Sentences with phrase «cells repair dna»

This new function for GFI1 is a new piece of the puzzle to understand how cells repair their DNA.
Their technique has shed light on how cells repair DNA strand breaks, which could help scientists learn how to protect astronauts from cosmic rays as well as refine radiotherapy protocols designed to kill tumors.
Berkeley Lab scientists are using a similar approach to study how cells repair DNA damage.
«Although we are investigating a very basic problem in biology — how cells repair DNA damage — our discoveries have potential ramifications in the clinic,» says de Lange.

Not exact matches

Its drug Niraparib kills cancer cells by inhibiting the production of proteins called PARPs, which help repair damaged DNA strands, thereby hastening the death of some types of cancer cells.
This makes me happy: Microglia cells migrate into tumors and supply cancer cells with a substance needed for the repair of DNA damage.
The DNA damage builds up and checkpoints that repair or kill damage cells are impaired.
Catalyst AC - 11 Serum goes right to work restoring your skin's DNA and creating more active cells by activating your skin's own zinc finger remodeling process which is a critical part of DNA repair.
PARP inhibitors prevent DNA repair causing cancer cells to die rather than repair.
Natural DNA - repair mechanisms then kick in and put the pieces back together, but in a complete hotchpotch, which usually means the cell will die.
A type of immune therapy known as PD - 1 blockade controlled cancer in 77 percent of patients with defects in DNA mismatch repair — the system cells use to spell - check and fix errors in DNA (SN Online: 10/7/15).
One strategy is to stop a cell from dividing until it self - destructs or its DNA can be repaired.
«The study culminates years of work and provides physical evidence that sleep deprivation injures cells and that sleep recovery restores the balance between, among other parameters, DNA damage and repair,» Dr. Everson said.
The most common mutations, occurring in five of the women, occurred in genes including ARID1A, PIK3CA, KRAS and PPP2R1A, all known for controlling cell growth, cell invasion and DNA damage repair.
Mice with fragile beta cells that were poor at repairing DNA damage would rapidly develop diabetes when those beta cells were challenged by cellular stress.
Zika induced changes that were more focused on genes involved on DNA replication and repair, indicating that Zika infection disrupts cell replication more.
Other mice, with robust beta cells that were good at repairing DNA damage, were able to stay non-diabetic for life, even when those islets were placed under severe cellular stress.
I had spent 4 years studying the interactions between two proteins involved in the cell cycle and DNA replication and repair.
The study found that carfilzomib and irinotecan have a potential synergistic effect in SCLC and other Irinotecan - sensitive cancers by allowing normal DNA damage repair and enabling normal cell - cycle death.
Fanconi anemia (FA) is a genomic instability syndrome caused by mutations inside a cluster of proteins normally responsible for DNA repair in cells.
A 2009 study by the same researchers showed that NF - kB helps normal cells in DNA repair, which may prevent them from harming the body.
Certain kinds of cancer cells depend heavily on PARP to repair DNA damage.
«For this reason, we decided to combine vitamin C with a PARP inhibitor, a drug type known to cause cancer cell death by blocking the repair of DNA damage, and already approved for treating certain patients with ovarian cancer.»
The mechanisms that promote or enable drug resistance include drug inactivation, drug target alteration, drug removal from cells, DNA damage repair, cell death inhibition and the epithelial - mesenchymal transition (EMT) that enable solid tumors to transform into more metastatic grades.
PARP inhibitors target and block proteins which cancer cells depend on to repair DNA for their survival.
This leads to massive DNA damage that can not be repaired, and the cancer cells self - destruct.
Injecting CRISPR / Cas9 along with sperm (bottom row) repairs the mutation before DNA replicates, leading to an embryo with all healthy cells.
The embryos lacking functional BRCA2 genes probably stopped growing because molecular «checkpoints» in the developing embryo either halt the division of cells with damaged DNA, so that the damage can be repaired, or kill the cells outright.
With a less efficient helicase and therefore less efficient DNA repair, Martin suggests, atherosclerotic lesions could arise like tumors from mutations in single cells, besides their well - known origin from chronic inflammation from high - fat diets.
Beyond this, we could take the DNA repair abilities from Polypedilum vanderplanki, a fly whose larvae can survive complete desiccation and extremes of heat and cold, and transplant them into human cells.
Taken together, these findings suggest that BRCA2 mutations increase susceptibility to breast cancer by disrupting DNA repair and allowing cells to accumulate mutations, including those that foster cancer development.
Now, results described in tomorrow's issue of Nature suggest that BRCA2 mutations could lead to cancer by interfering with cells» ability to repair damaged DNA.
Synthetic biocircuits made of DNA and encoded proteins could be inserted to detect and repair (or kill) cells with mutations known to cause cancer or aging.
PARP inhibitors prevent cancer cells from repairing themselves after experiencing DNA damage (for example from chemotherapy or radiation).
This can be exploited in the therapy, as Rottenberg explains: «DNA - repair - defective sleeper cells respond to particular substances that damage DNA
One big one: «Not everybody appreciates the way CRISPR technology works — it makes the cut in the DNA but it doesn't take care of the repair — so we rely on the cells» fundamental machinery to do that,» Doudna says.
The research group in Israel showed «that the Spalax p53 suppresses apoptosis (programmed cell death), however enhances cell cycle arrest and DNA repair mechanisms,» he said.
Ever wondered how a molecular nanomotor works when repairing DNA or transporting material such as organelles in the cell?
Now, the researchers have discovered an alternative in a mouse model: in the case of breast tumours with a specific defect in DNA repair, the animals can be cured using already established, cheap chemotherapy drugs, if enough DNA damage can be inflicted on the resting tumour cells.
Mesenchymal glioma stem cells show significantly higher radiation resistance and high expression of DNA - repair genes;
Olaparib is good at killing cancer cells that have errors in genes that have a role in repairing damaged DNA such as BRCA1 or BRCA2.
In response, cells activate an enzyme called poly (ADP - ribose) polymerase (PARP) to repair DNA damage.
«If the main DNA repair pathway, BRCA - mediated homologous recombination, becomes defective, cancer cells adapt and still proliferate.»
Dawson reasoned that in trying to repair the cell's DNA, PARP might seriously deplete energy resources and perhaps even kill the cell.
But scientists at the Lewis Katz School of Medicine at Temple University (LKSOM) now think they can help overcome that problem, thanks to their discovery of a small molecule that selectively kills BRCA - deficient cancer cells by blocking the activity of an alternative DNA repair pathway.
«We now know why a crucial DNA - repair process shuts down just when the cell starts to divide into two daughter cells,» says Dr. Daniel Durocher, a Senior Investigator at the Lunenfeld - Tanenbaum Research Institute at Mount Sinai Hospital in Toronto, Canada.
Our DNA is constantly exposed to damage and to protect the genome, cells have evolved mechanisms that monitor and repair these damages.
Rad3 signalling ensures that cells do not divide before DNA damages are repaired and thus provides cancer cells with a mechanism to resist chemotherapy by repairing these DNA damages.
They found that cancer cells had acquired new genetic changes that cancelled out the original errors in DNA repair — particularly in the genes BRCA2 and PALB2 — that had made the cancer susceptible to olaparib in the first place.
It is known that the ATM protein is one of the main proteins involved in DNA repair in somatic cells (any of the cells forming part of our organism, except for germline cells).
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