DNA single-strand break repair and spinocerebellar ataxia with axonal neuropathy-1

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DNA single-strand break repair and spinocerebellar ataxia with axonal neuropathy-1.

DNA single-strand breaks (SSBs) are the commonest DNA lesions arising spontaneously in cells, and if not repaired may block transcription or may be converted into potentially lethal/clastogenic DNA double-strand breaks (DSBs). Recently, evidence has emerged that defects in the rapid repair of SSBs preferentially impact the nervous system. In particular, spinocerebellar ataxia with axonal neurop...

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DNA Single-Strand Break Repair and Spinocerebellar Ataxia

DNA single-strand break repair (SSBR) is critical for the survival and genetic stability of mammalian cells. Three papers have recently associated mutations in putative human SSBR genes with hereditary spinocerebellar ataxia. The emerging links between SSBR and neurodegenerative disorders are discussed.

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Spinocerebellar Ataxia with Axonal Neuropathy (SCAN1): A Disorder of Nuclear and Mitochondrial DNA Repair

Spinocerebellar ataxias (SCAs) are a group of progressive and irreversible neurological diseases affecting gait and movement coordination. Many result from cerebellar degeneration or the impairment of a portion of the neuroaxis that contributes to cerebellar inflow or outflow (Embirucu et al., 2009). In the cerebellum, the dysfunction and death of Purkinje cells, granule cells or interneurons c...

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Defective DNA ligation during short-patch single-strand break repair in ataxia oculomotor apraxia 1.

Ataxia oculomotor apraxia 1 (AOA1) results from mutations in aprataxin, a component of DNA strand break repair that removes AMP from 5' termini. Despite this, global rates of chromosomal strand break repair are normal in a variety of AOA1 and other aprataxin-defective cells. Here we show that short-patch single-strand break repair (SSBR) in AOA1 cell extracts bypasses the point of aprataxin act...

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DNA Double-Strand Break Repair

ownloade C regulates a myriad of genes controlling cell proliferation, metabolism, differentiation, and apoptosis. lso controls the expression of DNA double-strand break (DSB) repair genes and therefore may be a ial target for anticancer therapy to sensitize cancer cells to DNA damage or prevent genetic instability. report, we studied whether MYC binds to DSB repair gene promoters and modulates...

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ژورنال

عنوان ژورنال: Neuroscience

سال: 2007

ISSN: 0306-4522

DOI: 10.1016/j.neuroscience.2006.08.048