DNA IR-Double Strand Breaks (DSBs) and cellular response via ATM (Homo sapiens)

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28, 76107, 229, 334, 39278, 100, 159, 206, 215...110, 143, 305, 33266, 81, 2572, 50, 146, 204, 2477871, 162, 32431, 17528934, 60, 31198, 35527956, 28328, 769, 382160, 197, 36534936, 29251139, 248230, 352, 39095, 156, 30928135729205, 28741438827025016496, 3854263018716053, 37033075, 24253, 18632898, 260, 3643, 191, 195, 29796, 193, 232323196, 258298, 40764, 314217223, 336, 353133, 337216921833573732244, 270243, 258, 3637833, 4365338617, 184292412190, 198, 34727, 102, 145, 189, 222...6428436932, 168, 256, 290, 33121839285188306309149, 2103158285339, 34528970164363167306199138, 26230335ATM-TRAF6-cIAP1moduleInhibition pathNuA4complexIonizing Radiation (IR)DNA DSBs21, 25, 63, 144, 174...12, 200, 207, 213, 249...TERF2M-Phase ProgressionRAD17ACTL6APARP1KAT5OBFC2BARF(CDKN2A)MRE11APCNABAK1TRIM28ApoptosisTP53BP1RAD51UPF1CASP9CHK1NBNRAD50MDC1RAD52BLMmRNA nonsense-mediateddecay (NMD)CHK2TP53CDK5SMC3MCPH1RASSF1SMC1ABRCA1STK3DCLRE1CATRp73CohesinEXO1APAF1DNA-PKBRCA2BAXNFkB activationThe intra-S-phasecheckpoint mediatedarrest of cell cycleprogressionMDM2TRAF6ATMLATS1HSF1MCPH1E2F120, 23, 103, 219, 243...13, 300, 402, 43815988, 131, 272, 377, 415...24, 72, 112, 116, 148...236, 354, 437108, 132, 212, 264, 365120, 254, 35091, 109, 157, 27498, 260, 310, 355, 364...420173, 230, 3525, 52, 282, 318, 320...205, 259, 287, 387133, 337, 34989, 275, 303, 342, 425178, 324, 373, 41173, 177, 243, 302, 391...129, 294, 317, 37837, 141, 245153, 159, 16418, 83, 124, 134, 137...165, 356, 358, 39614, 49, 152, 41214, 58, 152, 4108, 42, 99, 111, 160...62, 115, 130, 304, 31651, 344, 389221, 339, 38045, 296, 319, 34816, 84, 135, 147, 288...48, 116, 169, 276, 2774, 220, 321, 401113, 343, 4179, 149, 210, 361, 382...6, 172, 214, 280, 41311, 114, 241, 379, 40541, 55, 118, 126, 158...47, 125, 140, 171, 237...99, 226, 340, 39511, 69, 239154, 235, 253180, 238, 295, 42322, 308, 312211, 268, 371, 372PATM38, 43, 59, 93, 121...PBID74, 233, 419RAD9A80, 327H2AX1, 67, 105, 166, 176...DNA Repair15, 234, 267, 381, 429PAPAF1CASP9CASP37, 35, 54, 333, 416...RNF865, 299, 306RIF1Cell CycleCheckpoint Activation202, 291, 292101, 136, 246, 397, 399G2/M-Phase Checkpoint122, 150, 394Damage ProcessingDNA Polymerasedelta tetramer251, 40877, 261, 424Member of the groupIntermediate paths not shownPath to processStimulation pathRelation to pathRelation to path(intermediate steps not shown)CDC25C46, 90, 225Translocation pathATMTRAF6Cell Survival255ABL196, 104, 117, 346ACTL6AKAT53602653MDM2ARF(CDKN2A)Cell cycle arrestat G1 & G2ARF-MD2McomplexATF2123, 155, 27111, 69, 23919, 30478188MRE11A188RAD50NBNGammaH2AXMDC186MRNcomplexYAP119426, 106, 228, 375FANCD210, 57, 79, 97, 182...7, 61, 87, 94, 119...65, 299, 306, 328, 422FANCD1FANCD1BRCA2128, 358, 39613468, 286, 293217


Description

Wide-ranging correlations are found between the initial physical features of radiation exposure and the possibility of biological consequences. These persist even with the chain of physical, chemical and biological processes that eliminate the majority of the early damage.

Ionizing radiations (IRs) generate hundreds of different simple chemical products in DNA as well multitudes of clustered combinations. The simple products, including single-strand breaks (SSBs), tend to correlate poorly with biological effectiveness. However, when IR produce double-strand breaks (DSBs) in DNA it comes a large rise in relative biological response to cellular damage. In general terms, IRs produce a wide variety of DNA lesions and DSBs are considered to be the major actor responsible for cell death. If unrepaired or improperly repaired, DSBs contribute to chromosomal aberrations, which may lead to human disorders including cancer. The accurate preservation of chromosome continuity in human cells during either DNA replication or repair is critical for preventing the conversion of normal cells to an oncogenic status.

