Gene Report

Basic Information

Approved Symbol	ATM
Approved Name	ataxia telangiectasia mutated
Previous Symbol	ATA, ATDC, ATC, ATD
Previous Name	ataxia telangiectasia mutated (includes complementation groups A, C and D)
Symbol Alias	TEL1, TELO1
Name Alias	TEL1, telomere maintenance 1, homolog (S. cerevisiae)
Location	11q22-q23
Position	chr11:108093559-108239826 (+)
External Links	Entrez Gene: 472 Ensembl: ENSG00000149311 UCSC: uc001pkb.1 HGNC ID: 795
No. of Studies (Positive/Negative)	1(1/0)
Type	Literature-origin

Positive relationships between ATM and MDD (count: 1)

Name in Literature	Reference	Research Type	Statistical Result	Relation Description
ATM	Aston, 2005	patients and normal controls		Genes altered in major depressive disorder Genes altered in major depressive disorder

Positive relationships between ATM and other components at different levels (count: 0)

Positive relationship network of ATM in MK4MDD

Network loading ...

Note:
1. The different color of the nodes denotes the level of the nodes.

Genetic/Epigenetic Locus	Protein and Other Molecule	Cell and Molecular Pathway	Neural System	Cognition and Behavior	Symptoms and Signs	Environment	MDD

2. Besides the component related relationships from literature, gene mapped protein and protein mapped gene are also shown in the network. If the mapped gene or protein is not from literature, square node would be used instead of Circle node. Accordingly, the relationship is marked with dot line.
2. User can drag the nodes to rearrange the layout of the network. Click the node will enter the report page of the node. Right-click will show also the menus to link to the report page of the node and remove the node and related edges. Hover the node will show the level of the node and hover the edge will show the evidence/description of the edge.
3. The network is generated using Cytoscape Web

Negative relationships between ATM and MDD (count: 0)

Negative relationships between ATM and other components at different levels (count: 0)

ATM related SNPs in MK4MDD (count: 0)

ATM related proteins in MK4MDD (count: 1)

Approved Name	UniportKB	No. of Studies (Positive/Negative)	Source
Serine-protein kinase ATM	Q13315	0(0/0)	Gene mapped

ATM related GO terms (count: 50)

ID	Name	Type	Evidence
Literature-origin GO terms
GO:0032553	ribonucleotide binding	molecular function	IEA
GO:0032553	ribonucleotide binding	molecular function	IEA

