MRE11 Promotes Tumorigenesis by Facilitating Resistance to Oncogene-Induced Replication Stress.

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Unrepaired DNA damage in macrophages causes elevation of particulate matter- induced airway inflammatory response.Gene expression profiling reveals a close relationship between follicular lymphoma grade 3A and 3B, but distinct profiles of follicular lymphoma grade 1 and 2.

P2860

Q52319741-CC538ACB-7952-407B-91F3-148321C9D761 Q52806970-90E5E4B8-54AB-4FB1-BD7D-A9EA6336E23F

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MRE11 Promotes Tumorigenesis by Facilitating Resistance to Oncogene-Induced Replication Stress.

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2017 nî lūn-bûn

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2017年の論文

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2017年学术文章

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2017年学术文章

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2017年学术文章

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2017年学术文章

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2017年学术文章

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2017年学术文章

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2017年學術文章

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2017年學術文章

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name

MRE11 Promotes Tumorigenesis b ...... ne-Induced Replication Stress.

@en

MRE11 Promotes Tumorigenesis b ...... ne-Induced Replication Stress.

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type

Item

label

MRE11 Promotes Tumorigenesis b ...... ne-Induced Replication Stress.

@en

MRE11 Promotes Tumorigenesis b ...... ne-Induced Replication Stress.

@nl

prefLabel

MRE11 Promotes Tumorigenesis b ...... ne-Induced Replication Stress.

@en

MRE11 Promotes Tumorigenesis b ...... ne-Induced Replication Stress.

@nl

P1476

MRE11 Promotes Tumorigenesis b ...... ne-Induced Replication Stress.

@en

P2093

Cheryl J Smith

http://www.w3.org/2001/XMLSchema#string

David O Ferguson

http://www.w3.org/2001/XMLSchema#string

Elizabeth Spehalski

http://www.w3.org/2001/XMLSchema#string

Jeffrey Buis

http://www.w3.org/2001/XMLSchema#string

JoAnn M Sekiguchi

http://www.w3.org/2001/XMLSchema#string

Kayla M Capper

http://www.w3.org/2001/XMLSchema#string

Maria Dinkelmann

http://www.w3.org/2001/XMLSchema#string

Mary J Morgan

http://www.w3.org/2001/XMLSchema#string

P2860

Activation of the ATM kinase by ionizing radiation and phosphorylation of p53

The hMre11/hRad50 protein complex and Nijmegen breakage syndrome: linkage of double-strand break repair to the cellular DNA damage response

Functional interaction of H2AX, NBS1, and p53 in ATM-dependent DNA damage responses and tumor suppression

Oncogenic transformation in the absence of Xrcc4 targets peripheral B cells that have undergone editing and switching

Recruitment and activation of the ATM kinase in the absence of DNA-damage sensors.

Mre11 Dimers Coordinate DNA End Bridging and Nuclease Processing in Double-Strand-Break Repair

DNA Double-Strand Break Repair Pathway Choice Is Directed by Distinct MRE11 Nuclease Activities

The DNA double-strand break repair gene hMRE11 is mutated in individuals with an ataxia-telangiectasia-like disorder

Interplay of p53 and DNA-repair protein XRCC4 in tumorigenesis, genomic stability and development

IgH class switching and translocations use a robust non-classical end-joining pathway

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5327-5338

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scholarly article

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10.1158/0008-5472.CAN-17-1355

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English

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2017-08-17T00:00:00Z

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28819025

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5831255

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MRE11 Promotes Tumorigenesis by Facilitating Resistance to Oncogene-Induced Replication Stress.

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P2860

P2860

MRE11 Promotes Tumorigenesis by Facilitating Resistance to Oncogene-Induced Replication Stress.

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P932