Articles tagged with Cell Apoptosis
Researchers at the University of Kentucky discovered that tumor-suppressor protein Par-4 is secreted by most human and rodent cells and can target large numbers of cancer cells by binding to receptors on the cell surface.
A team of researchers has identified XIAP as the critical factor determining which cell death pathway is followed to culminate in a cell's death. This finding has implications for cancer patients with underlying liver conditions who are being treated with IAP inhibitors.
Scientists at Stanford University School of Medicine have created fluorescent probes that can noninvasively image apoptosis in living tumors, allowing for the gauge of treatment effectiveness. The probes bind exclusively to caspases, enzymes regulating cell death, and respond with light emission, highlighting dying cells.
Researchers at the Bioprocessing Technology Institute discovered a novel function of the FAIM gene, which protects immune and liver cells from apoptosis. They propose that manipulating this process could lead to new treatments for liver cirrhosis and neurodegenerative diseases like Alzheimer's and Parkinson's.
Research reveals Alisol B acetate inhibits proliferation of gastric cancer cells and induces apoptosis through mitochondrial and PI3K/Akt signaling pathways. This could lead to the development of a new anticancer agent for treating gastric cancer, one of the most common cancers worldwide.
Researchers have developed novel compounds that absorb by cancer cells and release nitric oxide upon specific light wavelengths, inducing apoptosis and killing tumor cells. The compounds, called dye-sensitized ruthenium nitrosyls, offer a localized delivery of high concentrations of nitric oxide without causing inflammation.
Death receptors, which eliminate unwanted cells, may also be used to strengthen cells against illnesses. Researchers can develop new therapeutics that target these receptors to treat various diseases.
Researchers discovered a novel compound, ADFMChR, with potent anti-tumor activity against human liver carcinoma cells. The compound induces apoptosis and modulates key proteins, providing new insights into its potential as a cancer-preventive agent.
A CSHL-led team has identified a critical role for the protein EYA in setting the machinery for DNA repair, allowing cells to either fix broken DNA or die. The discovery sheds light on how cells make decisions when faced with catastrophic DNA damage.
Research reveals cathepsin B's role in hepatocyte apoptosis and liver injury in fulminant hepatic failure. Inhibition of cathepsin B attenuates apoptosis and liver damage.
The study investigates the anti-apoptotic effects of Astragalus saponin extract on human peritoneal mesothelial cells during peritoneal gastric cancer metastasis. The results show that gastric cancer cell supernatant induces apoptosis in mesothelial cells, while Astragalus injection can partly suppress this effect and regulate the expr...
Scientists at A*STAR's IMCB have discovered a human protein called Bax-beta (Baxβ) that can induce cancer cell death. The protein is normally degraded by proteasomes in healthy cells, but its levels are elevated in cancer cells, leading to apoptosis.
Scientists at Albert Einstein College of Medicine identified a small intracellular protein, p115, that helps cells commit suicide and is required for the pro-apoptotic function of the Golgi protein. This discovery could lead to drugs for combating cancer and other diseases characterized by overproduction of cells.
Researchers discovered how defective DNA repair in ATLD and NBS causes distinct pathologies, including neurodegeneration and microcephaly. The study provides insights into the links between brain disease and cancer vulnerability in people carrying these diseases.
Researchers have shown that maslinic acid significantly inhibits cell proliferation and induces apoptosis in colon-cancer cells. The compound may provide a cheap and effective way to control colon cancer and is being investigated as a potential chemotherapeutic agent.
Research on Scutellaria barbata extract reveals growth inhibitory effects on human cancers, including lung, breast, and digestive system cancer. The extract induces apoptosis in hepatoma cells through the mitochondrial pathway, suggesting a potential therapeutic approach.
Researchers at Vanderbilt University Medical Center have identified prostaglandin-E2 receptors as crucial players in atherosclerosis development. Mice with impaired EP4 receptors showed reduced atherosclerosis and increased macrophage programmed cell death, highlighting the importance of these signaling pathways in disease progression.
Researchers found that cancer cells use apoptosis inhibitors to prevent programmed cell death while also controlling cell migration. This discovery challenges current treatment strategies and highlights the need for more targeted approaches.
HBV infection induces increased steady state of ATR protein and phosphorylation of downstream targets including Chk1, p53, and H2AX. The level of Mre11 and p21 were reduced after HBV-positive serum addition. This suggests that HBV escapes the consequences of activation of the DNA damage checkpoint by degradation of checkpoint proteins.
Researchers have identified a new combination therapy that targets tumors with B-RAF mutations by combining MEK inhibitors with BH3 mimetics, showing promise in treating melanomas and other solid tumors.