ID	Name	Type	Evidence
Gene mapped GO terms
GO:0051402	neuron apoptotic process	biological process	IEA
GO:0043525	positive regulation of neuron apoptotic process	biological process	IEA
GO:0043065	positive regulation of apoptotic process	biological process	IMP[17875758]
GO:0016023	cytoplasmic membrane-bounded vesicle	cellular component	IEA
GO:0007420	brain development	biological process	IEA
GO:0005515	protein binding	molecular function	IPI
GO:0035174	histone serine kinase activity	molecular function	IEA
GO:0007050	cell cycle arrest	biological process	IMP[15149599]
GO:0004677	DNA-dependent protein kinase activity	molecular function	IDA[15790808]
GO:0018105	peptidyl-serine phosphorylation	biological process	IDA[9733515]
GO:0036092	phosphatidylinositol-3-phosphate biosynthetic process	biological process	IMP[11375976]
GO:0043066	negative regulation of apoptotic process	biological process	IEA
GO:0005654	nucleoplasm	cellular component	TAS
GO:0007292	female gamete generation	biological process	IEA
GO:0000723	telomere maintenance	biological process	IEA
GO:0007507	heart development	biological process	IEA
GO:0031572	G2/M transition DNA damage checkpoint	biological process	IMP[15149599]
GO:0090399	replicative senescence	biological process	IMP[15149599]
GO:0042159	lipoprotein catabolic process	biological process	IEA
GO:0004674	protein serine/threonine kinase activity	molecular function	IDA[9733515]
GO:0002331	pre-B cell allelic exclusion	biological process	ISS
GO:0071480	cellular response to gamma radiation	biological process	IDA[9925639]
GO:0006977	DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrest	biological process	TAS
GO:0007165	signal transduction	biological process	TAS[7792600]
GO:0006974	response to DNA damage stimulus	biological process	IMP[15790808]
GO:0046777	protein autophosphorylation	biological process	IDA[9733515]
GO:0006975	DNA damage induced protein phosphorylation	biological process	IDA[9733515]
GO:0000075	cell cycle checkpoint	biological process	TAS
GO:0007094	mitotic cell cycle spindle assembly checkpoint	biological process	IMP[11943150]
GO:0046983	protein dimerization activity	molecular function	IDA[15790808]
GO:0030889	negative regulation of B cell proliferation	biological process	IMP[17875758]
GO:0006281	DNA repair	biological process	TAS
GO:0001756	somitogenesis	biological process	IEA
GO:0047485	protein N-terminus binding	molecular function	IDA[11375976]
GO:0016303	1-phosphatidylinositol-3-kinase activity	molecular function	IMP[11375976]
GO:0005819	spindle	cellular component	IEA
GO:0008630	intrinsic apoptotic signaling pathway in response to DNA damage	biological process	IEA
GO:0032403	protein complex binding	molecular function	IDA[15790808]
GO:0006302	double-strand break repair	biological process	TAS
GO:0043517	positive regulation of DNA damage response, signal transduction by p53 class mediator	biological process	IMP[9733515]
GO:0010212	response to ionizing radiation	biological process	IDA[9733515]
GO:0071044	histone mRNA catabolic process	biological process	IDA[16086026]
GO:0007131	reciprocal meiotic recombination	biological process	TAS[7792600]
GO:0003677	DNA binding	molecular function	IEA
GO:0005524	ATP binding	molecular function	IEA
GO:0000724	double-strand break repair via homologous recombination	biological process	TAS
GO:0001666	response to hypoxia	biological process	IEA
GO:0000781	chromosome, telomeric region	cellular component	IDA[15149599]

ATM related KEGG pathways (count: 3)

ID	Name	Brief Description	Full Description
Gene mapped KEGG pathways
hsa04210	apoptosis	Apoptosis	Apoptosis is a genetically controlled mechanisms of cell dea...... Apoptosis is a genetically controlled mechanisms of cell death involved in the regulation of tissue homeostasis. The 2 major pathways of apoptosis are the extrinsic (Fas and other TNFR superfamily members and ligands) and the intrinsic (mitochondria-associated) pathways, both of which are found in the cytoplasm. The extrinsic pathway is triggered by death receptor engagement, which initiates a signaling cascade mediated by caspase-8 activation. Caspase-8 both feeds directly into caspase-3 activation and stimulates the release of cytochrome c by the mitochondria. Caspase-3 activation leads to the degradation of cellular proteins necessary to maintain cell survival and integrity. The intrinsic pathway occurs when various apoptotic stimuli trigger the release of cytochrome c from the mitochondria (independently of caspase-8 activation). Cytochrome c interacts with Apaf-1 and caspase-9 to promote the activation of caspase-3. Recent studies point to the ER as a third subcellular compartment implicated in apoptotic execution. Alterations in Ca2+ homeostasis and accumulation of misfolded proteins in the ER cause ER stress. Prolonged ER stress can result in the activation of BAD and/or caspase-12, and execute apoptosis. More...
hsa04115	p53 signaling_pathway	p53 signaling pathway	p53 activation is induced by a number of stress signals, inc...... p53 activation is induced by a number of stress signals, including DNA damage, oxidative stress and activated oncogenes. The p53 protein is employed as a transcriptional activator of p53-regulated genes. This results in three major outputs; cell cycle arrest, cellular senescence or apoptosis. Other p53-regulated gene functions communicate with adjacent cells, repair the damaged DNA or set up positive and negative feedback loops that enhance or attenuate the functions of the p53 protein and integrate these stress responses with other signal transduction pathways. More...
hsa04110	cell cycle	Cell cycle	Mitotic cell cycle progression is accomplished through a rep...... Mitotic cell cycle progression is accomplished through a reproducible sequence of events, DNA replication (S phase) and mitosis (M phase) separated temporally by gaps known as G1 and G2 phases. Cyclin-dependent kinases (CDKs) are key regulatory enzymes, each consisting of a catalytic CDK subunit and an activating cyclin subunit. CDKs regulate the cell's progression through the phases of the cell cycle by modulating the activity of key substrates. Downstream targets of CDKs include transcription factor E2F and its regulator Rb. Precise activation and inactivation of CDKs at specific points in the cell cycle are required for orderly cell division. Cyclin-CDK inhibitors (CKIs), such as p16Ink4a, p15Ink4b, p27Kip1, and p21Cip1, are involved in the negative regulation of CDK activities, thus providing a pathway through which the cell cycle is negatively regulated. Eukaryotic cells respond to DNA damage by activating signaling pathways that promote cell cycle arrest and DNA repair. In response to DNA damage, the checkpoint kinase ATM phosphorylates and activates Chk2, which in turn directly phosphorylates and activates p53 tumor suppressor protein. p53 and its transcriptional targets play an important role in both G1 and G2 checkpoints. ATR-Chk1-mediated protein degradation of Cdc25A protein phosphatase is also a mechanism conferring intra-S-phase checkpoint activation. More...

