Apoptosis Regulatory Proteins
TOR Serine-Threonine Kinases
Class III Phosphatidylinositol 3-Kinases
Lysosomal-Associated Membrane Protein 2
Microscopy, Electron, Transmission
RNA, Small Interfering
Endoplasmic Reticulum Stress
Reactive Oxygen Species
Gene Knockdown Techniques
Adaptor Proteins, Signal Transducing
Proteasome Endopeptidase Complex
AMP-Activated Protein Kinases
Green Fluorescent Proteins
LB-AUT7, a novel symbiosis-regulated gene from an ectomycorrhizal fungus, Laccaria bicolor, is functionally related to vesicular transport and autophagocytosis. (1/5833)We have identified LB-AUT7, a gene differentially expressed 6 h after ectomycorrhizal interaction between Laccaria bicolor and Pinus resinosa. LB-Aut7p can functionally complement its Saccharomyces cerevisiae homolog, which is involved in the attachment of autophagosomes to microtubules. Our findings suggest the induction of an autophagocytosis-like vesicular transport process during ectomycorrhizal interaction. (+info)
Apg7p/Cvt2p is required for the cytoplasm-to-vacuole targeting, macroautophagy, and peroxisome degradation pathways. (2/5833)Proper functioning of organelles necessitates efficient protein targeting to the appropriate subcellular locations. For example, degradation in the fungal vacuole relies on an array of targeting mechanisms for both resident hydrolases and their substrates. The particular processes that are used vary depending on the available nutrients. Under starvation conditions, macroautophagy is the primary method by which bulk cytosol is sequestered into autophagic vesicles (autophagosomes) destined for this organelle. Molecular genetic, morphological, and biochemical evidence indicates that macroautophagy shares much of the same cellular machinery as a biosynthetic pathway for the delivery of the vacuolar hydrolase, aminopeptidase I, via the cytoplasm-to-vacuole targeting (Cvt) pathway. The machinery required in both pathways includes a novel protein modification system involving the conjugation of two autophagy proteins, Apg12p and Apg5p. The conjugation reaction was demonstrated to be dependent on Apg7p, which shares homology with the E1 family of ubiquitin-activating enzymes. In this study, we demonstrate that Apg7p functions at the sequestration step in the formation of Cvt vesicles and autophagosomes. The subcellular localization of Apg7p fused to green fluorescent protein (GFP) indicates that a subpopulation of Apg7pGFP becomes membrane associated in an Apg12p-dependent manner. Subcellular fractionation experiments also indicate that a portion of the Apg7p pool is pelletable under starvation conditions. Finally, we demonstrate that the Pichia pastoris homologue Gsa7p that is required for peroxisome degradation is functionally similar to Apg7p, indicating that this novel conjugation system may represent a general nonclassical targeting mechanism that is conserved across species. (+info)
Glucose-induced autophagy of peroxisomes in Pichia pastoris requires a unique E1-like protein. (3/5833)Cytosolic and peroxisomal enzymes necessary for methanol assimilation are synthesized when Pichia pastoris is grown in methanol. Upon adaptation from methanol to a glucose environment, these enzymes are rapidly and selectively sequestered and degraded within the yeast vacuole. Sequestration begins when the vacuole changes shape and surrounds the peroxisomes. The opposing membranes then fuse, engulfing the peroxisome. In this study, we have characterized a mutant cell line (glucose-induced selective autophagy), gsa7, which is defective in glucose-induced selective autophagy of peroxisomes, and have identified the GSA7 gene. Upon glucose adaptation, gsa7 cells were unable to degrade peroxisomal alcohol oxidase. We observed that the peroxisomes were surrounded by the vacuole, but complete uptake into the vacuole did not occur. Therefore, we propose that GSA7 is not required for initiation of autophagy but is required for bringing the opposing vacuolar membranes together for homotypic fusion, thereby completing peroxisome sequestration. By sequencing the genomic DNA fragment that complemented the gsa7 phenotype, we have found that GSA7 encodes a protein of 71 kDa (Gsa7p) with limited sequence homology to a family of ubiquitin-activating enzymes, E1. The knockout mutant gsa7Delta had an identical phenotype to gsa7, and both mutants were rescued by an epitope-tagged Gsa7p (Gsa7-hemagglutinin [HA]). In addition, a GSA7 homolog, APG7, a protein required for autophagy in Saccharomyces cerevisiae, was capable of rescuing gsa7. We have sequenced the human homolog of GSA7 and have shown many regions of identity between the yeast and human proteins. Two of these regions align to the putative ATP-binding domain and catalytic site of the family of ubiquitin activating enzymes, E1 (UBA1, UBA2, and UBA3). When either of these sites was mutated, the resulting mutants [Gsa7(DeltaATP)-HA and Gsa7(C518S)-HA] were unable to rescue gsa7 cells. We provide evidence to suggest that Gsa7-HA formed a thio-ester linkage with a 25-30 kDa protein. This conjugate was not observed in cells expressing Gsa7(DeltaATP)-HA or in cells expressing Gsa7(C518S)-HA. Our results suggest that this unique E1-like enzyme is required for homotypic membrane fusion, a late event in the sequestration of peroxisomes by the vacuole. (+info)
Apg7p/Cvt2p: A novel protein-activating enzyme essential for autophagy. (4/5833)In the yeast Saccharomyces cerevisiae, the Apg12p-Apg5p conjugating system is essential for autophagy. Apg7p is required for the conjugation reaction, because Apg12p is unable to form a conjugate with Apg5p in the apg7/cvt2 mutant. Apg7p shows a significant similarity to a ubiquitin-activating enzyme, Uba1p. In this article, we investigated the function of Apg7p as an Apg12p-activating enzyme. Hemagglutinin-tagged Apg12p was coimmunoprecipitated with c-myc-tagged Apg7p. A two-hybrid experiment confirmed the interaction. The coimmunoprecipitation was sensitive to a thiol-reducing reagent. Furthermore, a thioester conjugate of Apg7p was detected in a lysate of cells overexpressing both Apg7p and Apg12p. These results indicated that Apg12p interacts with Apg7p via a thioester bond. Mutational analyses of Apg7p suggested that Cys507 of Apg7p is an active site cysteine and that both the ATP-binding domain and the cysteine residue are essential for the conjugation of Apg7p with Apg12p to form the Apg12p-Apg5p conjugate. Cells expressing mutant Apg7ps, Apg7pG333A, or Apg7pC507A showed defects in autophagy and cytoplasm-to-vacuole targeting of aminopeptidase I. These results indicated that Apg7p functions as a novel protein-activating enzyme necessary for Apg12p-Apg5p conjugation. (+info)
