ATM signaling pathway (WP2516)

Ataxia-telangiectasia (A-T) is a highly pleiotropic, autosomal recessive disease that leads to multisystem defects and has an intricate cellular phenotype, all linked to the functional inactivation of a single gene. Extensive research on the phenotype and the recent discovery and cloning of the responsible gene point to a defect as a central biochemical locus which links several signal transduction pathways that operate under stress as well as in normal physiological conditions. Ataxia is the first symptom in all patients and is predominantly truncal, first manifested in swaying of the head and trunk on standing and even sitting. Truncal ataxia precedes appendicular cerebellar disease. In the first years of life, certain manifestations are present such as dysarthria, muscular hypotonia, the slow initiation and performance of all voluntary movements, characteristic hypotonic facies and postures, and drooling. Dyssynergia and intention tremor of the upper extremities become a major feature after the fifth year of life. The tendon reflexes are diminished or lost, but may be normal or even hyperactive in the early stages. All these observations show a clear ataxia of cerebellar type, initially of station and gait, and later of intention. Early observations of brains from patients with A-T showed neurodegenerative changes, particularly in the Purkinje and granular cells of the cerebellum. Neuronal degeneration is also present in the brainstem, and dentate and olivary nuclei atrophy. Neuronal loss occurs in the substantial nigra and oculomotor nuclei, dorsal root ganglia, and degenerative changes are evident in spinal motor neurons, and dorsal root and sympathetic motor neurons. Moreover, multiple abnormalities in Purkinje cell development have been observed in an Atm-deficient mouse model. Misplaced Purkinje cells have been observed in both the granular and molecular cell layers. In addition, Purkinje cell dendrites tend to grow laterally instead of extending towards the surface of the cerebellum. ATM (for Ataxia-telangiectasia mutated) has been located by restriction-fragment length polymorphism in the chromosome 11, location: 108,093,211-108,239,829. Interestingly, the site of ATM is the same or adjacent to the region occupied by CD3 (Antigen, Delta subunit), THY1 (T-Cell antigen), and NCAM (Cell Adhesion Molecule, Neural, 1) genes, all of which are members of the immunoglobulin-gene superfamily and consequently may be subject to the same defect that afflicts the T-cell receptor and immunoglobulin molecules in A-T. The ATM gene presents an open reading frame (ORF) of 9,165 kb cDNA and is constituted by 66 exons spread over 150 kb of genomic DNA which has a transcript of 12 kb. The ORF of this transcript predicts a 370-kDa protein composed of 3056 amino acids. Over 300 mutations have been found in A-T patients, distributed across the full length (150 kb of genomic DNA) of the ATM gene. Sequence homology indicates that the atm gene product falls into a family of proteins that are related to the catalytic subunit of phosphatidylinositol 3-kinase (PI 3-kinase). This family includes TEL1, MEC1, TOR1, and TOR2 of the budding yeast Saccharomyces cerevisiae, RAD3 of the fission yeast Schizosaccharomyces pombe, and MEI-41 of Drosophila melanogaster. The mammalian family member most closely related to ATM is the ATR/FRP1 protein and, like its yeast homologs, it mediates cellular responses to unreplicated or damaged DNA. In humans the PI 3-kinase family includes the catalytic subunit of the DNA-dependent protein kinase (DNA-PKcs) and FRAP. These sequence homologies appear to reflect functional homology because many of the PI 3-kinase family members are involved in DNA repair, recombination and cell cycle control. Despite the resemblance to lipid kinases, members of this family, including ATM, possess a serine/threonine protein kinase activity, which is wortmannin sensitive. ATM phosphoprotein is ubiquitously expressed and predominantly found in nuclei of proliferating cells, but subcellular fractionation and immunofluorescence revealed that 10-20% of the protein is present in cytoplasmic vesicles, including peroxisomes and endosomes and a prominent cytoplasmic fraction in mouse oocytes. ATM is endosome-bound in mouse neurons, suggesting molecular sorting of the protein occurs in the cytoplasm. In Purkinje cells, distribution of ATM protein is primarily in cytoplasm, and this may be related to the differentiation state of the cells. ATM mRNA is present in all human and mouse tissues. In situ hybridization shows that ATM mRNA is expressed throughout the whole mouse embryo. Furthermore, ATM has been associated with beta-adaptin in lymphoblast vesicles indicating that it may play a role in intracellular vesicle and/or protein transport mechanisms. No obvious nuclear localization signals have been detected in ATM. Neither an ectopically expressed N-terminal fragment of the protein nor a C-terminal fragment is capable of entering the nucleus.
last edited