ATM related BioCarta pathways (count: 8)

ID	Name	Brief Description	Full Description
Literature-origin BioCarta pathway
G1_PATHWAY	g1 pathway	Cell Cycle: G1/S Check Point	The G1/S cell cycle checkpoint controls the passage of eukar...... The G1/S cell cycle checkpoint controls the passage of eukaryotic cells from the first 'gap' phase (G1) into the DNA synthesis phase (S). Two cell cycle kinases, CDK4/6-cyclin D and CDK2-cyclin E, and the transcription complex that includes Rb and E2F are pivotal in controlling this checkpoint. During G1 phase, the Rb-HDAC repressor complex binds to the E2F-DP1 transcription factors, inhibiting the downstream transcription. Phosphorylation of Rb by CDK4/6 and CDK2 dissociates the Rb-repressor complex, permitting transcription of S-phase genes encoding for proteins that amplify the G1 to S phase switch and that are required for DNA replication. Many different stimuli exert checkpoint control including TGFb, DNA damage, contact inhibition, replicative senescence, and growth factor withdrawal. The first four act by inducing members of the INK4 or Kip/Cip families of cell cycle kinase inhibitors. TGFb additionally inhibits the transcription of Cdc25A, a phosphatase that activates the cell cycle kinases. Growth factor withdrawal activates GSK3b, which phosphorylates cyclin D, leading to its rapid ubiquitination and proteosomal degradation. Ubiquitination, nuclear export, and degradation are mechanisms commonly used to rapidly reduce the concentration of cell-cycle control proteins. More...