A 60 kDa plasma membrane protein changes its localization to autophagosome and autolysosome membranes during induction of autophagy in rat hepatoma cell line, H-4-II-E cells. (5/5833)We previously reported the preparation and characterization of an antibody against membrane fraction of autolysosomes from rat liver (J. Histochem. Cytochem. 38, 1571-1581, 1990). Immunoblot analyses of total membrane fraction of a rat hepatoma cell line, H-4-II-E cells by this antibody suggested that H-4-II-E cells expressed several autolysosomal proteins, including a protein with apparent molecular weight of 60 kDa. It was suggested that this 60 kDa protein was a peripheral membrane protein, because it was eluted from the membrane by sodium carbonate treatment. We prepared an antibody against this 60 kDa protein by affinity purification method, and examined its behavior during induction of autophagy. Autophagy was induced by transferring the cells from Dulbecco's modified Eagle medium (DMEM) containing 12% fetal calf serum into Hanks' balance salt solution. In DMEM, the 60 kDa protein showed diffused immunofluorescence pattern, and immunoelectron microscopy suggested that this protein was located on the extracellular side of the plasma membrane. After inducing autophagy, the immunofluorescence configuration of the 60 kDa protein changed from the diffused pattern to a granulous one. Immunoelectron microscopy showed that the 60 kDa protein was localized on the luminal side of the limiting membrane of autolysosomes and endosomes. In the presence of bafilomycin A1 which prevents fusion between autophagosomes and lysosomes, the 60 kDa protein was localized on the limiting membrane of the autophagosomes and endosomes. These results suggest that the 60 kDa protein is transported from the plasma membrane to the autophagosome membrane through the endosomes. (+info)
A human intracellular apyrase-like protein, LALP70, localizes to lysosomal/autophagic vacuoles. (6/5833)Using antibodies against autophagic vacuole membrane proteins we identified a human cDNA with an open reading frame of 1848 bp, encoding a protein of 70 kDa, which we named lysosomal apyrase-like protein of 70 kDa (LALP70). Sequence analysis revealed that LALP70 belongs to the apyrase or GDA1/CD39 family and is almost identical to a human uridine diphosphatase, with the exception of nine extra amino acids in LALP70. Members of this family were originally described as ectoenzymes, with some intracellular exceptions. Transfected LALP70 fused to the green fluorescent protein localized in the cytoplasm with a punctate pattern in the perinuclear space. These structures colocalized with the autophagic marker monodansylcadaverine and the lysosomal protein lamp1. Hydrophobicity analysis of the encoded protein revealed a transmembrane region at the N and C termini. Most of the sequence is arranged between these transmembrane domains, and contains four apyrase conserved regions. In vitro transcription/translation in the presence of microsomes showed that no signal sequence is cleaved off and that the translation product is protected from trypsin treatment. Our data indicate that LALP70 is a type III lysosomal/autophagic vacuole membrane protein with the apyrase conserved regions facing the luminal space of the vacuoles. (+info)
Apg16p is required for the function of the Apg12p-Apg5p conjugate in the yeast autophagy pathway. (7/5833)Autophagy is an intracellular bulk degradation system that is ubiquitous for eukaryotic cells. In this process, cytoplasmic components are enclosed in autophagosomes and delivered to lysosomes/vacuoles. We recently found that a protein conjugation system, in which Apg12p is covalently attached to Apg5p, is indispensable for autophagy in yeast. Here, we describe a novel coiled-coil protein, Apg16p, essential for autophagy. Apg16p interacts with Apg12p-conjugated Apg5p and less preferentially with unconjugated Apg5p. Moreover, the coiled-coil domain of Apg16p mediates self-multimerization that leads to cross-linking of Apg5p molecules and formation of a stable protein complex. Apg16p is not essential for the Apg12p-Apg5p conjugation reaction. These results suggest that the Apg12p-Apg5p conjugate requires Apg16p to accomplish its role in the autophagy pathway, and Apg16p is a key molecule as a linker to form the Apg12p-Apg5p-Apg16p multimer. (+info)
Clathrin functions in the absence of heterotetrameric adaptors and AP180-related proteins in yeast. (8/5833)The major coat proteins of clathrin-coated vesicles are the clathrin triskelion and heterotetrameric associated protein (AP) complexes. The APs are thought to be involved in cargo capture and recruitment of clathrin to the membrane during endocytosis and sorting in the trans-Golgi network/endosomal system. AP180 is an abundant coat protein in brain clathrin-coated vesicles, and it has potent clathrin assembly activity. In Saccharomyces cerevisiae, there are 13 genes encoding homologs of heterotetrameric AP subunits and two genes encoding AP180-related proteins. To test the model that clathrin function is dependent on the heterotetrameric APs and/or AP180 homologs, yeast strains containing multiple disruptions in AP subunit genes, as well as in the two YAP180 genes, were constructed. Surprisingly, the AP deletion strains did not display the phenotypes associated with clathrin deficiency, including slowed growth and endocytosis, defective late Golgi protein retention and impaired cytosol to vacuole/autophagy function. Clathrin-coated vesicles isolated from multiple AP deletion mutants were morphologically indistinguishable from those from wild-type cells. These results indicate that clathrin function and recruitment onto membranes are not dependent upon heterotetrameric adaptors or AP180 homologs in yeast. Therefore, alternative mechanisms for clathrin assembly and coated vesicle formation, as well as the role of AP complexes and AP180-related proteins in these processes, must be considered. (+info)
Autophagy is a cellular process in which cells break down and recycle their own damaged or unnecessary components. This process is essential for maintaining cellular health and function, as it helps to eliminate damaged organelles, misfolded proteins, and other cellular debris that can accumulate over time. Autophagy involves the formation of double-membrane vesicles called autophagosomes, which engulf and sequester the targeted cellular components. These autophagosomes then fuse with lysosomes, which contain enzymes that break down the contents of the autophagosome into smaller molecules that can be recycled by the cell. Autophagy plays a critical role in a variety of physiological processes, including cell growth, differentiation, and survival. It is also involved in the immune response, as it helps to eliminate intracellular pathogens and damaged cells. Dysregulation of autophagy has been implicated in a number of diseases, including neurodegenerative disorders, cancer, and infectious diseases.
Microtubule-associated proteins (MAPs) are a group of proteins that bind to microtubules, which are important components of the cytoskeleton in cells. These proteins play a crucial role in regulating the dynamics of microtubules, including their assembly, disassembly, and stability. MAPs are involved in a wide range of cellular processes, including cell division, intracellular transport, and the maintenance of cell shape. They can also play a role in the development of diseases such as cancer, where the abnormal regulation of microtubules and MAPs can contribute to the growth and spread of tumors. There are many different types of MAPs, each with its own specific functions and mechanisms of action. Some MAPs are involved in regulating the dynamics of microtubules, while others are involved in the transport of molecules along microtubules. Some MAPs are also involved in the organization and function of the mitotic spindle, which is essential for the proper segregation of chromosomes during cell division. Overall, MAPs are important regulators of microtubule dynamics and play a crucial role in many cellular processes. Understanding the function of these proteins is important for developing new treatments for diseases that are associated with abnormal microtubule regulation.
