Adenovirus E3 Proteins
Apoptosis Regulatory Proteins
Apoptosis
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
Caspases
A family of intracellular CYSTEINE ENDOPEPTIDASES that play a role in regulating INFLAMMATION and APOPTOSIS. They specifically cleave peptides at a CYSTEINE amino acid that follows an ASPARTIC ACID residue. Caspases are activated by proteolytic cleavage of a precursor form to yield large and small subunits that form the enzyme. Since the cleavage site within precursors matches the specificity of caspases, sequential activation of precursors by activated caspases can occur.
RNA-Binding Proteins
Cell Death
Molecular Sequence Data
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Cause of Death
Amino Acid Sequence
bcl-Associated Death Protein
Death
Death, Sudden, Cardiac
Unexpected rapid natural death due to cardiovascular collapse within one hour of initial symptoms. It is usually caused by the worsening of existing heart diseases. The sudden onset of symptoms, such as CHEST PAIN and CARDIAC ARRHYTHMIAS, particularly VENTRICULAR TACHYCARDIA, can lead to the loss of consciousness and cardiac arrest followed by biological death. (from Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 7th ed., 2005)
Proto-Oncogene Proteins c-bcl-2
Membrane proteins encoded by the BCL-2 GENES and serving as potent inhibitors of cell death by APOPTOSIS. The proteins are found on mitochondrial, microsomal, and NUCLEAR MEMBRANE sites within many cell types. Overexpression of bcl-2 proteins, due to a translocation of the gene, is associated with follicular lymphoma.
Brain Death
A state of prolonged irreversible cessation of all brain activity, including lower brain stem function with the complete absence of voluntary movements, responses to stimuli, brain stem reflexes, and spontaneous respirations. Reversible conditions which mimic this clinical state (e.g., sedative overdose, hypothermia, etc.) are excluded prior to making the determination of brain death. (From Adams et al., Principles of Neurology, 6th ed, pp348-9)
Attitude to Death
Genes, bcl-2
Cell Survival
Proto-Oncogene Proteins
Signal Transduction
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
bcl-2-Associated X Protein
Receptors, Death Domain
A family of cell surface receptors that signal via a conserved domain that extends into the cell CYTOPLASM. The conserved domain is referred to as a death domain due to the fact that many of these receptors are involved in signaling APOPTOSIS. Several DEATH DOMAIN RECEPTOR SIGNALING ADAPTOR PROTEINS can bind to the death domains of the activated receptors and through a complex series of interactions activate apoptotic mediators such as CASPASES.
CARD Signaling Adaptor Proteins
A family of intracellular signaling adaptor proteins that contain caspase activation and recruitment domains. Proteins that contain this domain play a role in APOPTOSIS-related signal transduction by associating with other CARD domain-containing members and in activating INITIATOR CASPASES that contain CARD domains within their N-terminal pro-domain region.
Lymphoma, B-Cell
Caspase 3
Translocation, Genetic
Risk Factors
Chromosomes, Human, Pair 14
Mitochondria
Semiautonomous, self-reproducing organelles that occur in the cytoplasm of all cells of most, but not all, eukaryotes. Each mitochondrion is surrounded by a double limiting membrane. The inner membrane is highly invaginated, and its projections are called cristae. Mitochondria are the sites of the reactions of oxidative phosphorylation, which result in the formation of ATP. They contain distinctive RIBOSOMES, transfer RNAs (RNA, TRANSFER); AMINO ACYL T RNA SYNTHETASES; and elongation and termination factors. Mitochondria depend upon genes within the nucleus of the cells in which they reside for many essential messenger RNAs (RNA, MESSENGER). Mitochondria are believed to have arisen from aerobic bacteria that established a symbiotic relationship with primitive protoeukaryotes. (King & Stansfield, A Dictionary of Genetics, 4th ed)
Colorectal Neoplasms
ras Proteins
Small, monomeric GTP-binding proteins encoded by ras genes (GENES, RAS). The protooncogene-derived protein, PROTO-ONCOGENE PROTEIN P21(RAS), plays a role in normal cellular growth, differentiation and development. The oncogene-derived protein (ONCOGENE PROTEIN P21(RAS)) can play a role in aberrant cellular regulation during neoplastic cell transformation (CELL TRANSFORMATION, NEOPLASTIC). This enzyme was formerly listed as EC 3.6.1.47.