ID	Name	Brief Description	Full Description
Gene mapped BioCarta pathways
ATM_PATHWAY	atm pathway	ATM Signaling Pathway	The ataxia telangiectasia-mutated gene (ATM) encodes a prote...... The ataxia telangiectasia-mutated gene (ATM) encodes a protein kinase that acts as a tumor suppressor. ATM activation by ionizing radiation damage to DNA stimulates DNA repair and blocks progression through the cell cycle. Mutation of the ATM gene causes the disease ataxia telangiectasia which which involves an inherited predisposition to some cancers. To play this role ATM interacts with a broad network of proteins, including checkpoint factors (chk1, chk2), tumor suppressors (p53 and BRCA), DNA repair factors (RAD50, RAD51, GADD45), and other signaling molecules (c-Abl and NF-kB). In addition to regulating DNA repair and the cell cycle, ATM can also trigger apoptosis in radiation treated cells. More...
G2_PATHWAY	g2 pathway	Cell Cycle: G2/M Checkpoint	The G2/M DNA damage checkpoint prevents the cell from enteri...... The G2/M DNA damage checkpoint prevents the cell from entering mitosis (M phase) if the genome is damaged. The Cdc2-cyclin B kinase is pivotal in regulating this transition. During G2 phase, Cdc2 is maintained in an inactive state by the kinases Wee1 and Mt1. As cells approach M phase, the phosphatase Cdc25 is activated, perhaps by the polo-kinase Pik1. Cdc25 then activates Cdc2, establishing a feedback amplification loop that efficiently drives the cell into mitosis. DNA damage activates the DNA-PK/ATM/ATR kinases, initiating two parallel cascades that inactivate Cdc2-cyclin B. The first cascade rapidly inhibits progression into mitosis: the CHK kinases phosphorylate and inactivate Cdc25, which can no longer activate Cdc2. The second cascade is slower. Phosphorylation of p53 dissociates it from MDM2, activating its DNA binding activity. Acetylation by p300/PCAF further activates its transcriptional activity. The genes that are turned on by p53 constitute effectors of this second cascade. They include 14-3-3s, which binds to the phosphorylated Cdc2-cyclin B kinase and exports it from the nucleus; GADD45, which apparently binds to and dissociates the Cdc2-cyclin B kinase; and p21Cip1, an inhibitor of a subset of the cyclin-dependent kinases including Cdc2 (CDK1). More...
ATRBRCA_PATHWAY	atrbrca pathway	Role of BRCA1, BRCA2 and ATR in Cancer Susceptibility	BRCA1 and BRCA2 were identified genetically as breast cancer...... BRCA1 and BRCA2 were identified genetically as breast cancer susceptibility genes when a single copy of the gene is mutated and are involved in the cellular response to DNA damage, including blocking cell cycle progression and inducing DNA repair to preserve the integrity of the genome during cell division. BRCA1 and BRCA2 induce double-stranded repair of breaks using homologous recombination, in part through activation of RAD51. BRCA1 acts as a ubiquitin ligase targeting the protein FancD2 that activates checkpoint control, integrating the ATM response to ionizing radiation and the FA response to cross-linking agents like mitomycin C. Mutation of one of the several components of the FA complex involved in maintaining integrity of the genome leads to the condition Fanconi anemia. One member of the FA complex was recently identified as BRCA2, which leads to Fanconi anemia when both copies of the gene are mutated. Another related factor involved in the response of cells to DNA damage is the kinase ATM. ATM is mutated in patients with AT, a condition with many similar traits to Fanconi anemia. Like ATM, ATR serves as a checkpoint kinase that halts cell cycle progression and induces DNA repair when DNA is damaged. Loss of ATR results in a loss of checkpoint control in response to DNA damage, leading to cell death, and deletion of the ATR gene in mice is embryonic lethal. ATRIP is a protein that interacts with ATR and is a substrate for its kinase activity. ATRIP is required for ATR function, and removal of ATRIP also leads to a loss of checkpoint control of the cell cycle. ATR and ATM kinase targets include repair enzymes like Rad51, and the checkpoint kinases Chk1 and Chk2, as well as BRCA1 and BRCA2. The close relationship of the genes involved in breast cancer and Fanconi anemia has helped illuminate this signaling system, and may help lead to improved understanding and treatment of these conditions. More...
