Articles tagged with Dna Damage Responses
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A team of researchers found that chromatin motion on damaged DNA sites moves faster than those away from damage, with the group moving as a unit over short distances. This coherent movement is crucial for effective DNA repair, preventing damaged DNA from harmful contact and improving accuracy.
Researchers discovered that combining a new target with an old chemotherapy drug can reduce resistance and potentially improve treatment outcomes for small cell lung cancer. The study used mouse models to show that inhibiting a protein called SMYD3, along with cyclophosphamide, stopped tumors in their tracks.
A Johns Hopkins Medicine study found that a protein called STING responds to clean-up signals in brain cells damaged by Parkinson’s disease by creating a cycle of inflammation that accelerates the disease’s progression. In mice with deactivated STING proteins, there was less microglial activity and brain cell death.
Researchers discovered hundreds of new gene functions in algae, which have counterparts in plants, enabling better understanding of photosynthesis, DNA repair, and stress responses. The findings can improve biofuel production and develop heat-tolerant crops.
Scientists at Van Andel Institute and Rockefeller University have revealed the structure of the 911 DNA checkpoint clamp, which loads onto DNA to repair damage. The novel finding shows that the 911 clamp is loaded onto DNA from the opposite end, a surprise in the field of DNA replication.
Researchers at the University of Copenhagen have discovered that the BRCA2 gene requires a specific enzyme, PP2A-B56, to repair DNA damage. This finding may pave the way for more targeted treatment of cancer patients with certain mutations.
A novel lncRNA, Caren, has been identified as a potential therapeutic target for heart failure. It enhances energy production in cardiomyocytes and inhibits the activation of the ATM protein, which accelerates heart failure severity. Increasing Caren expression may inhibit heart failure progression.
Researchers discovered that plants use combined control of cytokinin and auxin to organize DNA damage responses, allowing continuous root growth. The study reveals a sophisticated way for plants to retain stem cells while maintaining their genomes in damaged plants.
Researchers used molecular imaging to track DNA damage in neuroendocrine tumors treated with 177Lu-DOTATATE. The technique enabled visualization of γH2AX foci just days after treatment, providing insights into therapeutic outcomes and potential dose adjustments.
Researchers identify a hyperploid salvage survival pathway in high-grade serous carcinoma cell line models that bypasses apoptosis and emerges as viable large hyperploid cells. This pathway may contribute to acquired resistance and genomic diversity of recovering tumor cells.
Researchers discovered that Par3 regulates contractility of keratinocytes, essential for accurate cell division and preventing DNA damage. The findings suggest that Par3 plays a key role in maintaining skin self-renewal capacity, with dysfunction linked to premature aging and skin cancer.
Researchers have discovered that inhibiting two key proteins, ATM and ATR, can reduce BK polyomavirus levels in infected cells. This finding may provide an opportunity to use existing cancer drugs to combat the virus without reducing immunosuppressing drugs, which are needed to prevent transplant rejection.
The study reveals that gene transcription is equally important to DNA damage response, with activated transcription facilitating DNA repair and limiting abnormal transcripts. Cells become hypersensitive to DNA damage-inducing agents when the RBM7-P-TEFb axis is interfered with.
Scientists at the Salk Institute discovered a complex gene regulation network that helps plants cope with DNA damage. The research identified approximately 2,400 genes responding to DNA damage, with only 200 directly activated by SOG1, revealing its 'hands-off' overseer role.
Researchers from Mayo Clinic have made significant progress in understanding the DNA damage response proteins and their role in repairing double-strand breaks. The study reveals how these proteins work together to fix damaged DNA, potentially leading to new therapeutic strategies for cancer treatment.
Research reveals that stem cells from heavy smokers use error-prone DNA repair pathway, leading to accumulation of mutations and squamous cell carcinoma. The study suggests targeting DNA repair processes may be a promising approach to preventing and treating this form of lung cancer.
A new study by Lomonosov Moscow State University researchers clarifies the DNA alarm-system, which detects single-strand breaks and activates kinase ATM to signal repair. This system prevents cancer-causing mutations and cell death.
Researchers found similarities between field and laboratory studies on Gulf killifish responses to Deepwater Horizon oil spill. Changes in genome expression were detected, with high concentrations causing developmental defects and DNA damage.
Researchers discovered that DNA damage triggers dramatic reorganization of the Golgi, leading to its dispersal throughout the cell. This dispersal involves a novel signaling pathway directly linking DNA damage response to the Golgi, affecting cell survival and chemotherapy efficacy.
Researchers discovered SIRT4 plays a crucial role in preventing DNA damage-induced cancer by controlling glutamine metabolism and arresting cell cycle. In mice lacking SIRT4, lung cancer developed spontaneously, highlighting its potential as a therapeutic target.
Researchers have discovered that TRF2 suppresses DNA damage response by blocking signaling pathways, preventing chromosomes from sticking together. This finding has implications for understanding cancer and the aging process, as telomere shortening can lead to chromosomal instability.
Researchers at Stanford University School of Medicine have separated two distinct ways in which the p53 protein works, with implications for developing treatments that mitigate radiotherapy and chemotherapy side effects. The study reveals that disabling one part of the protein could allow healthy cells to survive DNA damage without pro...