Apoptosis Regulatory Proteins are a group of proteins that play a crucial role in regulating programmed cell death, also known as apoptosis. These proteins are involved in the initiation, execution, and termination of apoptosis, which is a natural process that occurs in the body to eliminate damaged or unnecessary cells. There are several types of apoptosis regulatory proteins, including caspases, Bcl-2 family proteins, and inhibitors of apoptosis proteins (IAPs). Caspases are proteases that cleave specific proteins during apoptosis, leading to the characteristic changes in cell structure and function. Bcl-2 family proteins regulate the permeability of the mitochondrial outer membrane, which is a key step in the execution of apoptosis. IAPs, on the other hand, inhibit the activity of caspases and prevent apoptosis from occurring. Apoptosis regulatory proteins are important in many areas of medicine, including cancer research, neurology, and immunology. Dysregulation of these proteins can lead to a variety of diseases, including cancer, autoimmune disorders, and neurodegenerative diseases. Therefore, understanding the function and regulation of apoptosis regulatory proteins is crucial for developing new treatments for these diseases.
Ubiquitin-activating enzymes (E1 enzymes) are a class of enzymes that play a central role in the ubiquitin-proteasome system (UPS), a major pathway for protein degradation in cells. The UPS is responsible for the degradation of a wide range of cellular proteins, including misfolded or damaged proteins, as well as proteins that are no longer needed or are involved in signaling pathways. E1 enzymes are responsible for the activation of ubiquitin, a small protein that is covalently attached to target proteins by a series of enzymatic reactions. The E1 enzyme binds to ubiquitin and transfers it to a ubiquitin-conjugating enzyme (E2 enzyme), which then transfers the ubiquitin to a ubiquitin ligase (E3 enzyme). The E3 enzyme is responsible for recognizing specific target proteins and facilitating the transfer of ubiquitin to those proteins. The addition of ubiquitin to a protein serves as a signal for the protein to be degraded by the proteasome, a large protein complex that breaks down proteins into smaller peptides. The UPS plays a critical role in regulating a wide range of cellular processes, including cell cycle progression, signal transduction, and protein homeostasis. Disruptions in the UPS can lead to a variety of diseases, including cancer, neurodegenerative disorders, and autoimmune diseases. Therefore, understanding the function and regulation of E1 enzymes and the UPS is important for developing new therapeutic strategies for these diseases.
TOR (Target of Rapamycin) Serine-Threonine Kinases are a family of protein kinases that play a central role in regulating cell growth, proliferation, and metabolism in response to nutrient availability and other environmental cues. The TOR kinase complex is a key regulator of the cell's response to nutrient availability and growth signals, and is involved in a variety of cellular processes, including protein synthesis, ribosome biogenesis, and autophagy. Dysregulation of TOR signaling has been implicated in a number of diseases, including cancer, diabetes, and neurodegenerative disorders. Inhibitors of TOR have been developed as potential therapeutic agents for the treatment of these diseases.
Class III phosphatidylinositol 3-kinases (PI3Ks) are a family of enzymes that play a crucial role in various cellular processes, including cell growth, survival, and metabolism. They are involved in the regulation of the phosphatidylinositol signaling pathway, which is a key signaling pathway in cells. Class III PI3Ks are unique among the other classes of PI3Ks because they do not contain a catalytic domain. Instead, they consist of a regulatory domain and a lipid-binding domain. They function by recruiting other proteins to the plasma membrane, where they can activate downstream signaling pathways. In the medical field, Class III PI3Ks have been implicated in various diseases, including cancer, diabetes, and neurodegenerative disorders. In particular, mutations in genes encoding Class III PI3Ks have been identified in some types of cancer, such as acute myeloid leukemia and breast cancer. Targeting Class III PI3Ks has therefore become an area of active research in the development of new cancer therapies.
Adenine is a nitrogenous base that is found in DNA and RNA. It is one of the four nitrogenous bases that make up the genetic code, along with guanine, cytosine, and thymine (in DNA) or uracil (in RNA). Adenine is a purine base, which means it has a double ring structure with a six-membered ring fused to a five-membered ring. It is one of the two purine bases found in DNA and RNA, the other being guanine. Adenine is important in the function of DNA and RNA because it forms hydrogen bonds with thymine (in DNA) or uracil (in RNA) to form the base pairs that make up the genetic code.
Apoptosis is a programmed cell death process that occurs naturally in the body. It is a vital mechanism for maintaining tissue homeostasis and eliminating damaged or unwanted cells. During apoptosis, cells undergo a series of changes that ultimately lead to their death and removal from the body. These changes include chromatin condensation, DNA fragmentation, and the formation of apoptotic bodies, which are engulfed by neighboring cells or removed by immune cells. Apoptosis plays a critical role in many physiological processes, including embryonic development, tissue repair, and immune function. However, when apoptosis is disrupted or dysregulated, it can contribute to the development of various diseases, including cancer, autoimmune disorders, and neurodegenerative diseases.
Lysosomal-Associated Membrane Protein 2 (LAMP2) is a type of protein that is found on the surface of lysosomes, which are organelles within cells that are responsible for breaking down and recycling cellular waste. LAMP2 plays a role in regulating the flow of materials in and out of the lysosome, and it is also involved in the process of autophagy, which is the degradation of cellular components. In the medical field, LAMP2 is sometimes studied in the context of various diseases, including lysosomal storage disorders, which are a group of rare genetic disorders that affect the function of lysosomes.
A cell line, tumor is a type of cell culture that is derived from a cancerous tumor. These cell lines are grown in a laboratory setting and are used for research purposes, such as studying the biology of cancer and testing potential new treatments. They are typically immortalized, meaning that they can continue to divide and grow indefinitely, and they often exhibit the characteristics of the original tumor from which they were derived, such as specific genetic mutations or protein expression patterns. Cell lines, tumor are an important tool in cancer research and have been used to develop many of the treatments that are currently available for cancer patients.
Sirolimus is a medication that belongs to a class of drugs called immunosuppressants. It is primarily used to prevent organ rejection in people who have received a kidney, liver, or heart transplant. Sirolimus works by inhibiting the growth of T-cells, which are a type of white blood cell that plays a key role in the immune response. By suppressing the immune system, sirolimus helps to prevent the body from attacking the transplanted organ as a foreign object. It is also used to treat certain types of cancer, such as lymphoma and renal cell carcinoma.
Membrane proteins are proteins that are embedded within the lipid bilayer of a cell membrane. They play a crucial role in regulating the movement of substances across the membrane, as well as in cell signaling and communication. There are several types of membrane proteins, including integral membrane proteins, which span the entire membrane, and peripheral membrane proteins, which are only in contact with one or both sides of the membrane. Membrane proteins can be classified based on their function, such as transporters, receptors, channels, and enzymes. They are important for many physiological processes, including nutrient uptake, waste elimination, and cell growth and division.
In the medical field, "cell survival" refers to the ability of cells to survive and continue to function despite exposure to harmful stimuli or conditions. This can include exposure to toxins, radiation, or other forms of stress that can damage or kill cells. Cell survival is an important concept in many areas of medicine, including cancer research, where understanding how cells survive and resist treatment is crucial for developing effective therapies. In addition, understanding the mechanisms that regulate cell survival can also have implications for other areas of medicine, such as tissue repair and regeneration.