The production of DSBs can be quantified by biochemical techniques, e.g., pulsed field gel electrophoresis (PFGE) and cell imaging, either globally or damage specific, through immunostaining of marker proteins or recruitment of fluorescent proteins to the DNA breaks.

In vertebrate cells, the elimination of DSBs with minimal nucleotide sequence change involves the spatiotemporal orchestration of an apparently endless number of proteins ranging, according to their action, from the nucleotide level to nucleosome organization and chromosome architecture. DSBs trigger a multitude of post-translational modifications that alter both, catalytic activities and the specificity of protein interactions including: phosphorylation, methylation, ubiquitylation, acetylation, and SUMOylation, followed by the turnaround of these changes as repair has been completed.

In mammalian cells, the formation of DSBs initiates a massive global cellular response, either checkpoint signaling and repair or cell death (apoptosis). A major role is that of the MRN (MRE11/RAD50/NBS1) complex binding to DSBs and facilitating the activation of ATM (Ataxia Telangiectasia Mutated) protein, a key PI3K (Phosphatidylinositol 3-kinase) related kinase in the DNA damage response (DDR). At the break site, ATM autophosphorylates, allowing its activation and the following phosphorylation of several substrates in the surrounding chromatin.

The following pathway diagrams the early events of the cellular response after DSBs by IR through the activation of ATM in human cells.

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History

View all...
CompareRevisionActionTimeUserComment
101991view19:16, 22 November 2018EgonwRemove
101834view13:03, 12 November 2018EgonwReplaced an old Uniprot data source with the new one.
95280view18:09, 29 November 2017AmanzoImprovements in conection lines.
95274view17:36, 28 November 2017AmanzoCorrection in line connections.
91367view20:47, 10 February 2017KhanspersModified title
91329view19:06, 31 January 2017Amanzo1 Datanode updated
91328view18:45, 31 January 2017Amanzo2 Datanodes updated
91327view18:13, 31 January 2017Amanzo5 Datanodes updated
91072view18:17, 30 December 2016AmanzoOntology Term : 'disease of cellular proliferation' added !
91071view18:15, 30 December 2016AmanzoOntology Term : 'altered programmed cell death pathway' added !
91070view18:14, 30 December 2016AmanzoOntology Term : 'pathway pertinent to DNA replication and repair, cell cycle, maintenance of genomic integrity, RNA and protein biosynthesis' added !
91069view18:13, 30 December 2016AmanzoOntology Term : 'altered double-strand DNA repair pathway' added !
91068view18:09, 30 December 2016AmanzoModified description
91065view17:29, 29 December 2016AmanzoNew pathway

External references

DataNodes

View all...
NameTypeDatabase referenceComment
ABL1ProteinP00519 (Uniprot-TrEMBL)
ACTL6AProteinO96019 (Uniprot-TrEMBL)
APAF1ProteinO14727 (Uniprot-TrEMBL)
ARF (CDKN2A)ProteinQ8N726 (Uniprot-TrEMBL)
ATF2GeneProductENSG00000115966 (Ensembl)
ATMGeneProductENSG00000149311 (Ensembl)
ATMProteinQ13315 (Uniprot-TrEMBL)
ATRProteinQ13535 (Uniprot-TrEMBL) From Pathway: SPIKE 00003
ApoptosisPathwayR-HSA-109581 (Reactome)
BAK1ProteinQ16611 (Uniprot-TrEMBL)
BAXProteinQ07812 (Uniprot-TrEMBL)
BIDProteinP55957 (Uniprot-TrEMBL)
BLMProteinP54132 (Uniprot-TrEMBL)
BRCA1ProteinP38398 (Uniprot-TrEMBL)
BRCA2ProteinP51587 (Uniprot-TrEMBL)
CASP3ProteinP42574 (Uniprot-TrEMBL)
CASP9ProteinP55211 (Uniprot-TrEMBL)
CDC25CProteinP30307 (Uniprot-TrEMBL)
CDK5ProteinQ00535 (Uniprot-TrEMBL)
CHK1ProteinO14757 (Uniprot-TrEMBL)
CHK2ProteinO96017 (Uniprot-TrEMBL)
Cell Cycle Checkpoint ActivationPathwayWP1775 (WikiPathways)
Cell SurvivalPathway
Cell cycle arrest at G1 & G2Pathway
CohesinProtein
DCLRE1CProteinQ96SD1 (Uniprot-TrEMBL)
DNA Polymerase delta tetramerProteinP30261 (Uniprot-TrEMBL)
DNA RepairPathwayWP707 (WikiPathways)
DNA-PKProteinP78527 (Uniprot-TrEMBL)
Damage ProcessingPathway
E2F1ProteinQ01094 (Uniprot-TrEMBL)