Map Key
Generic Enzyme
Generic kinase
Protein kinase
Lipid kinase
Generic phosphatase
Protein phosphatase
Lipid phosphatase
Generic phospholipase
Generic protease
Metalloprotease
G-alpha
RAS - superfamily
G beta/gamma
Regulators (GDI, GAP, GEF)
Generic channel
Ligand-gated channel
Voltage-gated channel
Transporter
Normal process
Pathological process
Positive effect
Negative effect
Unspecified effect
Technical link
Disrupts in disease
Emerges in disease
Enhances in disease
Weakens in disease
Organsim specific interaction

Generic binding protein
Receptor ligand
Cell membrane glycoprotein
Transcription factor
DNA
RNA
Compound
Inorganic ion
Predicted metabolite or user's structure
Reaction
Generic receptor
GPCR
Receptors with enzyme activity
Mitochondria
EPR
Golgi
Nucleus
Lysosome
Peroxisome
Cytoplasm
Extracellular

Normal process
Pathological process
Binding
Cleavage
Covalent modifications
Phosphorylation
Dephosphorylation
Transformation
Transport
Catalysis
Transcription regulation
MicroRNA binding
Competition
Influence on expression
Unspecified interactions
Pharmacological effect
Toxic effect
Group relation
Complex subunit
Similarity reaction
A complex or a group
Organism specific object

DNA damage DNA-damage-induced responses


Log In to Post A Comment

DNA damage DNA-damage-induced responses

DNA-damage-induced responses

If the DNA damage is double-strand breaks (DSB) caused by ionizing radiation orradiomimetic agents, ataxia telangiectasia mutated serine-protein kinase ( ATM )is activated [1]. If the DNA is damaged by UV light or UV-mimeticagents, ataxia telangiectasia and Rad3 related protein kinase ( ATR ) andDNA-activated protein kinase ( DNA-PK ) are activated [2]. ATM,ATR and DNA-PK belong to phosphoinositide-3-kinases family. These stimulatedkinases signal the presence of DNA damage in mammalian cells by phosphorylating proteinsthat initiate cell-cycle arrest, apoptosis, and DNA repair [3], [4]. There are three basic pathways, which participate in DNA-damages-induced cellresponse.

Phosphorylation of the c ell cycle checkpoint kinase 2 ( Chk2 ) or c ell cyclecheckpoint kinase 1 ( Chk1 ) [5] are the initial steps in the checkpoint arrest [6] and Brca1 [7] participate in DNA-damage-induced cell cycleregulation (see maps 426. ATM/ATR regulation of G1/S checkpoint and 441.ATM/ATR regulation of G1/S checkpoint ).

It is shown that DNA-damages-induced apoptosis is realized via the activatedp53, Brca1, c-Abl and Chk2 (see map 542 DNA-damages-inducedapoptosis ) [8], [9], [10].

DNA repair is mediated mainly by Brca1 [11] (see map 427. Roleof Brca1 and Brca2 in DNA Repair ).