Chloroquine is an antimalarial drug that was first discovered in the 1930s. It is a synthetic derivative of quinine, a natural alkaloid found in the bark of the cinchona tree. Chloroquine is used to treat and prevent malaria caused by Plasmodium falciparum, Plasmodium vivax, and other species of Plasmodium. Chloroquine works by inhibiting the growth and reproduction of the Plasmodium parasite within red blood cells. It does this by interfering with the parasite's ability to synthesize heme, a vital component of hemoglobin, which is necessary for the survival of the parasite. Chloroquine is also used to treat autoimmune diseases such as rheumatoid arthritis and lupus. It works by suppressing the immune system's response to foreign substances, reducing inflammation and pain. Chloroquine is available in tablet form and is usually taken orally. It can cause side effects such as nausea, vomiting, headache, and dizziness. Long-term use of chloroquine can also cause retinopathy, a condition that affects the eyes and can lead to vision loss.
In the medical field, cell death refers to the process by which a cell ceases to function and eventually disintegrates. There are two main types of cell death: apoptosis and necrosis. Apoptosis is a programmed form of cell death that occurs naturally in the body as a way to eliminate damaged or unnecessary cells. It is a highly regulated process that involves the activation of specific genes and proteins within the cell. Apoptosis is often triggered by signals from the surrounding environment or by internal cellular stress. Necrosis, on the other hand, is an uncontrolled form of cell death that occurs when cells are damaged or stressed beyond repair. Unlike apoptosis, necrosis is not a programmed process and can be caused by a variety of factors, including infection, toxins, and physical trauma. Both apoptosis and necrosis can have important implications for health and disease. For example, the loss of cells through apoptosis is a normal part of tissue turnover and development, while the uncontrolled death of cells through necrosis can contribute to tissue damage and inflammation in conditions such as infection, trauma, and cancer.
RNA, Small Interfering (siRNA) is a type of non-coding RNA molecule that plays a role in gene regulation. siRNA is approximately 21-25 nucleotides in length and is derived from double-stranded RNA (dsRNA) molecules. In the medical field, siRNA is used as a tool for gene silencing, which involves inhibiting the expression of specific genes. This is achieved by introducing siRNA molecules that are complementary to the target mRNA sequence, leading to the degradation of the mRNA and subsequent inhibition of protein synthesis. siRNA has potential applications in the treatment of various diseases, including cancer, viral infections, and genetic disorders. It is also used in research to study gene function and regulation. However, the use of siRNA in medicine is still in its early stages, and there are several challenges that need to be addressed before it can be widely used in clinical practice.
Reactive Oxygen Species (ROS) are highly reactive molecules that are produced as a byproduct of normal cellular metabolism. They include oxygen radicals such as superoxide, hydrogen peroxide, and hydroxyl radicals, as well as non-radical species such as singlet oxygen and peroxynitrite. In small amounts, ROS play important roles in various physiological processes, such as immune responses, cell signaling, and the regulation of gene expression. However, when produced in excess, ROS can cause oxidative stress, which can damage cellular components such as lipids, proteins, and DNA. This damage can lead to various diseases, including cancer, cardiovascular disease, and neurodegenerative disorders. Therefore, ROS are often studied in the medical field as potential therapeutic targets for the prevention and treatment of diseases associated with oxidative stress.
Multiprotein complexes are groups of two or more proteins that interact with each other to form a functional unit in the cell. These complexes can be involved in a wide range of cellular processes, including signal transduction, gene expression, metabolism, and protein synthesis. Multiprotein complexes can be transient, meaning they assemble and disassemble rapidly in response to changes in the cellular environment, or they can be stable and persist for longer periods of time. Some examples of well-known multiprotein complexes include the proteasome, the ribosome, and the spliceosome. In the medical field, understanding the structure and function of multiprotein complexes is important for understanding how cells work and how diseases can arise. For example, mutations in genes encoding proteins that make up multiprotein complexes can lead to the formation of dysfunctional complexes that contribute to the development of diseases such as cancer, neurodegenerative disorders, and metabolic disorders. Additionally, drugs that target specific components of multiprotein complexes are being developed as potential treatments for these diseases.
Cytoprotection is a term used in the medical field to describe the process of protecting cells from damage or injury. This can be achieved through various mechanisms, such as the production of antioxidants, the activation of cellular repair pathways, or the inhibition of cell death pathways. In the context of medicine, cytoprotection is often used to describe the use of drugs or other interventions to protect cells from damage caused by various factors, such as toxins, infections, or radiation. For example, some drugs used in chemotherapy are cytoprotective, as they help to protect healthy cells from the toxic effects of the chemotherapy drugs. Cytoprotection is also an important concept in the field of neurology, where it is used to describe the use of drugs or other interventions to protect neurons from damage caused by conditions such as stroke, traumatic brain injury, or neurodegenerative diseases like Alzheimer's and Parkinson's. Overall, cytoprotection is a critical process for maintaining the health and function of cells, and understanding the mechanisms of cytoprotection is an important area of research in medicine and biology.
In the medical field, starvation refers to a severe lack of nutrition and energy due to a prolonged period of not eating enough food. Starvation can occur as a result of various factors, including malnutrition, illness, and intentional fasting. The body requires a certain amount of nutrients, including carbohydrates, proteins, fats, vitamins, and minerals, to function properly. When a person does not consume enough of these nutrients, the body begins to break down its own tissues, including muscle and fat, to provide energy. This can lead to a range of symptoms, including weakness, fatigue, dizziness, and weight loss. In severe cases of starvation, the body may also experience more serious complications, such as organ failure, electrolyte imbalances, and even death. Treatment for starvation typically involves providing adequate nutrition and hydration, as well as addressing any underlying medical conditions that may have contributed to the starvation.
Neurodegenerative diseases are a group of disorders characterized by the progressive loss of structure and function of neurons, the nerve cells that make up the brain and spinal cord. These diseases are typically associated with aging, although some can occur at a younger age. Neurodegenerative diseases can affect different parts of the brain and spinal cord, leading to a wide range of symptoms and complications. Some of the most common neurodegenerative diseases include Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS). The exact causes of neurodegenerative diseases are not fully understood, but they are believed to involve a combination of genetic and environmental factors. Some neurodegenerative diseases are caused by mutations in specific genes, while others may be triggered by exposure to toxins, infections, or other environmental factors. Treatment for neurodegenerative diseases is often focused on managing symptoms and slowing the progression of the disease. This may involve medications, physical therapy, speech therapy, and other forms of supportive care. While there is currently no cure for most neurodegenerative diseases, ongoing research is aimed at developing new treatments and improving the quality of life for people living with these conditions.