Leucovorin
Camptothecin
Antibodies, Monoclonal, Humanized
Antibodies from non-human species whose protein sequences have been modified to make them nearly identical with human antibodies. If the constant region and part of the variable region are replaced, they are called humanized. If only the constant region is modified they are called chimeric. INN names for humanized antibodies end in -zumab.
Organoplatinum Compounds
Subcellular distribution and redistribution of Bcl-2 family proteins in human leukemia cells undergoing apoptosis. (1/660)
It has been suggested that the ratio of Bcl-2 family proapoptotic proteins to antiapoptotic proteins determines the sensitivity of leukemic cells to apoptosis. However, it is believed that Bcl-2 family proteins exert their function on apoptosis only when they target to the mitochondrial outer membrane. The vinblastine-resistant T-lymphoblastic leukemic cell line CEM/VLB100 has increased sensitivity to tumor necrosis factor-alpha (TNF-alpha)-induced cytochrome c release, mitochondrial respiratory inhibition, and consequently apoptosis, compared with parental CEM cells. However, there was no difference between the two cell lines in the expression of Bcl-2 family proteins Bcl-2, Bcl-XL, Bcl-XS, Bad, and Bax at the whole cell level, as analyzed by Western blotting. Bcl-2 mainly located to mitochondria and light membrane as a membrane-bound protein, whereas Bcl-XL was located in both mitochondria and cytosol. Similar levels of both Bcl-2 and Bcl-XL were present in the resting mitochondria of the two cell lines. Although the proapoptotic proteins Bcl-XS, Bad, and Bax were mainly located in the cytosol, CEM/VLB100 mitochondria expressed higher levels of these proapoptotic proteins. Subcellular redistribution of the Bcl-2 family proteins was detected in a cell-free system by both Western blotting and flow cytometry after exposure to TNF-alpha. The levels of Bcl-2 family proteins were not altered at the whole cell level by TNF-alpha. However, after exposure to TNF-alpha, Bax, Bad, and Bcl-XS translocated from the cytosol to the mitochondria of both cell lines. An increase in Bcl-2 levels was observed in CEM mitochondria, which showed resistance to TNF-alpha-induced cytochrome c release. By contrast, decreased mitochondrial Bcl-2 was observed in CEM/VLB100 cells, which released cytochrome c from the mitochondria and underwent apoptosis as detected by fluorescence microscopy. We conclude that mitochondrial levels of Bcl-2 family proteins may determine the sensitivity of leukemic cells to apoptosis and that, furthermore, these levels may change rapidly after exposure of cells to toxic stimuli. (+info)Dissociation of apoptosis from proliferation, protein kinase B activation, and BAD phosphorylation in interleukin-3-mediated phosphoinositide 3-kinase signaling. (2/660)
Interleukin-3 (IL-3) acts as both a growth and survival factor for many hemopoietic cells. IL-3 treatment of responsive cells leads to the rapid and transient activation of Class IA phosphoinositide-3-kinases (PI3Ks) and the serine/threonine kinase Akt/protein kinase B (PKB) and phosphorylation of BAD. Each of these molecules has been implicated in anti-apoptotic signaling in a wide range of cells. Using regulated expression of dominant-negative p85 (Deltap85) in stably transfected IL-3-dependent BaF/3 cells, we have specifically investigated the role of class IA PI3K in IL-3 signaling. The major functional consequence of Deltap85 expression in these cells is a highly reproducible, dramatic reduction in IL-3-induced proliferation. Expression of Deltap85 reduces IL-3-induced PKB phosphorylation and activation and phosphorylation of BAD dramatically, to levels seen in unstimulated cells. Despite these reductions, the levels of apoptosis observed in the same cells are very low and do not account for the reduction in IL-3-dependent proliferation we observe. These results show that Deltap85 inhibits both PKB activity and BAD phosphorylation without significantly affecting levels of apoptosis, suggesting that there are targets other than PKB and BAD that can transmit survival signals in these cells. Our data indicate that the prime target for PI3K action in IL-3 signaling is at the level of regulation of proliferation. (+info)Ca2+-induced apoptosis through calcineurin dephosphorylation of BAD. (3/660)