Dr. Yosef Shiloh is recognized for his groundbreaking work on ataxia-telangiectasia (A-T), a rare disease caused by a defect in the cellular response to DNA damage. His identification of the ATM gene has revolutionized the field, leading to significant advances in our understanding of DNA damage response and repair.
Yosef Shiloh, a renowned expert in ataxia-telangiectasia (A-T) research, has been awarded the 51st Annual AACR G.H.A. Clowes Memorial Award for his groundbreaking work on cellular DNA damage response and A-T. His discoveries have significantly advanced our understanding of this rare genomic instability syndrome.
Researchers at Salk Institute identify viral protein ICP0 that shuts down host cell's DNA damage response, enabling HSV to infect cells. By removing specific ubiquitin marks, ICP0 allows the virus to take over and multiply.
Researchers have identified a crucial biochemical step involved in nerve cells' response to DNA damage. Cdk5 activation is necessary before ATM can function in neurons, suggesting it as a potential drug target for neurodegenerative diseases. This discovery sheds light on the underlying mechanisms of ataxia telangiectasia and other neur...
Researchers investigated DNA damage response pathway in HBV infection and replication, finding ATR-dependent activation triggered by HBV infection. The study suggests targeting specific cellular factors for inhibition or restoration of p21 expression as potential therapeutic strategies.
Scientists at the Salk Institute report that ATM protein activation depends on both damaged DNA and surrounding flanking regions. This discovery reveals a new mechanism for efficient DNA repair, highlighting the importance of intact chromatin in activating the cellular response.
Activation of DNA damage response in early stages of Kaposi's sarcoma development functions as an anti-cancer barrier also in virus-induced malignancies. The study found that viral oncogene-induced DNA damage response is activated in Kaposi's sarcoma tumorigenesis, leading to growth arrest or apoptosis.
Researchers discovered that herpes viruses trick mouse cells into activating the DNA damage response, allowing them to replicate more efficiently. Blocking this activation significantly reduces viral replication rates, providing a promising target for antiviral therapy.
A new database developed by researchers at the Howard Hughes Medical Institute provides a detailed portrait of the army of over 700 proteins that helps maintain DNA's integrity. The study reveals that two critical enzymes, ATM and ATR, act as sensors to detect trouble and initiate repair pathways.
Researchers have identified a minimal DNA structure that activates the ATR-mediated DNA damage checkpoint in a cell-free system. This discovery enables precise control and quantitative probing of checkpoint signaling responses.
Researchers at Cold Spring Harbor Laboratory discovered that DNA damage response pathways mediate oncogene-induced senescence. The study suggests that targeting these pathways could lead to novel approaches for preventing cancer formation.
A recent study published in Cell reveals that mice have two proteins working together to protect chromosome ends, suggesting rapid evolution. The findings identify the distinct functions of POT1a and POT1b proteins, which could impact human telomere biology.
Researchers identified a unique stretch of internal telomeric repeats that suppress the DNA damage checkpoint response. The arrest duration was significantly shorter than expected, indicating a potential mechanism for preventing normal telomeres from being recognized as damaged DNA.
Researchers have identified a common intermediate to activate ATR in response to various forms of genotoxic stress, including UV-induced cross-links and oxidative damage. This discovery highlights the importance of proper DNA detection and response to prevent genome instability and cancer.
Researchers have identified a crucial function for microcephalin, a protein involved in primary microcephaly, a rare neurological disorder. The discovery links microcephalin's function to DNA damage responses that prevent cancer development, suggesting potential therapeutic applications.
A new study reveals that ATR kinase plays a crucial role in maintaining genome integrity by regulating cell cycle checkpoints and preventing DNA damage. The study shows that ATR is essential for ensuring cells leave the cell cycle without DNA damage, which can lead to diseases such as cancer.
Scientists have discovered that the protein ATR is responsible for activating BRCA1 in response to UV light-induced DNA damage, increasing breast cancer susceptibility. This discovery provides new evidence for ATR as a breast cancer susceptibility gene.
A team of scientists has discovered a group of enzymes capable of duplicating damaged genetic material, allowing cells to 'compromise' and replicate with a certain 'sloppiness'. This mechanism increases genetic diversity and enables natural selection, driving the evolutionary process.
Researchers have identified a gene called Mre11 as a critical component of the regulatory network that cells activate in response to DNA damage. This discovery explains how mutations in Mre11 can cause ataxia-telangiectasia, a genetic disorder characterized by progressive nerve and muscle loss and increased susceptibility to cancer.
Researchers at UCSF have identified a transcription factor, human Cdc5 (hCdc5), that regulates the cell cycle and may help stimulate heart muscle cell repair after damage. The discovery could lead to new treatments for children with heart abnormalities and potentially benefit 900,000 American adults affected by heart attacks each year.
Researchers identified a mechanism by which cytosine substitution can occur in non-dividing cells, leading to the production of mutant proteins. This process has significant implications for understanding age-related cell death, neurodegenerative diseases, and malignant transformation.
Scientists have identified a specific gene, the AH receptor, as a vital link in the chemical cascade that causes cancer when exposed to cigarette smoke. The study found that mice without this receptor showed no damage from cigarette smoke, suggesting it plays a crucial role in controlling gene damage.