In the medical field, a cell line refers to a group of cells that have been derived from a single parent cell and have the ability to divide and grow indefinitely in culture. These cells are typically grown in a laboratory setting and are used for research purposes, such as studying the effects of drugs or investigating the underlying mechanisms of diseases. Cell lines are often derived from cancerous cells, as these cells tend to divide and grow more rapidly than normal cells. However, they can also be derived from normal cells, such as fibroblasts or epithelial cells. Cell lines are characterized by their unique genetic makeup, which can be used to identify them and compare them to other cell lines. Because cell lines can be grown in large quantities and are relatively easy to maintain, they are a valuable tool in medical research. They allow researchers to study the effects of drugs and other treatments on specific cell types, and to investigate the underlying mechanisms of diseases at the cellular level.
Ubiquitin is a small, highly conserved protein that is found in all eukaryotic cells. It plays a crucial role in the regulation of various cellular processes, including protein degradation, cell cycle progression, and signal transduction. In the medical field, ubiquitin is often studied in the context of various diseases, including cancer, neurodegenerative disorders, and autoimmune diseases. For example, mutations in genes encoding ubiquitin or its regulatory enzymes have been linked to several forms of cancer, including breast, ovarian, and prostate cancer. Additionally, the accumulation of ubiquitinated proteins has been observed in several neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease. Overall, understanding the role of ubiquitin in cellular processes and its involvement in various diseases is an active area of research in the medical field.
Adaptor proteins, signal transducing are a class of proteins that play a crucial role in transmitting signals from the cell surface to the interior of the cell. These proteins are involved in various cellular processes such as cell growth, differentiation, and apoptosis. Adaptor proteins function as molecular bridges that connect signaling receptors on the cell surface to downstream signaling molecules inside the cell. They are characterized by their ability to bind to both the receptor and the signaling molecule, allowing them to transmit the signal from the receptor to the signaling molecule. There are several types of adaptor proteins, including SH2 domain-containing adaptor proteins, phosphotyrosine-binding (PTB) domain-containing adaptor proteins, and WW domain-containing adaptor proteins. These proteins are involved in a wide range of signaling pathways, including the insulin, growth factor, and cytokine signaling pathways. Disruptions in the function of adaptor proteins can lead to various diseases, including cancer, diabetes, and immune disorders. Therefore, understanding the role of adaptor proteins in signal transduction is important for the development of new therapeutic strategies for these diseases.
The proteasome endopeptidase complex is a large protein complex found in the cells of all eukaryotic organisms. It is responsible for breaking down and recycling damaged or unnecessary proteins within the cell. The proteasome is composed of two main subunits: the 20S core particle, which contains the proteolytic active sites, and the 19S regulatory particle, which recognizes and unfolds target proteins for degradation. The proteasome plays a critical role in maintaining cellular homeostasis and is involved in a wide range of cellular processes, including cell cycle regulation, immune response, and protein quality control. Dysregulation of the proteasome has been implicated in a number of diseases, including cancer, neurodegenerative disorders, and autoimmune diseases.
AMP-Activated Protein Kinases (AMPK) are a family of enzymes that play a critical role in regulating cellular energy metabolism and maintaining cellular homeostasis. They are activated in response to a decrease in the ratio of ATP to AMP, which occurs under conditions of energy stress, such as during exercise or fasting. AMPK acts as a cellular energy sensor, and its activation leads to a variety of metabolic changes that help to restore energy balance. These changes include increasing glucose uptake and metabolism, inhibiting fatty acid synthesis, and stimulating fatty acid oxidation. AMPK also plays a role in regulating cell growth and survival, and has been implicated in the development of a number of diseases, including diabetes, obesity, and cancer. In the medical field, AMPK is a target for the development of new drugs for the treatment of metabolic disorders and other diseases. Activation of AMPK has been shown to improve insulin sensitivity, reduce body weight, and lower blood pressure, making it a promising therapeutic target for the treatment of type 2 diabetes, obesity, and cardiovascular disease.
Green Fluorescent Proteins (GFPs) are a class of proteins that emit green light when excited by blue or ultraviolet light. They were first discovered in the jellyfish Aequorea victoria and have since been widely used as a tool in the field of molecular biology and bioimaging. In the medical field, GFPs are often used as a marker to track the movement and behavior of cells and proteins within living organisms. For example, scientists can insert a gene for GFP into a cell or organism, allowing them to visualize the cell or protein in real-time using a fluorescent microscope. This can be particularly useful in studying the development and function of cells, as well as in the diagnosis and treatment of diseases. GFPs have also been used to develop biosensors, which can detect the presence of specific molecules or changes in cellular environment. For example, researchers have developed GFP-based sensors that can detect the presence of certain drugs or toxins, or changes in pH or calcium levels within cells. Overall, GFPs have become a valuable tool in the medical field, allowing researchers to study cellular processes and diseases in new and innovative ways.
Autophagy-related protein 13
Autophagy-related protein 101
Chaperone-assisted selective autophagy
Myopathy, X-linked, with excessive autophagy
Daniel J. Klionsky
Carbonyl cyanide m-chlorophenyl hydrazone
Gram domain containing 1a
Apoptosis regulator BAX
Goldilocks and the Three Bears
Steven J. Fliesler
Chloroquine autophagy inhibitor
Detection of autophagy using automated imaging
SESAME-catalyzed H3T11 phosphorylation inhibits Dot1-catalyzed H3K79me3 to regulate autophagy and telomere silencing
Autophagy Inhibitors | Autophagy | Tocris Bioscience
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AKC Canine Health Foundation | Enhancing Autophagy to Control Canine Myxomatous Mitral Valve Disease
A microfluidic chip for screening individual cancer cells via eavesdropping on autophagy-inducing crosstalk in the stroma niche...
Apolipoprotein E4 inhibits autophagy gene products through direct, specific binding to CLEAR motifs. | ALZFORUM
Autophagy is Protective Against Hematopoietic Stem Cell Aging - Fight Aging!
The Role of Calcium Signalling in Autophagy - Open Research Online
Frontiers | Human Antimicrobial RNases Inhibit Intracellular Bacterial Growth and Induce Autophagy in Mycobacteria-Infected...
Can the science of autophagy boost your health?
X-linked myopathy with excessive autophagy (XMEA) - ENMC
Did you know your body eats itself daily? Learn about autophagy (self-eating) fasting and exercises for numerous health...
Fairlie - Apoptosis, autophagy, cancer, drug development and peptides
Autophagy restricts fungal accommodation in the roots of Arabidopsis thaliana | bioRxiv
Autophagy-related protein 2 (Neurospora crassa OR74A) | Protein Target - PubChem
Autophagy: 2 Books in 1 - Discover Why Keto and Fasting Works, Ultimate Guide to Fat Loss and Anti-Aging (Paperback) |...
Fluoride Action Network | [In vivo and in vitro experimental study on the effect of fluoride-induced autophagy in rat HAT-7...
Expression of Concern: Alamandine attenuates hepatic fibrosis by regulating autophagy induced by NOX4-dependent ROS | Clinical...
Homocysteine accelerates hepatocyte autophagy by upregulating TFEB via DNMT3b-mediated DNA hypomethylation | Lund University...