P53HYPOXIA_PATHWAY	p53hypoxia pathway	Hypoxia and p53 in the Cardiovascular system	Hypoxic stress, like DNA damage, induces p53 protein accumul...... Hypoxic stress, like DNA damage, induces p53 protein accumulation and p53-dependent apoptosis in oncogenically transformed cells. Unlike DNA damage, hypoxia does not induce p53-dependent cell cycle arrest, suggesting that p53 activity is differentially regulated by these two stresses. Hypoxia induces p53 protein accumulation, but in contrast to DNA damage, hypoxia fails to induce endogenous downstream p53 effector mRNAs and proteins, such as p21, Bax, CIP1, WAF1 etc. Hypoxia does not inhibit the induction of p53 target genes by ionizing radiation, indicating that p53-dependent transactivation requires a DNA damage-inducible signal that is lacking under hypoxic treatment alone. The phosphatidylinositol 3-OH-kinase-Akt pathway inhibits p53-mediated transcription and apoptosis. Mdm2, a ubiquitin ligase for p53, plays a central role in regulation of the stability of p53 and serves as a good substrate for Akt. Mdm-2 targets the p53 tumor suppressor for ubiquitin-dependent degradation by the proteasome, but, in addition, the p53 transcription factor induces Mdm-2, thus, establishing a feedback loop. Hypoxia or DNA damage by abrogating binding of HIF-1 with VHL and p53 with Mdm-2, respectively, leads to stabilization and accumulation transcriptionally active HIF-1 and p53. At the molecular level, DNA damage induces the interaction of p53 with the transcriptional activator p300 as well as with the transcriptional corepressor mSin3A. In contrast, hypoxia primarily induces an interaction of p53 with mSin3A, but not with p300. More...
RB_PATHWAY	rb pathway	RB Tumor Suppressor/Checkpoint Signaling in response to DNA damage	Cell cycle checkpoint controls at the G1 to S transition and...... Cell cycle checkpoint controls at the G1 to S transition and the G2 to M transition prevent the cell cycle from progressing when DNA is damaged. The ATM protein kinase detects DNA damage and in response to this activates DNA repair factors and inhibits cell cycle progression. Two of the proteins that ATM phosphorylates in response to DNA damage are the tumor suppressor p53 and the checkpoint kinase chk1. In turn, the tumor suppressor p53 interacts with p21 to block the activity of cdk2 (cyclin dependent kinase 2) preventing passage from G1 to S phase and harmful replication of damaged DNA. One of the targets of cdk2 is the Rb gene product, another tumor suppressor. When dephosphorylated, Rb interacts with E2F transcription factors and prevents transcription of genes required for progression through the cell cycle. When phosphorylated by cell cycle dependent kinases like cdk2 and cdk4, Rb no longer interacts with E2F and the cell cycle proceeds through the G1-S checkpoint. DNA damage also regulates the G2-M phase transition by acting on the cell cycle regulator cdc2. More...
CHEMICAL_PATHWAY	chemical pathway	Apoptotic Signaling in Response to DNA Damage	The cellular activation of the caspase cascade resulting in ...... The cellular activation of the caspase cascade resulting in cell death is triggered by chemical damage to DNA which stimulates a sequence resulting in the cleavage of Bid in a manner similar to the binding of so called death-receptors or directly initiates the permeability transition of the mitochondrial membrane. The permiability transition releases several factors including cytochrome c, AIF and other factors in to the cytoplasm. Cytochrome c, a key protein in electron transport, is released from mitochondria in response to apoptotic signals, and activates Apaf-1, a protease released from mitochondria. Activated Apaf-1 activates caspase-9 and the rest of the caspase cascade. The caspases are a class of cysteine proteases that includes several representatives involved in apoptosis. The caspases convey the apoptotic signal in a proteolytic cascade, with caspases cleaving and activating other caspases that then degrade other cellular targets that lead to cell death. More...
P53_PATHWAY	p53 pathway	p53 Signaling Pathway	p53 is a transcription factor who's activity is regulated by...... p53 is a transcription factor who's activity is regulated by phosphorylation. The function is p53 is to keep the cell from progressing through the cell cycle if there is damage to DNA present. It may do this in multiple ways from holding the cell at a checkpoint until repairs can be made to causing the cell to enter apoptosis if the damage cannot be repaired. The critical role of p53 is evidenced by the fact that it is mutated in a very large fraction of tumors from nearly all sources. More...