Researchers have identified genes that control cell death as contributing to age-related hearing loss. The study used mice to chart the activity of over 22,000 genes, finding eight genes involved in the apoptotic process whose activity differed between normal and hearing-loss mice.
A single dose of EPO immediately after a heart attack reduces apoptosis and limits damage to the heart. The study found a 2.7-fold reduction in tracer accumulation, indicating less damage to heart tissue.
Researchers at Burnham Institute have created a peptide that converts Bcl-2, a protein protecting cancer cells from programmed death, into a pro-apoptotic molecule. This breakthrough may lead to novel cancer therapies, as the peptide induces cell death in cancer cells.
Researchers developed a secretory Apoptin fusion protein that induces apoptosis in hepatocellular carcinoma HepG2 cells, offering new potential for cancer gene therapy. The study's findings suggest the therapeutic usage of Apoptin may be increased with its secretory characteristic.
The study found that Curcuma wenyujin essential oil exhibits antiproliferative effects in HepG2 cells by inducing apoptosis, associated with cell cycle arrest and mitochondrial membrane potential loss. The results suggest the potential value of developing ezhu as a chemotherapeutic agent for liver cancer treatment.
Research finds that anti-apoptotic Bcl-2 proteins, such as Bcl-xL and Mcl-1, contribute to apoptosis resistance in colorectal cancer cells. Knockdown of these proteins sensitizes CRC cells to chemotherapy and targeted therapies, suggesting a potential new approach to improving treatment outcomes.
Research found that apoptosis in liver cells leads to decreased total and free choline compound concentrations, but synthetical choline remains unchanged, providing insight into the puzzle of early-stage apoptosis changes.
Cells undergoing apoptosis exert substantial forces on surrounding cells, contributing to processes like wound formation and organ development. Apoptotic cells imploding and withdrawing create a force that aids in closing eye-shaped openings during embryonic development.
Researchers at Rockefeller University amplify cell death signals to induce self-destruction in precancerous cells. By inactivating a protein called IAP, they found that mice without the RING domain lived twice as long as those with it, highlighting a potential breakthrough in cancer therapy.
Researchers have discovered a mechanism to overcome the resistance of human glioblastoma multiforme cells to growth factor inhibitors by blocking inhibitor of apoptosis proteins. Combining drugs targeting IAPs with RTK inhibitors showed enhanced efficacy in inhibiting tumor growth. Additionally, targeting liver CB1 receptors may provid...
Researchers found that RTK inhibitors can be less effective in treating glioblastoma multiforme (GBM) due to cell death inhibition. Combining RTK and IAP inhibitors showed promise in inducing apoptosis in GBM cells, with enhanced efficacy in orthotopic mouse models.
Researchers have discovered that isoforms from Novel Structure Proteins (NSPs) could be involved in apoptosis, a process of programmed cell death. The NSPs were found to interact with the protein B23, and silencing their expression led to increased cell viability but reduced apoptosis.
A molecule called HMGB1 is released by dying cells, determining whether the immune system responds to cell death. Apoptotic cells produce free radicals that modify HMGB1, preventing it from stimulating an immune response. This finding may have implications for treating autoimmune diseases and cancer.
Researchers at German Cancer Research Center discovered that tumor cells degrade HIPK2 to prevent programmed cell death. Blocking this degradation may increase effectiveness of radiotherapy or chemotherapy. The study suggests a new approach to cancer treatment by targeting the Siah-1 enzyme.
A Phase 2 clinical trial of GCS-100, a polysaccharide targeting galectin-3, demonstrates apoptosis induction and reduced leukocyte counts in relapsed CLL patients. The treatment was generally well tolerated with mild-to-moderate adverse events.
Researchers at Baylor College of Medicine discovered that caspases, known as 'killer enzymes,' play a crucial role in cell differentiation. By manipulating programmed cell death pathways and caspase targets, scientists may be able to revert somatic cells into embryonic stem cell-like states.
Researchers found that HIV protease inhibitors can decrease photoreceptor apoptosis in mouse models of retinal detachment. The study suggests that these drugs may prevent vision loss after retinal detachment by inhibiting mitochondrial apoptosis.
At 15 mmHg CO2 insufflation pressure, gastric cancer cells' proliferation was inhibited and apoptosis improved. The extracellular pH changed significantly with CO2 versus helium exposure, affecting tumor-cell implantation during laparoscopic surgery.
Researchers found that thymoquinone blocked pancreatic cancer cell growth and killed cells by enhancing programmed cell death, with 80% of cancer cells killed. Thymoquinone also triggered epigenetic changes, including acetylation of histones, which could lead to new cancer treatments.