The Ca2+-activated protein phosphatase calcineurin induces apoptosis, but the mechanism is unknown. Calcineurin was found to dephosphorylate BAD, a pro-apoptotic member of the Bcl-2 family, thus enhancing BAD heterodimerization with Bcl-xL and promoting apoptosis. The Ca2+-induced dephosphorylation of BAD correlated with its dissociation from 14-3-3 in the cytosol and translocation to mitochondria where Bcl-xL resides. In hippocampal neurons, L-glutamate, an inducer of Ca2+ influx and calcineurin activation, triggered mitochondrial targeting of BAD and apoptosis, which were both suppressible by coexpression of a dominant-inhibitory mutant of calcineurin or pharmacological inhibitors of this phosphatase. Thus, a Ca2+-inducible mechanism for apoptosis induction operates by regulating BAD phosphorylation and localization in cells. (+info)Trophic support promotes survival of bcl-x-deficient telencephalic cells in vitro. (4/660)
Survival of immature neurons is regulated by Bcl-xL, as targeted disruption of bcl-x significantly increases cell death in vivo and in vitro. Death of cultured bcl-x-deficient and wild-type telencephalic cells can be prevented by fetal calf serum or chemically-defined medium (ITS), suggesting trophic factors in these media potentiate survival through a pathway independent of Bcl-xL. Addition of trophic factors to basal medium revealed that insulin and insulin-like growth factors (IGFs), but not other trophic factors, reduced apoptosis of wild-type and bcl-x-deficient telencephalic cells. Antibodies raised against IGF-I receptors and wortmannin both attenuated the effects of IGF-I, indicating survival was mediated by IGF-I receptors and phosphatidylinositol 3'-kinase signaling, whereas effects of ITS were only partially reduced by these agents. The survival promoting effects of ITS were reduced in cells lacking both bcl-x and bcl-2, indicating Bcl-2 plays a supportive role to Bcl-xL in maintaining telencephalic cell survival. Furthermore, the ratio of expression of the pro-apoptotic bax gene to the anti-apoptotic bcl-2 gene was reduced in bcl-x-deficient cultures grown in ITS, suggesting that the interaction between these bcl-2 family members may, in part, regulate a Bcl-xL independent survival pathway. Finally, the pro-apoptotic bad gene does not appear to play a role in these interactions as targeted disruption of bad did not alter apoptosis in telencephalic cultures. (+info)Phosphorylation and inactivation of BAD by mitochondria-anchored protein kinase A. (5/660)
Signaling pathways between cell surface receptors and the BCL-2 family of proteins regulate cell death. Survival factors induce the phosphorylation and inactivation of BAD, a proapoptotic member. Purification of BAD kinase(s) identified membrane-based cAMP-dependent protein kinase (PKA) as a BAD Ser-112 (S112) site-specific kinase. PKA-specific inhibitors blocked the IL-3-induced phosphorylation on S112 of endogenous BAD as well as mitochondria-based BAD S112 kinase activity. A blocking peptide that disrupts type II PKA holoenzyme association with A-kinase-anchoring proteins (AKAPs) also inhibited BAD phosphorylation and eliminated the BAD S112 kinase activity at mitochondria. Thus, the anchoring of PKA to mitochondria represents a focused subcellular kinase/substrate interaction that inactivates BAD at its target organelle in response to a survival factor. (+info)Developmental regulation of Bcl-2 family protein expression in the involuting mammary gland. (6/660)
