Articles tagged with Cell Cycle
Researchers observed the evolution of simple self-reproducing groups of cells from individual cells, revealing a reproductive division of labour. Cheats that initially exploited others' cooperation eventually became seeds for future generations, leading to the emergence of multicellular organisms with improved fitness.
Researchers at IRB Barcelona reveal a mechanism that allows differentiated cells to reactivate as stem cells again, a phenomenon seen in the liver's regenerative capacity. The key feature is the inhibition of endocycle entry, a modified cell cycle that prevents irreversible changes in gene expression.
Researchers identify two critical controls that tie DNA replication to cell division in bacteria, enabling them to enter a 'zombie-like' state when blocked. This discovery opens doors to developing new drugs that target the bacterial cell cycle to combat infections.
Cells with oncogenic H-RAS activate ROS, which inactivates PTP1B, leading to AGO2 phosphorylation and gene silencing. This results in the accumulation of p21 proteins and halting the cell cycle.
Researchers discovered that cell division in mammalian cells synchronises with the body's daily rhythm, known as the circadian clock. This synchronization can help explain why people with disrupted circadian rhythms are more susceptible to cancer and may also inform an optimal timing for administering chemotherapy.
New mutations in cohesin proteins are common in various cancers, including bladder cancer and melanoma. Cohesin regulates cell division and DNA repair, making it a potential driver or facilitator for tumours.
Researchers have discovered that cell division time is programmed by the 'parent' cell and varies between parent and offspring cells. The study's findings challenge a 40-year-old theory on cell division and provide a new model to predict how populations of cells divide.
A new UCSB study uncovers unique evolutionary adaptations in the primate brain, highlighting the crucial role of microRNAs in a portion of the brain called the outer subventricular zone (OSVZ). These findings suggest that microRNAs are responsible for controlling gene expression and regulating complex cellular processes.
Yale researchers discovered that accelerating cell cycle speed reduces barriers to changing a cell's fate, allowing for pluripotent cells to be created more efficiently. The study found that cells with faster cycles can become multiple cell types, whereas slower cycles remain in their original state.
Researchers found that silencing the gene encoding p57 Kip2 in adult human islets promotes beta cell replication. These new cells exhibit properties associated with normal beta cells, providing a potential explanation for excessive beta cell expansion in children with focal hyperinsulinism.
New research reveals that macrophage populations mediate tumor cell removal following monoclonal antibody treatment. Additionally, targeting the p57Kip2 pathway in adults with type 2 diabetes may improve β cell function and expand β cell mass.
Researchers at the University of Cincinnati identified serine/threonine protein kinase-29 (STK-29) as a key component linking circadian rhythms and cell division cycles. The study, led by Christian Hong, provided insights that could lead to improved disease treatments and drug delivery.
Researchers at IDIBELL describe the key role of separase protein in regulating mitosis and ensuring correct genetic inheritance. The study identifies two new substrates that contribute to the Hippo tumor suppressor pathway, advancing knowledge of this process.
Researchers at UCSF have discovered a new way to target cancer by controlling cell growth and boosting protein production during the S phase of the cell cycle. This study has implications for the development of new cancer therapies.
A recent study published in Neural Regeneration Research identified cell cycle-related genes as crucial factors in the development of neural tube defects. The research found that retinoic acid treatment differentially expressed three cell cycle-related genes: p57kip2, Cdk5, and Spin.
Researchers at Caltech have discovered a new mechanism for creating macrophages by increasing the accumulation of regulatory protein PU.1 through slowed cell division. The process involves an unexpected cycle where cell division slows, allowing higher PU.1 levels to accumulate and prompt macrophage generation.
Researchers have found that pancreatic β cells can be regenerated at least three times using a mechanism that involves the forced activation of the Pax 4 gene. This breakthrough suggests that the pancreas has a virtually inexhaustible source of cells capable of replacing lost β cells, offering new hope for treating Type 1 diabetes.
Researchers found that Wip1 mutations can lead to the shortening of this protein, allowing cancer cells to circumvent p53's protective mechanisms. These mutations were detected in colorectal and breast cancer patients, suggesting they may be a new target for cancer treatment.
Scientists at the University of Pittsburgh School of Medicine have discovered a novel mechanism that regulates the replication of insulin-producing beta cells in the pancreas. The findings, published in Diabetes, provide new insights into how to regenerate beta cells and potentially lead to new therapies for Type 1 and 2 diabetes.