ATM related Reactome pathways (count: 6)

ID	Name	Description
Gene mapped Reactome pathways
REACT_1538	cell cycle_checkpoints	A hallmark of the human cell cycle in normal somatic cells i...... A hallmark of the human cell cycle in normal somatic cells is its precision. This remarkable fidelity is achieved by a number of signal transduction pathways, known as checkpoints, which monitor cell cycle progression ensuring an interdependency of S-phase and mitosis, the integrity of the genome and the fidelity of chromosome segregation. Checkpoints are layers of control that act to delay CDK activation when defects in the division program occur. As the CDKs functioning at different points in the cell cycle are regulated by different means, the various checkpoints differ in the biochemical mechanisms by which they elicit their effect. However, all checkpoints share a common hierarchy of a sensor, signal transducers, and effectors that interact with the CDKs. The stability of the genome in somatic cells contrasts to the almost universal genomic instability of tumor cells. There are a number of documented genetic lesions in checkpoint genes, or in cell cycle genes themselves, which result either directly in cancer or in a predisposition to certain cancer types. Indeed, restraint over cell cycle progression and failure to monitor genome integrity are likely prerequisites for the molecular evolution required for the development of a tumor. Perhaps most notable amongst these is the p53 tumor suppressor gene, which is mutated in >50% of human tumors. Thus, the importance of the checkpoint pathways to human biology is clear. More...
REACT_309	stabilization of_p53	Later studies pin-pointed that a single serine. ATM also reg...... Later studies pin-pointed that a single serine. ATM also regulates the phosphorylation of p53 at other sites, especially Ser-20, by activating other serine/threonine kinases in response to IR. Phosphorylation of p53 at Ser-20 interferes with p53-MDM2 interaction. MDM2 is transcriptionally activated by p53 and is a negative regulator of p53 that targets it for degradation. In addition modification of MDM2 by ATM also affects p53 stabilization. More...
REACT_828	g2 m_checkpoints	G2/M checkpoints include the checks for damaged DNA, unrepli...... G2/M checkpoints include the checks for damaged DNA, unreplicated DNA, and checks that ensure that the genome is replicated once and only once per cell cycle. If cells pass these checkpoints, they follow normal transition to the M phase. However, if any of these checkpoints fail, mitotic entry is prevented by specific G2/M checkpoint events. The G2/M checkpoints can fail due to the presence of unreplicated DNA or damaged DNA. In such instances, the cyclin-dependent kinase, Cdc2(Cdk1), is maintained in its inactive, phosphorylated state, and mitotic entry is prevented. Events that ensure that origins of DNA replication fire once and only once per cell cycle are also an example of a G2/M checkpoint. In the event of high levels of DNA damage, the cells may also be directed to undergo apopotosis (not covered). More...
REACT_2054	double strand_break_repair	Numerous types of DNA damage can occur within a cell due to ...... Numerous types of DNA damage can occur within a cell due to the endogenous production of oxygen free radicals, normal alkylation reactions, or exposure to exogenous radiations and chemicals. Double-strand breaks. HRR functions primarily in repairing both one-sided DSBs that arise at DNA replication forks and two-sided DSBs arising in S or G2-phase chromatid regions that have replicated. More...
REACT_216	dna repair	DNA repair is a phenomenal multi-enzyme, multi-pathway syste...... DNA repair is a phenomenal multi-enzyme, multi-pathway system required to ensure the integrity of the cellular genome. These cellular mechanisms that must cope with the plethora of DNA base pair adducts that arise. DNA damage can arise spontaneously in the cellular milieu through chemical alteration of base nucleotides or as a consequence of errors during DNA replication. For example, it is well known that normal cellular pH and temperature offer an environment, which is hostile to the integrity of DNA and its nucleotide components. Additionally, DNA damage may be induced in response to environmental exposures, including exposure to physical agents such as ionizing or ultraviolet (UV) radiation. Finally, specific chemical agents are known to alkylate or cross-link DNA bases, produce bulky adducts on DNA bases, or break DNA phosphate-sugar backbone. The pioneering work from a number of laboratories have elucidated the basic mechanisms underlying distinct DNA repair pathways that include nucleotide excision repair (NER), base excision repair (BER), DNA strand break repair (DSBR), direct reversal of DNA damage, and the replication past DNA lesions by specialized DNA bypass polymerases (bypass replication). Defects in most of these repair pathways have been associated with one or more specific human diseases. Additionally, the repair of damaged DNA is intimately associated with a number of other distinct cellular processes such as DNA replication, DNA recombination, cell cycle checkpoint arrest, and other basic cellular mechanisms as outlined herein. More...
REACT_1874	homologous recombination_repair	The HRR pathway is an error free DNA repair mechanism that u...... The HRR pathway is an error free DNA repair mechanism that utilizes information encoded by homologous sequence to repair double-strand breaks (DSBs). HRR acts on DSBs occurring within replicated DNA (replication-independent DSBs) or on DSBs that are generated at broken replication forks (replication-dependent DSBs). Repair by homologous recombination involves processing of the ends of the DNA double-strand break, homologous DNA pairing and strand exchange, repair DNA synthesis, and resolution of the heteroduplex molecules. More...

