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Evolution of p53 in hypoxia-stressed Spalax mimics human tumor mutation
Osnat Ashur-Fabian
, Aaron Avivi
, Luba Trakhtenbrot
, Konstantin Adamsky
, Meytal Cohen
, Gadi Kajakaro
, Alma Joel
, Ninette Amariglio
, Eviatar Nevo
, Gideon Rechavi
Sheba Medical Center at Tel Hashomer
Tel Aviv University
University of Haifa
Research output
:
Contribution to journal
›
Article
›
peer-review
107
Scopus citations
Overview
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Dive into the research topics of 'Evolution of p53 in hypoxia-stressed Spalax mimics human tumor mutation'. Together they form a unique fingerprint.
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Keyphrases
Human Tumors
100%
Hypoxia
100%
Tumor mutation Burden
100%
Spalax
100%
Tumor Progression
33%
Growth Arrest
22%
Apoptosis
22%
Apaf-1
22%
Cellular Response
11%
Arginine
11%
Stress Conditions
11%
P53 Stabilization
11%
Human Cancer
11%
Selective Advantage
11%
Tumor Protein p53 (TP53)
11%
Adaptive Mechanism
11%
Lysine
11%
Homeostasis
11%
Structure Model
11%
Dimerization
11%
Epigenetic Modification
11%
P53 Protein
11%
Apoptosis Induction
11%
Low Oxygen
11%
Cell Cycle Arrest
11%
DNA Damage
11%
DNA-binding Domain
11%
Reporter Assay
11%
Hypoxic Stress
11%
Sequence Alignment
11%
DNA-free
11%
Noxa
11%
Puma
11%
Hypoxic Microenvironment
11%
Hypoxia Adaptation
11%
Respiratory Adaptation
11%
Pten
11%
K Substitution
11%
Tumor-associated
11%
Genetics/epigenetics
11%
Entire Life Cycle
11%
Mole Rat
11%
Biochemistry, Genetics and Molecular Biology
Spalax
100%
P53
100%
Arginine
40%
Tumor Progression
30%
Programmed Cell Death
30%
Genetics
10%
Dimerization
10%
Tumor Suppressor Gene
10%
DNA-binding Domain
10%
Homeostasis
10%
DNA Damage
10%
Sequence Alignment
10%
Cell Cycle Arrest
10%
Life Cycle
10%
Cell Cycle Checkpoint
10%
Puma
10%
Oxygen Tension
10%
DnaA
10%
Mole Rat
10%
Lysine
10%