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ichthyosis/arabidopsis
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8 risultati
Evidence for sub-functionalization of tandemly duplicated XPB nucleotide excision repair genes in Arabidopsis thaliana
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Plants are continuously exposed to agents that can generate DNA lesions. Nucleotide Excision Repair (NER) is one of the repair pathways employed by plants to protect their genome, including from sunlight. The Xeroderma Pigmentosum type B (XPB) protein is a DNA helicase shown to be involved in NER
RAD7 homologues contribute to Arabidopsis UV tolerance.
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Frequent exposure of plants to solar ultraviolet radiation (UV) results in damaged DNA. One mechanism of DNA repair is the light independent pathway Global Genomic Nucleotide Excision Repair (GG-NER), which repairs UV damaged DNA throughout the genome. In mammals, GG-NER DNA damage recognition is
Functional XPB/RAD25 redundancy in Arabidopsis genome: characterization of AtXPB2 and expression analysis.
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The xeroderma pigmentosum complementation group B (XPB) protein is involved in both DNA repair and transcription in human cells. It is a component of the transcription factor IIH (TFIIH) and is responsible for DNA helicase activity during nucleotide (nt) excision repair (NER). Its high evolutionary
Cloning of a cDNA from Arabidopsis thaliana homologous to the human XPB gene.
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The human gene XPB, defective in xeroderma pigmentosum patients complementation group B, encodes a DNA helicase involved in several DNA metabolic pathways, including DNA repair and transcription. The high conservation of this gene has allowed the cloning of homologs in various species, such as
Binding of calcium and target peptide to calmodulin-like protein CML19, the centrin 2 of Arabidopsis thaliana.
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Calmodulin-like protein 19 (CML19) is an Arabidopsis centrin that modulates nucleotide excision repair (NER) by binding to RAD4 protein, the Arabidopsis homolog of human Xeroderma pigmentosum complementation group C protein. Although the necessity of CML19 as a part of the RAD4 plant recognition
RAD4 and RAD23/HMR Contribute to Arabidopsis UV Tolerance.
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In plants, exposure to solar ultraviolet (UV) light is unavoidable, resulting in DNA damage. Damaged DNA causes mutations, replication arrest, and cell death, thus efficient repair of the damaged DNA is essential. A light-independent DNA repair pathway called nucleotide excision repair (NER) is
De-etiolated 1 and damaged DNA binding protein 1 interact to regulate Arabidopsis photomorphogenesis.
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BACKGROUND
Plant development is exquisitely sensitive to light. Seedlings grown in the dark have a developmentally arrested etiolated phenotype, whereas in the light they develop leaves and complete their life cycle. Arabidopsis de-etiolated 1 (det1) mutants develop like light-grown seedlings even
Novel human and mouse homologs of Saccharomyces cerevisiae DNA polymerase eta.
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The Saccharomyces cerevisiae RAD30 gene encodes a novel eukaryotic DNA polymerase, pol eta that is able to replicate across cis-syn cyclobutane pyrimidine dimers both accurately and efficiently. Very recently, a human homolog of RAD30 was identified, mutations in which result in the
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