Hif-2α promotes degradation of Mammalian peroxisomes by selective autophagy - Zurich Open Repository and Archive
Autophagy attenuates the catabolic effect during inflammatory conditions in nucleus pulposus cells, as sustained by NF-κB and...
Glucose-starved cells do not engage in prosurvival autophagy - Enlighten Publications
Cannabinoid-induced autophagy regulates suppressor of cytokine signaling (SOCS)-3 in intestinal epithelium - Lancaster EPrints
Overexpression of the clock gene Per2 suppresses oral squamous cell carcinoma progression by activating autophagy via the PI3K...
Autophagy may be the key to finding treatments for early Huntington's disease
Systematic review of the statistical scope used in studies based on skeletal muscle autophagy and exercise [PeerJ Preprints]
Valosin containing protein associated inclusion body myopathy: abnormal vacuolization, autophagy and cell fusion in myoblasts
- Online Apotheke Viagra Ohne Rezept chloroquine autophagy inhibitor . (apsia.org)
- Se trata de una formación avanzada de carácter profesionalizante y chloroquine autophagy inhibitor . (apsia.org)
- Manufactured and distributed by Cipla, chloroquine autophagy inhibitor . (apsia.org)
- Pharmacie online chloroquine autophagy inhibitor . (apsia.org)
- Puede encontrar en nuestra seccion 'Green' de la pagina, toda la linea de productos chloroquine autophagy inhibitor . (apsia.org)
- Somos Farmacia Familiar, un negocio de salud orientado a mejorar la calidad de vida de sus clientes a través de la provisión de productos y servicios, siempre chloroquine autophagy inhibitor . (apsia.org)
- Furthermore, cotreatment with PCA and autophagy inhibitor attenuated the cytotoxicity induced by PCA in OVCAR-3 cells. (nih.gov)
- In the present study, autophagy activator and inhibitor were used to demonstrate the impact of autophagy on the catabolic effect induced by TNF‑α. (spandidos-publications.com)
- In addition, nuclear factor κB (NF‑κB), c‑Jun N‑terminal kinase (JNK), extracellular signal‑regulated kinases and p38 mitogen‑activated protein kinase inhibitors and TNF‑α were used to determine the molecular mechanism of autophagy during the inflammatory conditions, and only the NF‑κB and JNK inhibitor were found to enhance the autophagy of rat NP cells. (spandidos-publications.com)
- In contrast, the glycolytic inhibitor 2-deoxyglucose induced prosurvival autophagy. (gla.ac.uk)
- In summary, TSN reduces podocyte damage induced by high glucose via inhibiting mTORC1 pathway and downstream targets and restoring podocyte autophagy. (hindawi.com)
- This study aims to clarify the contribution of the autophagy pathway to development of MMVD and contribute data to inform potential future clinical trials or development of future treatments, that may even be in the form of dietary supplements. (akcchf.org)
- Additional studies used a well-characterised Ca 2+ transport pathway to generate cellular Ca 2+ signals, and examined their ability to trigger autophagy. (open.ac.uk)
- Communication between the cell survival pathway of autophagy and the cell death pathway of apoptosis is crucial for determining the best outcome for the cell, and ultimately its fate. (edu.au)
- The second approach is to use either the new gene editing CRISPR/Cas9 technology or mass spectrometric/proteomics approaches (or both) to undertake screens to identify factors that can inhibit the cell death that occurs as a consequence of disarming the autophagy pathway through deletion of Beclin. (edu.au)
- Here we show that autophagy, a major degradation pathway plays a key role in the beneficial interaction between S. indica and Arabidopsis. (biorxiv.org)
- Macroautophagy (hereafter referred to as autophagy) is a vacuolar lysosomal degradation pathway for organelles and cytoplasmic macromolecules ( 9 ). (spandidos-publications.com)
- Autophagy is a catabolic process involved in homeostatic and regulated cellular protein recycling and degradation via the lysosomal degradation pathway. (lancs.ac.uk)
- In contrast, CBD was able to bypass both the CB1 receptor and the canonical pathway to induce autophagy, albeit to a lesser extent. (lancs.ac.uk)
- In conclusion, our research results demonstrate that Per2 suppresses OSCC progression by motivating autophagy, as well as inhibiting cell proliferation and promoting apoptosis, which were mediated by autophagy, in a PI3K/AKT/mTOR pathway-dependent manner. (jcancer.org)
- Our data revealed that PCA could modulate apoptosis and autophagy, suggesting the potential of PCA for chemoprevention and chemotherapy of ovarian cancer. (nih.gov)
- Complementary projects in the lab focus on autophagy, a cell survival process that has significant cross-talk with apoptosis. (edu.au)
- The first is to use an in vivo approach to analyse transgenic mice in which the autophagy regulator known as Beclin has been engineered to either disrupt or enhance its regulation by key components (i.e. proteins) of the apoptosis pathways. (edu.au)
- Inhibition of autophagy by chemical or genetic means by using 3-methyladenine, chloroquine, a dominant negative form of ATG4B or silencing Beclin-1, Atg7, or p62 indicated that macroautophagy does not protect cells undergoing necrosis or apoptosis upon glucose deprivation. (gla.ac.uk)
- Overexpression of Per2 promoted autophagy and apoptosis in OSCC cells and inhibited proliferation. (jcancer.org)
- When the AKT activator SC79 was added to Per2-overexpressing OSCC cells, the increased autophagy, apoptosis and decreased proliferation were significantly rescued. (jcancer.org)
- Verapamil induces autophagy while chloroquine inhibits degradation of autophagosomes that lead to accumulation of particles. (moleculardevices.com)
- mTORC1 activation inhibits autophagy, and it is considered to be a molecular marker of diabetic nephropathy [ 7 , 8 ], as the decrease in podocyte autophagic activity caused by mTORC1 activation plays a vital role in the progression of this disease [ 9 ]. (hindawi.com)
- Apolipoprotein E4 inhibits autophagy gene products through direct, specific binding to CLEAR motifs. (alzforum.org)
- Rapamycin and spermidine can induce autophagy within a few hours of administration. (fightaging.org)
- Intermittent fasting is another great way to induce autophagy. (indiatimes.com)
- Our findings show that all three cannabinoids induce autophagy in a dose-dependent manner in fully differentiated CaCo2 cells, a model of mature intestinal epithelium. (lancs.ac.uk)
- Furthermore, while ENM induce autophagy, increasing autophagic flux can block IL-1beta release from macrophages. (cdc.gov)
Suggest that autophagy2
- These data suggest suggest that autophagy is a key regulator of MMVD and a is a promising potential therapeutic target to treat MMVD in dogs. (akcchf.org)
- Some studies suggest that autophagy may be enhanced during and immediately after exercise, particularly during aerobic activities like running or cycling. (fightaging.org)
- By inhibiting mTOR, they remove the inhibition on autophagy and allow it to proceed. (fightaging.org)
- Using pharmacological inhibition of various Ca 2+ -sensitive kinases, it was found that at least part of the autophagy that occurred during SOCE was due to activation of Ca 2+ /calmodulin-dependent kinase kinase-β (CaMKK-β, also known as CaMKK-2). (open.ac.uk)
- A critical role of autophagy was identified in rat nucleus pulposus (NP) cells: Inhibition of autophagy suppresses, while activation of autophagy enhances, the catabolic effect of cytokines. (spandidos-publications.com)