ATM related interactors from protein-protein interaction data in HPRD (count: 40)

Gene	Interactor	Interactor in MK4MDD?	Experiment Type	PMID
ATM	STK11	No	in vitro;in vivo	11853558 , 12234250
ATM	CHEK1	No	in vitro;in vivo	11390642 , 11252893
ATM	E2F1	No	in vitro	11459832
ATM	RAD9A	No	in vitro;in vivo	12709442 , 11278446
ATM	XRCC5	No	in vivo	15758953
ATM	PRKDC	No	in vitro	10464290
ATM	MDM2	No	in vitro;in vivo	11331603
ATM	TP53BP1	No	in vitro;in vivo	12697768
ATM	TP53	No	in vitro;in vivo	9765199 , 11551930 , 11709713 , 10673501 , 11875057 , 16858402 , 17157788 , 9843217
ATM	RAD51	No	in vitro;in vivo	10212258
ATM	EIF4EBP1	No	in vitro;in vivo	9806882 , 11146653 , 12588975
ATM	FANCD2	No	in vitro;in vivo	12086603
ATM	TERF1	No	in vitro;in vivo	11375976 , 15314656
ATM	EEF1E1	Yes	in vitro;in vivo	15680327
ATM	AP1B1	No	in vitro;in vivo;yeast 2-hybrid	9707615
ATM	CHEK2	No	in vivo	11901158 , 12242661 , 10973490 , 12493754 , 16794575
ATM	AP3B2	No	in vitro;yeast 2-hybrid	9707615
ATM	H2AFX	No	in vivo	9488723 , 11893489 , 11571274
ATM	AATF	No	in vitro;in vivo	17157788
ATM	SMC1A	No	in vitro;in vivo	11877377
ATM	RHEB	No	in vitro	15854902
ATM	MRE11A	No	in vitro	10608806
ATM	RAD17	No	in vitro;in vivo	11418864 , 10608806
ATM	BRCA1	No	in vitro;in vivo	10550055 , 10866324 , 11114888
ATM	CREB1	Yes	in vitro	16293623 , 15073328
ATM	ABL1	No	in vitro;in vivo;yeast 2-hybrid	9168117 , 9168116
ATM	ATM	Yes	in vitro;in vivo	14519663 , 12556884 , 10608806 , 16858402 , 16906133
ATM	DCLRE1C	No	in vitro;in vivo	15456891
ATM	TIPARP	No	in vivo	11238919
ATM	TOPBP1	No	in vitro;in vivo	11756551
ATM	AP2B1	No	in vitro;in vivo;yeast 2-hybrid	9707615
ATM	NBN	No	in vitro;in vivo	10839544 , 11252893 , 10839545 , 10608806
ATM	WRN	No	in vitro	10608806 , 11252893 , 10839545
ATM	RBBP8	No	in vitro;in vivo	10910365 , 11689934
ATM	MDC1	No	in vivo	12607005
ATM	KAT5	Yes	in vitro;in vivo	16141325
ATM	TREX1	No	in vivo	15758953
ATM	PEX5	No	in vivo;yeast 2-hybrid	10567403
ATM	MDM4	No	in vitro;in vivo	15788536 , 16163388
ATM	XPA	No	in vitro	16540648

Gene Report

Literature-origin GO terms

Gene mapped GO terms

Gene mapped KEGG pathways

Literature-origin BioCarta pathway

Gene mapped BioCarta pathways

Gene mapped Reactome pathways