Amanzo, Mkutmon, MaintBot, Khanspers, Zari, AlexanderPico, Egonw, and Eweitz

Cited In


Homo sapiens




Pathway Ontology: aging pathway altered apoptotic cell death pathway ataxia telangiectasia-mutated (ATM) signaling pathway altered DNA repair pathway


Label Type Compact Identifier
Chk2 Protein uniprot:O96017
CDC25A GeneProduct ensembl:ENSG00000164045
DNA Repair Pathway wikipathways:WP707
Cyclin B GeneProduct ncbigene:891
GADD45A GeneProduct ncbigene:1647
CREB1 GeneProduct ncbigene:1385
p21 GeneProduct ensembl:ENSG00000124762
TP73 GeneProduct ensembl:ENSG00000078900
NEMO Protein uniprot:Q9Y6K9
CDC25C GeneProduct ensembl:ENSG00000158402
SMC1A Protein uniprot:Q14683
Apoptosis Pathway wikipathways:WP254
AP3B2 Protein uniprot:Q13367
Apoptosis Pathway wikipathways:WP254
G2/M Transition Pathway wikipathways:WP1859
CDK1 GeneProduct ensembl:ENSG00000170312
ATM GeneProduct ensembl:ENSG00000149311
H2AX Protein uniprot:P16104
RAD9A GeneProduct ensembl:ENSG00000172613
PIDD GeneProduct ensembl:ENSG00000177595
RAD51 GeneProduct ensembl:ENSG00000051180
TLK1 Protein uniprot:Q9UKI8
CDC2 GeneProduct ncbigene:983
IKBA Protein uniprot:P25963
RIP1 GeneProduct uniprot:Q13546
CCNE1 GeneProduct ensembl:ENSG00000105173
c-Abl GeneProduct ensembl:ENSG00000097007
Chk1 Protein uniprot:O14757
BRCA1 Protein uniprot:P38398
SAPK (MAPK9) GeneProduct ensembl:ENSG00000050748
Cell Death Pathway wikipathways:WP254
FANCD2 Protein uniprot:Q9BXW9
Senescence Pathway wikipathways:WP615
MDMX (MDM4) GeneProduct uniprot:O15151
S Phase Arrest Pathway wikipathways:WP45
TP53 GeneProduct ensembl:ENSG00000141510
DNA Repair Pathway wikipathways:WP707
MDM2 Protein uniprot:Q00987
CDK2 Protein uniprot:P24941
MDC1 Protein uniprot:Q14676
RAIDD GeneProduct uniprot:P78560
NF kappa B Pathway Pathway kegg.pathway:ko04064
G2/M Checkpoint Arrest Pathway wikipathways:WP1859
Caspase 2 GeneProduct uniprot:P42575
S PhaseProgression Pathway wikipathways:WP45
G1/S Checkpoint Arrest Pathway wikipathways:WP45
ATF2 GeneProduct ensembl:ENSG00000115966
DNA Repair Pathway wikipathways:WP707
BID Protein uniprot:P55957
c-Jun GeneProduct ensembl:ENSG00000177606
TP53BP1 GeneProduct ensembl:ENSG00000067369
S Phase Progression Pathway wikipathways:WP45
ATM GeneProduct ensembl:ENSG00000149311
ATM GeneProduct ensembl:ENSG00000149311
ATM GeneProduct ensembl:ENSG00000149311
Cell Cycle Checkpoint Activation Pathway wikipathways:WP1775
MRE11 Protein uniprot:P49959
NBS1 Protein uniprot:O60934
RAD50 Protein uniprot:Q92878
DNA DAMAGE Pathway wikipathways:WP707
CDK2 Protein uniprot:P24941
MDM2 Protein uniprot:Q00987
RAD50 Protein uniprot:Q92878
MRE11 Protein uniprot:P49959
NBS1 Protein uniprot:O60934
Recombination Pathway wikipathways:WP438


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