- However, the signals that promote autophagy in old HSCs and the mechanisms responsible for the increased regenerative potential of autophagy-activated old HSCs remain unknown. (fightaging.org)
- Diet: Low-carb or ketogenic diets may promote autophagy relatively quickly, within a few days to a week as the body adjusts to using ketones for energy. (fightaging.org)
- Starvation of glucose, an essential nutrient, is thought to promote autophagy in mammalian cells. (gla.ac.uk)
- Stress and Hormonal Factors: Stressors like heat or cold exposure, oxidative stress, and hormonal fluctuations can activate autophagy relatively quickly, within minutes to hours in some cases. (fightaging.org)
- In summary, this study shows that Hcy can activate autophagy by inhibiting DNMT3b-mediated DNA methylation and upregulating TFEB expression. (lu.se)
- To evaluate effects on autophagy, cells were treated with various concentrations of chloroquine or verapamil for 48 h. (moleculardevices.com)
- Chloroquine and verapamil treatment increased autophagy levels by 4.6 and 3.3-fold, respectively, as determined by total autophagosome counts (EC 50 values were 4.0 and 3.6 μM respectively). (moleculardevices.com)
- The top panel shows representative autophagy cells image and analysis mask for PC12 cells treated with an autophagy inducer chloroquine (30 μM) and stained with Cyto-ID dye. (moleculardevices.com)
- In this study, MDA-MB-231 (MDA) triple-negative breast carcinoma cells were used as a tumor cell model and mouse fibroblasts expressing an autophagy marker protein called GFP-LC3, were used as a stroma model. (nature.com)
- We also observed that PCA treatment significantly caused upregulation of autophagy-related protein LC3-II and induced GFP-LC3 puncta formation. (nih.gov)
- The protein induction of autophagy was analyzed by RT-qPCR, western blot, immunofluorescence, and electron microscopy. (frontiersin.org)
- Silencing of TFEB decreases the level of autophagy-related protein LC3BII/I and increases p62 expression level in hepatocytes after exposure to Hcy. (lu.se)
- Emerging data associates impaired autophagy, increased activity in the endocannabinoid system and upregulation of suppressor of cytokine signaling (SOCS)-3 protein expression during intestinal inflammatory states. (lancs.ac.uk)
- Functionally, all three cannabinoids reduced SOCS3 protein expression, which was reversed by blocking both early and late autophagy. (lancs.ac.uk)
- In conclusion, the regulatory protein, SOCS3, is itself regulated by autophagy and cannabinoids play a role in this process, which could be important when considering therapeutic applications for the cannabinoids in inflammatory conditions. (lancs.ac.uk)
- Recent studies, however, reveal that autophagy may be more subtle and selectively target ubiquitylated protein aggregates , protein complexes and even organelles for degradation to regulate vital cellular processes even during favourable conditions. (bvsalud.org)
- The selective nature of autophagy lends itself to potential manipulation and exploitation as part of designer protein turnover machinery for the development of stress-tolerant and disease -resistant crops, crops with increased yield potential and agricultural efficiency and reduced post-harvest losses. (bvsalud.org)
- The EPG5 gene provides instructions for making a protein that is involved in a cellular process called autophagy. (medlineplus.gov)
- In addition to its role in autophagy, the EPG5 protein aids in the cell's ability to recognize infection from foreign invaders such as bacteria and viruses. (medlineplus.gov)
- Autophagy is a catabolic process that is important for degradation of cellular components, and for cell survival, and has also been associated with pathological disorders and tumour growth. (open.ac.uk)
- 2 Mitophagy is the selective degradation of mitochondria by autophagy. (moleculardevices.com)
- Hif-2α activation augments peroxisome turnover by selective autophagy (pexophagy) and thereby changes lipid composition reminiscent of peroxisomal disorders. (uzh.ch)
- Initially, autophagy was considered a non-selective bulk degradation mechanism that provides energy and building blocks for homeostatic balance during stress. (bvsalud.org)
- We have also fond that by enhancing a mechanism called autophagy we can overcome senescence and transition diseased VICs back to a normal healthy state. (akcchf.org)
- Autophagy is a cellular homeostatic mechanism where proteins and organelles are digested and recycled to provide an alternative source of building blocks and energy to cells. (nature.com)
- High level of homocysteine (Hcy) promotes autophagy in hepatocytes, but the underlying mechanism is still unknown. (lu.se)
- These findings provide another new mechanism for Hcy-induced autophagy in hepatocytes. (lu.se)
- However, the autophagy induced by TNF‑α and IL‑1β and the corresponding molecular mechanism appear to be cell‑type dependent. (spandidos-publications.com)
- The effect and mechanism of autophagy regulated by TNF‑α and IL‑1β in IVDs remains unclear. (spandidos-publications.com)
- Autophagy may be called the recycling system of the cells: In short, molecules and cellular organelles, which have faulty structure or are worn out, are isolated into membrane bound vacuoles, so-called autophagic vacuoles. (enmc.org)
- The results show that Hcy-induced autophagy level is mediated by upregulation of TFEB. (lu.se)
- After treatment, live cells were stained with the CYTO-ID® Autophagy Detection Kit for tracking autophagosomes. (moleculardevices.com)
- Autophagy: renovation of cells and tissues. (moleculardevices.com)
- We used this system to study how tumor cells induced autophagy in the stromal niche. (nature.com)
- Firstly, we could confirm that transforming growth factor β1 (TGFβ1) secreted from breast tumor cells is a paracrine mediator of tumor-stroma interaction leading to the activation of autophagy in the stroma component fibroblasts. (nature.com)
- Through proof of concept experiments using TGFβ1 as a model factor, we could demonstrate real time monitoring of autophagy induction in fibroblasts by single tumor cells. (nature.com)
- The fundamental need for Ca 2+ in the activation of autophagy was demonstrated by loading cells with an exogenous Ca 2+ buffer, which prevented various stimuli from triggering autophagy. (open.ac.uk)
- When in autophagy mode, your body's cells create membranes that find dead, diseased, or worn-out cells, eat them up, and use the resulting molecules for energy or for making new cell parts. (indiatimes.com)
- Once your body enters autophagy, it will begin repairing damaged cells and breaking down old cells for fuel. (indiatimes.com)
- A research review found that intermittent fasting and autophagy can make cancer treatments more effective while protecting normal cells and reducing the side effects. (indiatimes.com)
- Finally, IKKβ knockdown was used to further confirm the effect of the NF‑κB signal on human NP cells autophagy, and the data showed that IKKβ knockdown upregulated the autophagy of NP cells during inflammatory conditions. (spandidos-publications.com)
- In addition, Shen et al ( 14 ) reported that the autophagy of rat AF cells was induced by serum deprivation in vitro and that IL-1β upregulated serum deprivation-induced autophagy in a dose-dependent manner. (spandidos-publications.com)
