Not exact matches
Tilivalline itself lacks the
DNA -
damaging activity of its antitumor antibiotic relatives because the chemical
site crucial for
DNA interference is blocked.
The study results indicate that patients who have abnormal levels of breaks at common fragile
sites (CFSs),
sites within the chromosomes that are sensitive to
DNA damage, are more likely to have their cancer to return — treatment failure.
«It also allows mapping rNMPs even in conditions in which the
DNA is exposed to environmental stressors that
damage the
DNA by generating breaks and / or abasic
sites.»
Now, the California Institute of Technology chemist is amassing evidence that cells harness this ability to help them home in on
sites of
DNA damage within each cell by revealing defects in
DNA that disrupt its charge - carrying ability.
This binding
site is occupied in case of nucleotide misincorporation in the RNA or
damage to the
DNA, and is termed the «P»
site because it supports proofreading.
When
DNA damage occurs in these cells, the GFP lights up at the
site of the repairs.
Although its raison d'être remains elusive, the gene appears to play an important role in
DNA repair: Mice lacking the protein Brca1 have trouble fixing
DNA damage induced by radiation, for instance, and the protein clumps in the nucleus at
sites where
DNA is broken.
When such
DNA damage occurs, proteins known as PARPs move to the
site of
damage and begin to mend these broken strands of
DNA, allowing cancerous cells and tumors to recover, grow and proliferate, thereby escaping the effects of treatment.
We thus envisage the molecular mechanism of interallelic complementation to involve the exchange of XPD molecules within the TFIIH complex or turnover of TFIIH complexes containing different XPD molecules at the
site of
DNA damage during the course of the global genome as well as transcription - coupled repair of either UV - induced or endogenous
DNA damage.
53BP1 exchanges slowly at the
sites of
DNA damage and appears to require RNA for its association with chromatin.
Guo R, Chen J, Zhu F, Biswas AK, Berton TR, Mitchell DL, Johnson DG (2010) E2F1 localizes to
sites of UV - induced
DNA damage to enhance nucleotide excision repair.
In the presence of
DNA damage, the macro domain of ALC1 is bound to PAR chains that accumulate at the
damage site.
Telomeres are repetitive
DNA sequences that protect the end of the chromosome from being recognized as
sites of
DNA damage.
Johnson and Cole Labs uncover a new role for a tumor suppressor in
DNA repair (11/15/16) Work from the Johnson lab previously showed that E2F1, a critical transcription factor target of the retinoblastoma (Rb) tumor suppressor protein, localizes to
sites of both UV and IR induced
DNA damage in a phosphorylation dependent manner.
At
sites of UV
damage, E2F1 recruits the histone acetyltransferase GCN5, which acetylates histone H3K9 in order to open chromatin structure and increase accessibility to the
damaged site by the
DNA repair machinery.
It has recently been described that Xpa is essential to recruit endonucleases and polymerases to the
damage sites to restore the original
DNA sequence [27].
Abasic
sites are where the
DNA has molecular
damage.