Researchers discovered that Alzheimer's disease is caused by faulty cell cycle control in neurons, triggered by the combination of amyloid-beta and tau proteins. In normal cells, these proteins do not induce cell cycle re-entry, but in AD neurons, they do, leading to cell death.
Researchers clarify how cells line up at the right time to receive signals about the next phase of their life by visualizing single-cell activity in living zebrafish embryos. The findings increase understanding of cyclical behaviors in all types of cells and could lead to new ways to treat certain human conditions.
Researchers at MIT and HMS have precisely measured the growth rates of single cells, revealing that mammalian cells divide when their growth rate hits a specific threshold. This breakthrough offers a possible explanation for how cells determine when to start dividing.
Weill Cornell researchers devise innovative boxer-like strategy to deliver one-two punch to multiple myeloma by weakening defenses and then killing cancer cells. The approach, using two anti-cancer drugs, shows potential for treating other tumor types.
Researchers from IDIBELL have discovered a new mechanism in cell division regulation through protein Zds1. This finding has significant implications for developing targeted and direct therapies against cancer by understanding the molecular mechanisms of mitosis.
Researchers have developed a new imaging method, spatial light interference microscopy (SLIM), that can measure cell mass with high accuracy. SLIM offers insights into the debated problem of whether cells grow at a constant rate or exponentially.
Embryos avoid fatal chaos through a synchronized cell cycle mechanism triggered by the calcium wave, which sets cells to the same developmental timetable. The researchers' simulation shows that this rapid spread of oscillation is crucial for preventing disarray and ensuring the embryo's survival.
The study proposes a novel molecular mechanism for detecting chromosome alignment on the mitotic spindle, preventing errors in cell division. The checkpoint mechanism ensures irreversible progression through the cell cycle, blocking further progress until problems are corrected.
Researchers have identified a protein produced by HIV-1 that drives infected cells out of dormancy and into the cell cycle. This finding sheds light on how HIV reactivates after entering a dormant state and may lead to new treatments for people with HIV infection.
Researchers discovered that the OGF-OGFr axis controls entry from cytoplasm to nucleus, critical for cell proliferation. Nucleocytoplasmic transport involves karyopherin β and Ran, and is dependent on nuclear localization signals.
A recent study reveals that the JNK protein controls the cell cycle by regulating key drivers of cell growth. The findings suggest that hyperactive JNK activity may contribute to genomic instability and promote tumor growth.
The study found that histone H1 phosphorylation is associated with changes in gene activity, particularly in active genes during interphase. H1 phosphorylation also controls ribosomal RNA gene transcription in the nucleolus, a novel discovery that could lead to new treatments for diseases.
Researchers identified two distinct mechanisms for nuclear pore complex assembly during interphase and post-mitotic stages, shedding light on cell cycle-dependent differences in nuclear membrane topology. The findings have implications for conditions such as cancer, developmental defects, and sudden cardiac arrest.
Researchers at the University of Florida have discovered that a gene called Sonic hedgehog controls the speed of cell division, which may contribute to genital defects. The study found that slower cell division rates can lead to underdeveloped and malformed genitalia in mice.
A team of scientists led by Caltech biologists found that cell-cycle length and chromosome duplication without division play key roles in determining sepal cell sizes in Arabidopsis thaliana. This probabilistic development process results in unique patterns and proportions among sepals.
A new screening system for hepatitis C has been developed by Texas A&M University researchers, allowing for the study of all aspects of the virus's life cycle. The system enables the discovery of small, low-cost molecules that block the HCV life cycle, which could lead to more effective and affordable therapies.
Yang Cao will use the five-year grant to develop computational methods and mathematical theories to integrate various models of the cell cycle. The project aims to improve understanding of the complex process, which is linked to cancer and cardiovascular disease.
Research suggests UbcH10 overexpression promotes aneuploidy and chromosome missegregation in tumors. High levels of UbcH10 in mice resulted in tumor formation across multiple tissues.
Researchers from Caltech have developed a new method to view the process of adding ubiquitin chains to cell-cycle proteins, revealing that enzymes add ubiquitins one at a time. This discovery could lead to the development of targeted cancer therapies by understanding how ubiquitin ligases work.
Researchers have found that the protein ERK cycles between the nucleus and cell proper in breast tissue cells, affecting cell growth and response to growth factors. The oscillations were regular and robust, providing a new insight into the internal signals controlling cell behavior.
Researchers have devised a new method to fix a broken heart by coaxing adult heart muscle cells into reentering the cell cycle, allowing them to divide and regenerate healthy heart tissue. The key ingredient is neuregulin1, which may one day be used to treat failing human hearts.