Epithelial cells within the mammary gland undergo developmental programmes of proliferation and apoptosis during the pregnancy cycle. After weaning, secretory epithelial cells are removed by apoptosis. To determine whether members of the Bcl-2 gene family could be involved in regulating this process, we have examined whether changes in their expression occur during this developmental apoptotic program in vivo. Bax and Bcl-x were evenly expressed throughout development. However, expression of Bak and Bad was increased during late pregnancy and lactation, and the proteins were present during the time of maximal apoptotic involution. Thereafter, their levels declined. In contrast, Bcl-w was expressed in pregnancy and lactation but was downregulated at the onset of apoptosis. Bcl-2 was not detected in lactating or early involuting mammary gland. Thus, the pro-apoptotic proteins Bax, Bak and Bad, as well as the death-suppressors Bcl-x, Bcl-2 and Bcl-w, are synthesised in mouse mammary gland, and dynamic changes in the expression profiles of these proteins occurs during development. To determine if changes in Bak and Bcl-w expression could regulate mammary apoptosis, their effect on cultured mouse mammary epithelial cells was examined in transient transfection assays. Enforced expression of Bak induced rapid mammary apoptosis, which could be suppressed by coexpression of Bcl-w. In extracts of mammary tissue in vivo, Bak heterodimerized with Bcl-x whereas Bax associated with Bcl-w, but Bak/Bcl-w heterodimers were not detected. Thus, Bak and Bcl-w may regulate cell death through independent pathways. These results support a model in which mammary epithelial cells are primed for apoptosis during the transition from pregnancy to lactation by de novo expression of the death effectors Bak and Bad. It is suggested that these proteins are prevented from triggering apoptosis by anti-apoptotic Bcl-2 family proteins until involution, when the levels of Bcl-w decline. Our study provides evidence that regulated changes in the expression of cell death genes may contribute to the developmental control of mammary apoptosis. (+info)Phosphorylation of the transcription factor forkhead family member FKHR by protein kinase B. (7/660)
Protein kinase B lies "downstream" of phosphatidylinositide (PtdIns) 3-kinase and is thought to mediate many of the intracellular actions of insulin and other growth factors. Here we show that FKHR, a human homologue of the DAF16 transcription factor in Caenorhabditis elegans, is rapidly phosphorylated by human protein kinase Balpha (PKBalpha) at Thr-24, Ser-256, and Ser-319 in vitro and at a much faster rate than BAD, which is thought to be a physiological substrate for PKB. The same three sites, which all lie in the canonical PKB consensus sequences (Arg-Xaa-Arg-Xaa-Xaa-(Ser/Thr)), became phosphorylated when FKHR was cotransfected with either PKB or PDK1 (an upstream activator of PKB). All three residues became phosphorylated when 293 cells were stimulated with insulin-like growth factor 1 (IGF-1). The IGF-1-induced phosphorylation was abolished by the PtdIns 3-kinase inhibitor wortmannin but not by PD 98059 (an inhibitor of the mitogen-activated protein kinase cascade) or by rapamycin. These results indicate that FKHR is a physiological substrate of PKB and that it may mediate some of the physiological effects of PKB on gene expression. DAF16 is known to be a component of a signaling pathway that has been partially dissected genetically and includes homologues of the insulin/IGF-1 receptor, PtdIns 3-kinase and PKB. The conservation of Thr-24, Ser-256, and Ser-319 and the sequences surrounding them in DAF16 therefore suggests that DAF16 is also a direct substrate for PKB in C. elegans. (+info)Cytokine-induced protein kinase B activation and Bad phosphorylation do not correlate with cell survival of hemopoietic cells. (8/660)
Activation of phosphoinositide-3 kinases (PI3Ks), their downstream target protein kinase B (PKB), and phosphorylation of Bad have all been implicated in survival signaling in many systems. However, it is not known whether these events are sufficient or necessary to universally prevent apoptosis. To address this issue, we have used three different factor-dependent hemopoietic cell lines, MC/9, BaF/3, and factor-dependent (FD)-6, which respond to a range of cytokines, to investigate the relationship between PI3K, PKB, and Bad activity with survival. The cytokines IL-3, IL-4, stem cell factor (SCF), GM-CSF, and insulin all induced the rapid and