- Ma et al ( 15 ) revealed that compression activated autophagy in NP cells and that compression-induced autophagy was closely associated with intracellular reactive oxygen species production. (spandidos-publications.com)
- Autophagy also helps cells use materials most efficiently when energy demands are high. (medlineplus.gov)
- Our Autophagy poster summarizes the molecular machinery, physiology and pathology of autophagy, and highlights chemical compounds that modulate autophagy. (tocris.com)
- Another study showed that removing the autophagy gene in mice caused weight gain, lethargy, higher cholesterol, and impaired brain function. (indiatimes.com)
- Autophagy is a highly conserved and lysosome-dependent bulk degradation process. (hindawi.com)
- Autophagy is a regulated process of degrading and recycling damaged proteins and organelles in response to cellular stress. (moleculardevices.com)
- Autophagy is the "self-eating" process of degrading damaged proteins and organelles, as well as recycling intracellular energy to maintain cellular homeostasis under stress conditions. (hindawi.com)
- The triggering of autophagy under these conditions was due to reduced cellular ATP levels. (open.ac.uk)
- The activation of autophagy absolutely required the presence of extracellular Ca 2+ , and was not due to cellular stress. (open.ac.uk)
- Autophagy is a genetically regulated, eukaryotic cellular degradation system that sequestrates cytoplasmic materials in specialised vesicles, termed autophagosomes , for delivery and breakdown in the lysosome or vacuole . (bvsalud.org)
- 2007). Autophagy: process and function, Genes & Dev. (moleculardevices.com)
- Autophagy plays a critical role in the physiology and pathophysiology of hepatocytes. (lu.se)
- In this context, we show that inflammation-mediated autophagy engagement preserves functional quiescence by enabling metabolic adaptation to glycolytic impairment. (fightaging.org)
- Autophagy makes us more efficient machines to get rid of faulty parts, stop cancerous growths, and stop metabolic dysfunction like obesity and diabetes," Champ says. (indiatimes.com)
- Detailed description of what changes take place in your body while in metabolic autophagy. (bookpeople.com)
- Moreover, we demonstrate that transient autophagy induction via a short-term fasting/refeeding paradigm normalizes glucose uptake and glycolytic flux and significantly improves old HSC regenerative potential. (fightaging.org)
- The 167th ENMC workshop organized June 19-21,2009 in Naarden, The Netherlands was the second (= follow-up) workshop on X-linked myopathy with excessive autophagy (XMEA) and related vacuolar myopathies, the first one having been the 77th ENMC workshop March 10-12, 2000. (enmc.org)
- Autophagy has a variety of complex physiological and pathophysiological roles, such as adaptation to nutrient starvation, clearance of damaged intracellular proteins and organelles, cell development, antiaging, elimination of microorganisms, cell death, tumor suppression, and antigen presentation. (moleculardevices.com)
- Here, we discuss our current understanding of autophagy and speculate its potential manipulation for improved agricultural performance. (bvsalud.org)
- Here, we demonstrate that autophagy activation is an adaptive survival response to chronic inflammation in the aging bone marrow (BM) niche. (fightaging.org)
- DN progression is associated with podocyte damage due to reduced autophagy caused by mTORC1 activation. (hindawi.com)
- Autophagy and its dysregulation has been found to play an important role in neurodegenerative diseases and cancers, therefore the discovery of novel therapeutic targets along this process has emerged as a promising approach for drug therapies. (moleculardevices.com)
- Our Autophagy review summarizes the molecular mechanisms and physiology of autophagy, as well as the role of autophagy in certain disease states. (tocris.com)
- The role of autophagy in cancer microenvironment is still poorly understood. (nature.com)
- We thus aimed to determine the role of autophagy in cell death induced by glucose deprivation. (gla.ac.uk)
- These data suggest that the role of autophagy in response to nutrient starvation should be reconsidered. (gla.ac.uk)
- In plants , autophagy plays essential roles in development (e.g., senescence ) and responses to abiotic (e.g., nutrient starvation , drought and oxidative stress ) and biotic stresses (e.g., hypersensitive response). (bvsalud.org)
- Studies suggest that a period of 12 to 24 hours of fasting can lead to significant activation of autophagy in various tissues. (fightaging.org)
- CONCLUSIONS: Excessive fluoride induced autophagy in ameloblasts both in vitro and in vivo. (fluoridealert.org)
- The method along with the CYTO-ID dye allows detection of autophagy particles and can be used for assay development and quantitation of the compound effects on the process of autophagy. (moleculardevices.com)
- Autophagy is a dynamic process that occurs at different levels in the body continuously, but it can be upregulated or enhanced in response to specific triggers. (fightaging.org)
- Sleep: Quality sleep is essential for autophagy, and the process occurs predominantly during the nighttime sleep cycle. (fightaging.org)
- Out of the seven tested recombinant human RNases, we have identified two members, RNase3 and RNase6, which were highly effective against Mycobacterium aurum extra- and intracellularly and induced an autophagy process. (frontiersin.org)
- In IVDs, autophagy is also present and associated with the increased pathological process of IVD degeneration in rats. (spandidos-publications.com)
- Two key steps regulate this process: 1) ENM-induced phagolysosomal membrane permeability (LMP) leading to the release of cathepsin B into the cytoplasm, which has been linked to NLRP3 Inflammasome assembly and Caspase-1 activation necessary for IL-1beta to be cleaved from its pro-form, and 2) elimination of the NLRP3 Inflammasome complex by autophagy. (cdc.gov)
- Taken together, we propose that autophagy-driven pro-survival responses are required to facilitate a long-lasting mutualistic interaction between S. indica and Arabidopsis. (biorxiv.org)
- With age, a subset of HSCs increases autophagy flux and preserves some regenerative capacity, while the rest fail to engage autophagy and become metabolically overactivated and dysfunctional. (fightaging.org)
- looks like 24hours to autophagy activation in mice, but how long for humans? (fightaging.org)
- Our results identify inflammation-driven glucose hypometabolism as a key driver of HSC dysfunction with age and establish autophagy as a targetable node to reset old HSC glycolytic and regenerative capacity. (fightaging.org)
- Autophagy is central for the benefits associated with activation of longevity signaling programs, and for HSC function and response to nutrient stress. (fightaging.org)
- Impairment of dAdo uptake in an autophagy mutant background confers resistance to dAdo-induced cell death and precludes the symbiosis-mediated cell death. (biorxiv.org)
- Autophagy is a response to stress, so to trigger it requires you to put your body through some hardship. (indiatimes.com)
- It's important to note that the degree of autophagy activation can vary among individuals, and the timeline can be influenced by factors like age, genetics, and overall health. (fightaging.org)
- Autophagy is everything from exercises to helpful nutritional information, this book outlines the simplest strategies to achieving your dream body. (bookpeople.com)