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「"pichierri p"[Author]」の検索結果

86件中 61件~80件表示    検索結果をPubMedで見る PubMedで見る

A case of primary botryoid conjunctival rhabdomyosarcoma.

Rituximab in primary conjunctiva lymphoma.

Werner syndrome protein and the MRE11 complex are involved in a common pathway of replication fork recovery.

BLM and the FANC proteins collaborate in a common pathway in response to stalled replication forks.

Fanconi anemia proteins and the s phase checkpoint.

Werner syndrome protein, the MRE11 complex and ATR: menage-à-trois in guarding genome stability during DNA replication?

The DNA crosslink-induced S-phase checkpoint depends on ATR-CHK1 and ATR-NBS1-FANCD2 pathways.

The Fanconi anemia pathway and the DNA interstrand cross-links repair.

Carotid cavernous fistula in a patient with Graves' ophthalmopathy.

The G2-phase decatenation checkpoint is defective in Werner syndrome cells.

The mammalian mismatch repair protein MSH2 is required for correct MRE11 and RAD51 relocalization and for efficient cell cycle arrest induced by ionizing radiation in G2 phase.

Werner's syndrome protein is phosphorylated in an ATR/ATM-dependent manner following replication arrest and DNA damage induced during the S phase of the cell cycle.

Transcription coupled repair efficiency determines the cell cycle progression and apoptosis after UV exposure in hamster cells.

DNA cross-link-dependent RAD50/MRE11/NBS1 subnuclear assembly requires the Fanconi anemia C protein.

Protecting genomic integrity during DNA replication: correlation between Werner's and Bloom's syndrome gene products and the MRE11 complex.

Bloom's syndrome protein is required for correct relocalization of RAD50/MRE11/NBS1 complex after replication fork arrest.

Hypersensitivity to camptothecin in MSH2 deficient cells is correlated with a role for MSH2 protein in recombinational repair.

Werner's syndrome protein is required for correct recovery after replication arrest and DNA damage induced in S-phase of cell cycle.

Investigation of G2-phase chromosomal radiosensitivity in hereditary non-polyposis colorectal cancer cells.

Werner's syndrome cell lines are hypersensitive to camptothecin-induced chromosomal damage.

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