transient activation of PKB in responsive cell lines. In all cases, cytokine-induced PKB activation was sensitive to inhibition by the PI3K inhibitor, LY294002. However, dual phosphorylation of the proapoptotic protein Bad was found not to correlate with PKB activation. In addition, we observed cell-type-specific differences in the ability of the same cytokine to induce Bad phosphorylation. Whereas IL-4 induced low levels of dual phosphorylation of Bad in FD-6, it was unable to in MC/9 or BaF/3. Insulin, which was the most potent inducer of PKB in FD-6, induced barely detectable Bad phosphorylation. In addition, the ability of a particular cytokine to induce PKB activity did not correlate with its ability to promote cell survival and/or proliferation. These data demonstrate that, in hemopoietic cells, activation of PKB does not automatically confer a survival signal or result in phosphorylation of Bad, implying that other survival pathways must be involved. (+info) Death is a process that occurs when a living organism ceases to function, and its vital organs stop working. This can happen due to various reasons such as old age, disease, injury, or other external factors. Death is a natural part of life, and it marks the end of an individual's physical existence.
In medical terms, death is defined as the irreversible cessation of all bodily functions that are necessary for life. This includes the loss of consciousness, the absence of breathing, heartbeat, and other vital signs. Brain death, which occurs when the brain no longer functions, is considered a definitive sign of death.
The medical professionals use various criteria to determine death, such as:
1. Cessation of breathing: When an individual stops breathing for more than 20 minutes, it is considered a sign of death.
2. Cessation of heartbeat: The loss of heartbeat for more than 20 minutes is another indicator of death.
3. Loss of consciousness: If an individual is unresponsive and does not react to any stimuli, it can be assumed that they have died.
4. Brain death: When the brain no longer functions, it is considered a definitive sign of death.
5. Decay of body temperature: After death, the body's temperature begins to decrease, which is another indicator of death.
In some cases, medical professionals may use advanced technologies such as electroencephalography (EEG) or functional magnetic resonance imaging (fMRI) to confirm brain death. These tests can help determine whether the brain has indeed ceased functioning and if there is no hope of reviving the individual.
It's important to note that while death is a natural part of life, it can be a difficult and emotional experience for those who are left behind. It's essential to provide support and care to the family members and loved ones of the deceased during this challenging time.
Sudden cardiac death refers to a condition where an individual experiences cardiac arrest and dies within minutes or hours of the onset of symptoms without any warning signs or diagnosed heart disease. It is often caused by an arrhythmia (abnormal heart rhythm) that originates in the heart's ventricles, such as ventricular fibrillation or tachycardia. Sudden cardiac death can be a result of inherited heart conditions, coronary artery disease, heart failure, or other factors that affect the heart's electrical system. It is a leading cause of death worldwide and can occur in individuals of all ages and backgrounds.
Some examples of the use of 'Death, Sudden, Cardiac' in medical contexts include:
1. Sudden cardiac death (SCD) is a major public health concern, affecting thousands of people each year in the United States alone. It is often caused by inherited heart conditions, such as hypertrophic cardiomyopathy or long QT syndrome.
2. The risk of sudden cardiac death is higher for individuals with a family history of heart disease or other pre-existing cardiovascular conditions.
3. Sudden cardiac death can be prevented by prompt recognition and treatment of underlying heart conditions, as well as by avoiding certain risk factors such as smoking, physical inactivity, and an unhealthy diet.
