tumorigenesis by stabilizing KRAS.
  • The AIMP2-DX2-KRAS interaction interface represents a promising therapeutic target for controlling KRAS-driven cancers.