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

Abnormal Proliferation02:23

Abnormal Proliferation

5.4K
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...
5.4K
Covalently Linked Protein Regulators02:04

Covalently Linked Protein Regulators

9.9K
Proteins can undergo many types of post-translational modifications, often in response to changes in their environment. These modifications play an important role in the function and stability of these proteins. Covalently linked molecules include functional groups, such as methyl, acetyl, and phosphate groups, and also small proteins, such as ubiquitin. There are around 200 different types of covalent regulators that have been identified.
These groups modify specific amino acids in a protein....
9.9K
Negative Regulator Molecules01:23

Negative Regulator Molecules

38.8K
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.
38.8K
Regulation of the Unfolded Protein Response01:31

Regulation of the Unfolded Protein Response

3.2K
Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
3.2K
Regulated Protein Degradation02:58

Regulated Protein Degradation

3.3K
3.3K
Regulated Protein Degradation02:58

Regulated Protein Degradation

9.2K
It is vital to regulate the activity of enzymatic as well as non-enzymatic proteins inside the cell. This can be achieved either through creating a balance between their rate of synthesis and degradation or regulating the intrinsic activity of the protein. Both these regulation mechanisms play an essential role in the normal functioning of cells.
Protein degradation plays two important roles in the cells. It helps to protect cells from misfolded or damaged proteins before they lead to a...
9.2K

You might also read

Related Articles

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

Sort by
Same author

A novel NAD(P)H:quinone oxidoreductase 1-responsive vascular endothelial growth factor-targeted antibody-drug conjugate induces dual apoptosis and ferroptosis in glioblastoma.

The Journal of pharmacology and experimental therapeutics·2026
Same author

The influence of retaining osteophyte on the coronal alignment and joint line height following medial unicompartmental knee arthroplasty.

Journal of orthopaedic surgery and research·2026
Same author

Real-time lane-level abnormal traffic detection on freeways using sparse telematics data.

Accident; analysis and prevention·2026
Same author

The coronal plane alignment of the knee classification cannot ignore the joint line convergence angle.

BMC musculoskeletal disorders·2026
Same author

Reprogramming chemoimmunotherapy via biomimetic cell membrane- clay platform to amplify prime-boost antitumor immunity.

Materials today. Bio·2026
Same author

Case Report: A liver metastasis 24 years after resection of a very low-risk jejunal gastrointestinal stromal tumor.

Frontiers in oncology·2026

Related Experiment Video

Updated: Mar 23, 2026

Purification of Ubiquitinated p53 Proteins from Mammalian Cells
10:55

Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Published on: March 21, 2022

2.9K

TRIM65 negatively regulates p53 through ubiquitination.

Yang Li1, Chengyuan Ma2, Tong Zhou3

  • 1Department of Respiration, The First Hospital of Jilin University, Changchun 130021, China.

Biochemical and Biophysical Research Communications
|March 26, 2016
PubMed
Summary

Tripartite-motif protein family member 65 (TRIM65) promotes non-small cell lung carcinoma (NSCLC) growth by degrading the tumor suppressor p53. Targeting TRIM65 may offer new NSCLC treatment strategies and overcome chemotherapy resistance.

Keywords:
NSCLCTRIM65Ubiquitinationp53

More Related Videos

Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

10.1K
Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence
04:56

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence

Published on: December 30, 2025

316

Related Experiment Videos

Last Updated: Mar 23, 2026

Purification of Ubiquitinated p53 Proteins from Mammalian Cells
10:55

Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Published on: March 21, 2022

2.9K
Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

10.1K
Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence
04:56

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence

Published on: December 30, 2025

316

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • The role of Tripartite-motif protein family member 65 (TRIM65) in human cancer is not well understood.
  • TRIM65 is implicated in white matter lesions.
  • Non-small cell lung carcinoma (NSCLC) is a major human cancer with ongoing research into its molecular drivers.

Purpose of the Study:

  • To investigate the role of TRIM65 in the development and progression of non-small cell lung carcinoma (NSCLC).
  • To elucidate the molecular mechanisms by which TRIM65 influences cancer cell behavior.
  • To explore the potential of TRIM65 as a therapeutic target in NSCLC.

Main Methods:

  • Analysis of TRIM65 expression in NSCLC patient data using The Cancer Genome Atlas (TCGA).
  • Cell proliferation assays to assess the impact of TRIM65 overexpression and knockdown.
  • Co-immunoprecipitation and Western blotting to study TRIM65-p53 interaction and p53 degradation.
  • Experiments involving p53-positive and p53-negative cell lines to determine p53's role in TRIM65 function.

Main Results:

  • TRIM65 is significantly upregulated in a subset of NSCLC patients.
  • Overexpression of TRIM65 enhances NSCLC cell proliferation, while its knockdown inhibits it.
  • TRIM65 functions as an E3 ligase, targeting the tumor suppressor p53 for poly-ubiquitination and proteasomal degradation.
  • TRIM65 attenuates cisplatin-induced p53 activation and its inhibitory effect on cell growth is dependent on p53 status.

Conclusions:

  • TRIM65 acts as an oncogenic protein in NSCLC, likely by inactivating p53.
  • TRIM65 promotes tumor growth and may contribute to chemotherapy resistance.
  • Targeting TRIM65 presents a potential therapeutic strategy for NSCLC treatment.