4. Cardiopulmonary resuscitation (CPR) and automated external defibrillators (AEDs) can be effective in restoring a normal heart rhythm during sudden cardiac death, especially when used promptly after the onset of symptoms.
The definition of "brain death" is a state of irreversible cessation of all brain function, including the absence of any clinical or electrophysiological signs of consciousness, brainstem reflexes, and the failure of all brain waves. This definition was established by the Ad Hoc Committee of the Harvard Medical School in 1968, and it is widely accepted by medical professionals and legal authorities as the criteria for determining death.
The committee defined "brain death" as follows:
* The absence of any clinical or electrophysiological signs of consciousness, including the lack of response to pain, light, sound, or other stimuli.
* The absence of brainstem reflexes, such as pupillary reactivity, oculocephalic reflex, and gag reflex.
* The failure of all brain waves, including alpha, beta, theta, delta, and epsilon waves, as detected by electroencephalography (EEG).
* The absence of any other clinical or laboratory signs of life, such as heartbeat, breathing, or blood circulation.
The definition of brain death is important because it provides a clear and consistent criteria for determining death in medical settings. It helps to ensure that patients who are clinically dead are not inappropriately kept on life support, and that organ donation can be performed in a timely and ethical manner.
Fetal death refers to the loss of life of a developing fetus during pregnancy, usually before the 24th week of gestation. It can occur due to various causes, such as genetic abnormalities, maternal infections, or pregnancy complications like placental abruption or umbilical cord compression.
There are different types of fetal death, including:
1. Stillbirth: This refers to the death of a fetus after the 20th week of gestation. It can be caused by various factors, such as infections, placental problems, or umbilical cord compression.
2. Miscarriage: This occurs before the 20th week of gestation and is usually due to chromosomal abnormalities or hormonal imbalances.
3. Ectopic pregnancy: This is a rare condition where the fertilized egg implants outside the uterus, usually in the fallopian tube. It can cause fetal death and is often diagnosed in the early stages of pregnancy.
4. Intrafamilial stillbirth: This refers to the death of two or more fetuses in a multiple pregnancy, usually due to genetic abnormalities or placental problems.
The diagnosis of fetal death is typically made through ultrasound examination or other imaging tests, such as MRI or CT scans. In some cases, the cause of fetal death may be unknown, and further testing and investigation may be required to determine the underlying cause.
There are various ways to manage fetal death, depending on the stage of pregnancy and the cause of the death. In some cases, a vaginal delivery may be necessary, while in others, a cesarean section may be performed. In cases where the fetus has died due to a genetic abnormality, couples may choose to undergo genetic counseling and testing to assess their risk of having another affected pregnancy.
Overall, fetal death is a tragic event that can have significant emotional and psychological impact on parents and families. It is essential to provide compassionate support and care to those affected by this loss, while also ensuring appropriate medical management and follow-up.
Lymphoma, B-cell refers to a type of cancer that develops in the B cells of the immune system. B cells are a type of white blood cell that produces antibodies to fight infections. In lymphoma, B-cell, the B cells become abnormal and grow uncontrollably, leading to a tumor.
There are several subtypes of lymphoma, B-cell, including:
1. Diffuse large B-cell lymphoma (DLBCL): This is the most common type of B-cell lymphoma and typically affects older adults.
2. Follicular lymphoma: This type of lymphoma grows slowly and often does not require treatment for several years.
3. Marginal zone lymphoma: This type of lymphoma develops in the marginal zone of the spleen or other lymphoid tissues.
4. Hodgkin lymphoma: This is a type of B-cell lymphoma that is characterized by the presence of Reed-Sternberg cells, which are abnormal cells that can be identified under a microscope.
The symptoms of lymphoma, B-cell can vary depending on the subtype and the location of the tumor. Common symptoms include swollen lymph nodes, fatigue, fever, night sweats, and weight loss.