Researchers have developed a novel drug discovery tool that uses baker's yeast to rapidly search for drugs to treat Parkinson's disease. The tool identifies cyclic peptides with protective effects on yeast cells and neurons in an animal model of the disease, offering new hope for treatment breakthroughs.
Researchers at the University of Pittsburgh School of Medicine have identified a key molecular pathway that regulates replication of pancreatic beta cells. Knocking out two cell cycle proteins leads to robust beta cell replication in mouse experiments.
The Opioid Growth Factor (OGF) and its receptor (OGFr) play a crucial role in regulating cell proliferation by modulating cyclin-dependent kinase inhibitors. The study found that transport of OGFr into the nucleus required two out of three nuclear localization signals, highlighting the importance of this pathway in cancer treatment.
Researchers at Rockefeller University Press have uncovered a mechanism that limits centriole duplication, allowing cells to fashion extra centrioles only once per cell cycle. This discovery could lead to the development of new cancer treatments by restricting tumor cells' ability to replicate centrioles.
JDRF-funded researchers at the University of Pittsburgh School of Medicine discovered a protein called cdk6 that regulates human beta cell replication. This finding provides proof-of-principle for stimulating human beta cell production and function.
Christine Jacobs-Wagner, a leading expert on bacteria, has been designated an HHMI investigator for her pioneering work on the internal mechanisms of bacteria. Her research has led to new insights into human illnesses and survival strategies of ancient organisms.
Researchers at Duke University have discovered a genetic 'tag team' that regulates the cell cycle, finding that nearly 70% of periodic genes continue to turn on and off without cyclins. The study suggests a new understanding of gene regulation in mammalian cells.
Researchers observed a group of six enzymes forming a cluster in living cells, which are essential for cell replication and DNA production. This discovery could lead to new cancer treatments by disrupting purine synthesis and halting cancer cell replication.
Scientists at UC San Diego discovered how cells of higher organisms change their movement speed, a discovery that may help prevent cancer cells from spreading. The study found that the frequency of the cell's motility cycle determines its crawling speed.
Two UI studies show that the NSAID celecoxib has potent anticancer activity, killing head and neck cancer cells in the S phase of the cell cycle. This finding suggests that combining celecoxib with chemotherapies may provide better tumor control than radiation alone.
Research by Nicholas Foulkes and colleagues found that peripheral clocks require cortisol to generate daily rhythms of cell proliferation. Constant levels of cortisol can restore normal cell-division rhythms in cortisol-deficient strains.
Researchers at Virginia Tech have developed models and algorithms that enable the simulation of cell division using the university's System X supercomputer. By characterizing protein interactions regulating the cell cycle, they aim to understand reproduction in human cells and combat cancer, tissue regeneration, and pathogens.
Researchers at UCSD find mechanical tension can switch on/off enzymes acting on DNA, revealing new mechanism for sensing and responding to cell stresses. The study demonstrates a tiny force of one pico-Newton can alter protein activity, sparking potential applications in biotechnology.
Researchers discovered that the cell cycle's temporal regulation evolves rapidly, with changes occurring every 100 million years. This fast evolution is unexpected for a fundamental process like cell division.
Researchers at the Ludwig Institute for Cancer Research discovered that SREBP1 regulates both lipid synthesis and cell cycle progression. Disrupting SREBP1 activity can prevent lipid production, which is essential for new cell wall construction.
DNA damage resets the cellular circadian clock, suggesting a link between circadian timing and cancer. The study implies that the biological clock has a protective dimension in addition to its pacemaker functions.
Scientists have made significant progress in understanding how to regenerate hair cells in the inner ear, a major breakthrough in the quest for new treatments for acquired hearing loss. The study found that blocking the Rb protein can promote hair cell regeneration, with specific areas of the inner ear exhibiting different responses.
Researchers have discovered that Alzheimer's disease is caused by abnormal cell division in neurons, which starts months before amyloid plaques form. The study suggests that another cellular problem triggers the disease process after abnormal cell cycling begins.
Researchers have identified a new protein, Ptprv, that plays a crucial role in preventing and counteracting cancer. The protein works with p53 to halt the cell cycle and block tumor formation, offering new perspectives for cancer treatment.
A new study reveals that the SAR11 microbe's streamlined genome is key to its dominance in oceans, recycling organic carbon and supporting 50% of global photosynthesis. With a compact genetic makeup, SAR11 can survive in low-nutrient environments and efficiently reproduce by consuming dissolved organic matter.