A study reveals that immune killer T cells induce cell death by disrupting mitochondria in two distinct ways, targeting enzymes and reactive oxygen production. This understanding provides a new insight into the major T cell defense pathway against viral infections and cancer.
Recent research suggests that gastrin inhibits cell apoptosis in colorectal cancer by up-regulating FasL expression, allowing cancer cells to evade immune surveillance. Somatostatin promotes cell apoptosis in large intestine cancer by increasing caspase-3 levels and activating death receptor signaling pathways.
Researchers at Melbourne's Walter and Eliza Hall Institute have discovered a key step in the 'puncture' mechanism of cell death, which drives apoptosis. The discovery has important implications for the development of drugs that can regulate cell death, with potential applications in cancer and degenerative disease treatments.
Researchers suggest adopting apoptosis to restructure businesses, eliminating malfunctioning processes. This approach can prevent commercial decay and protect organizations from demise.
IGF-I exerts mitochondrial protection in experimental cirrhosis, reducing caspase activation and increasing ATP production. IGF-I supplementation shows beneficial effects on liver function and fibrosis in animal models.
The Nix protein plays a crucial role in the maturation of red blood cells by facilitating autophagy, a process that removes damaged organelles like mitochondria. This regulation is essential for maintaining cellular quality and preventing anemia.
Research by Tufts University biologists reveals that early exposure to atrazine leads to deformed hearts, impaired kidneys, and digestive systems in tadpoles. The study found a significant increase in abnormalities in organs after 48 hours of exposure, with 57% of tadpoles having smaller-than-normal hearts.
The study reveals that three specific inhibitors of necroptosis, a form of necrotic death, target and inhibit RIP1 kinase, a protein that can direct cells into necrosis. This finding presents a novel avenue for drug development to prevent extensive tissue damage in diseases such as heart attacks and strokes.
Researchers have identified a key player in the killing of brain cells after a stroke or seizure - asparagine endopeptidase (AEP). AEP unleashes enzymes that break down brain cells' DNA, causing permanent damage.
Researchers identify KIFBbeta as a potential new neuronal tumor suppressor gene that mediates apoptosis in neural crest-derived tumors. The study suggests that KIFBbeta provides a protective effect against the development of these tumors.
Researchers found that CD95 on glioblastoma cells is activated by CD95L, leading to the production of MMP9, which cuts through tissue layers and allows cancer cells to invade healthy tissue. Blocking this activation may be a new approach to stopping glioblastoma's spread.
A study by the University of Washington researchers found that infections and toxins can activate caspase-1, an enzyme involved in both beneficial apoptosis and harmful pyroptosis. This activation leads to inflammation and can be detrimental to vital tissues, but also plays a role in resistance to infection.
Researchers have discovered how isotretinoin, the most potent acne treatment, works by triggering cell death in sebaceous glands. The study found that agents targeting Neutrophil gelatinase-associated lipocalin may provide a new approach to treating acne.
Researchers at St. Jude Children's Research Hospital discovered a crucial role of the Hax1 protein in protecting cells from apoptosis. The findings provide valuable insights into the biochemical interactions that control programmed cell death, which may lead to new treatments for diseases like Parkinson's.
Researchers discovered a new genetic link between the MEGF10 gene and schizophrenia, finding that a variant of the gene is associated with increased heritability risk. The study also found that the MEGF10 gene is expressed more extensively in post-mortem brain tissue from individuals with schizophrenia.
Researchers have identified a new compound that blocks an early step in programmed cell death, known as apoptosis. This process is triggered by mitochondrial division and can lead to cell death during heart attacks and strokes.
Researchers at Saint Louis University find that immune cells with pro-survival proteins accumulate in the bodies of patients with lupus, contributing to disease progression. The team aims to develop a therapy that blocks these proteins to restore balance in the immune system.
Epstein-Barr virus uses LMP1 to activate TRADD, a critical signaling molecule. Without TRADD, LMP1 loses its ability to induce apoptosis, allowing uncontrolled cell growth and cancer formation.
Researchers at UMass Medical School discovered a complex pathway that allows cells to survive and die through autophagy, a process previously misunderstood. The study sheds light on the relationship between autophagy and cell death, with potential implications for cancer, Alzheimer's, and Parkinson's treatments.
Researchers at Harvard Medical School have discovered a new type of programmed cell death called entosis, where cells bore into their neighbors and died. This process, known as entosis, was found to be more common in cancerous cells than previously thought, and its role in tumor progression is still unclear.
New compounds that target Inhibitor-of-Apoptosis (IAP) proteins have been shown to induce apoptosis in tumor cells. The IAP antagonists block the anti-death proteins and engage other players that lead to cell death, with little effect on healthy cells.