Treatment for lymphoma, B-cell usually involves chemotherapy, which is a type of cancer treatment that uses drugs to kill cancer cells. Radiation therapy may also be used in some cases. In some cases, bone marrow or stem cell transplantation may be recommended.
Prognosis for lymphoma, B-cell depends on the subtype and the stage of the disease at the time of diagnosis. In general, the prognosis is good for patients with early-stage disease, but the cancer can be more difficult to treat if it has spread to other parts of the body.
Prevention of lymphoma, B-cell is not possible, as the exact cause of the disease is not known. However, avoiding exposure to certain risk factors, such as viral infections and pesticides, may help reduce the risk of developing the disease. Early detection and treatment can also improve outcomes for patients with lymphoma, B-cell.
Lymphoma, B-cell is a type of cancer that affects the immune system and can be treated with chemotherapy and other therapies. The prognosis varies depending on the subtype and stage of the disease at diagnosis. Prevention is not possible, but early detection and treatment can improve outcomes for patients with this condition.
Genetic Translocation Definition - MedicineNet
https://www.medicinenet.com › Medical Dictionary › G
A genetic translocation is a change in the number or arrangement of the chromosomes in a cell. It occurs when a portion of one chromosome breaks off and attaches to another chromosome. This can result in a gain or loss of genetic material, which can have significant effects on the individual.
Genetic Translocation | Definition & Facts | Britannica
https://www.britannica.com › science › Genetic-tr...
Genetic translocation, also called chromosomal translocation, a type of chromosomal aberration in which a portion of one chromosome breaks off and attaches to another chromosome. This can result in a gain or loss of genetic material. Genetic translocations are often found in cancer cells and may play a role in the development and progression of cancer.
Translocation, Genetic | health Encyclopedia - UPMC
https://www.upmc.com › health-library › gene...
A genetic translocation is a change in the number or arrangement of the chromosomes in a cell. It occurs when a portion of one chromosome breaks off and attaches to another chromosome. This can result in a gain or loss of genetic material, which can have significant effects on the individual.
Genetic Translocation | Genetics Home Reference - NIH
https://ghr.nlm.nih.gov › condition › ge...
A genetic translocation is a change in the number or arrangement of the chromosomes in a cell. It occurs when a portion of one chromosome breaks off and attaches to another chromosome. This can result in a gain or loss of genetic material, which can have significant effects on the individual.
In conclusion, Genetic Translocation is an abnormality in the number or arrangement of chromosomes in a cell. It occurs when a portion of one chromosome breaks off and attaches to another chromosome, resulting in a gain or loss of genetic material that can have significant effects on the individual.
Colorectal Neoplasms are tumors that occur in the colon or rectum, which are parts of the gastrointestinal tract. These neoplasms can be benign or malignant, and their impact on public health is significant. Colorectal cancer is the third most common cancer worldwide, and it is estimated that there were approximately 1.8 million new cases diagnosed in 2018 alone.
The causes of colorectal neoplasms are not fully understood, but factors such as age, genetics, diet, and lifestyle have been implicated. Symptoms of colorectal cancer can include changes in bowel habits, blood in the stool, abdominal pain, and weight loss. Screening for colorectal cancer is recommended for adults over the age of 50, as it can help detect early-stage tumors and improve survival rates.
There are several subtypes of colorectal neoplasms, including adenomas (which are precancerous polyps), carcinomas (which are malignant tumors), and lymphomas (which are cancers of the immune system). Treatment options for colorectal cancer depend on the stage and location of the tumor, but may include surgery, chemotherapy, radiation therapy, or a combination of these.
Research into the causes and treatment of colorectal neoplasms is ongoing, and there has been significant progress in recent years. Advances in screening and treatment have improved survival rates for patients with colorectal cancer, and there is hope that continued research will lead to even more effective treatments in the future.
Bcl-2-associated death promoter
"The proapoptotic BH3-only protein BAD transduces cell death signals independently of its interaction with Bcl-2". Cell Death ... encodes a protein that activates apoptosis and interacts selectively with survival-promoting proteins Bcl-2 and Bcl-X(L)". EMBO ... bcl-Associated+Death+Protein at the US National Library of Medicine Medical Subject Headings (MeSH) Human BAD genome location ... The BCL2 associated agonist of cell death (BAD) protein is a pro-apoptotic member of the Bcl-2 gene family which is involved in ...
Bcl-2-like protein 1
Bcl-2-related ovarian death gene) is an ovarian BH3 domain-containing proapoptotic Bcl-2 protein capable of dimerization with ... the gene encodes both of the human proteins Bcl-xL and Bcl-xS. The protein encoded by this gene belongs to the Bcl-2 protein ... encodes a protein that activates apoptosis and interacts selectively with survival-promoting proteins Bcl-2 and Bcl-X(L)". The ... "BNIP3 heterodimerizes with Bcl-2/Bcl-X(L) and induces cell death independent of a Bcl-2 homology 3 (BH3) domain at both ...
Bcl-2-associated X protein
Apoptosis Apoptosome Bcl-2 BH3 interacting domain death agonist (BID) Caspases Cytochrome c Noxa Mitochondrion p53 upregulated ... also known as bcl-2-like protein 4, is a protein that in humans is encoded by the BAX gene. BAX is a member of the Bcl-2 gene ... "Identification of the protein-protein contact site and interaction mode of human VDAC1 with Bcl-2 family proteins". Biochem. ... Bcl-2-associated X protein has been shown to interact with: Bcl-2, BCL2L1, BCL2A1 SH3GLB1, SLC25A4, VDAC1, TCTP, YWHAQ, Bid, ...
Bcl-2
Apoptosome Bcl-2 homologous antagonist killer (BAK) Bcl-2-associated X protein (BAX) BH3 interacting domain death agonist (BID ... Bcl-2-related ovarian death gene) is an ovarian BH3 domain-containing proapoptotic Bcl-2 protein capable of dimerization with ... "BNIP3 heterodimerizes with Bcl-2/Bcl-X(L) and induces cell death independent of a Bcl-2 homology 3 (BH3) domain at both ... encodes a protein that activates apoptosis and interacts selectively with survival-promoting proteins Bcl-2 and Bcl-X(L)". The ...
Bcl-2 family
Youle, Richard J.; Strasser, Andreas (2008). "The BCL-2 protein family: opposing activities that mediate cell death". Nature ... Bcl-x(S)) and the β-isoform (Bcl-xβ) promote cell death. Bcl-x(L), Bcl-x(S) and Bcl-xβ are three isoforms derived by ... Bcl-2, Bcl-x(L) and Bcl-w), which is also seen in some pro-apoptotic proteins like Bcl-x(S), Diva, Bok-L and Bok-S. On the ... The anti-apoptotic Bcl-2 proteins, such as Bcl-2 and Bcl-xL, conserve all four BH domains. The BH domains also serve to ...
C-Raf
"Structure-function analysis of Bcl-2 family proteins. Regulators of programmed cell death". Adv. Exp. Med. Biol. 406: 99-112. ... Like most protein kinases, c-Raf has multiple substrates. BAD (Bcl2-atagonist of cell death) is directly phosphorylated by c- ... Wang HG, Takayama S, Rapp UR, Reed JC (July 1996). "Bcl-2 interacting protein, BAG-1, binds to and activates the kinase Raf-1 ... Wang HG, Rapp UR, Reed JC (November 1996). "Bcl-2 targets the protein kinase Raf-1 to mitochondria". Cell. 87 (4): 629-38. doi: ...
Venetoclax
... blocks the anti-apoptotic B-cell lymphoma-2 (Bcl-2) protein, leading to programmed cell death of CLL cells. ... Venetoclax attaches to a protein called Bcl-2. This protein is present in high amounts in CLL cancer cells, where it helps the ... By attaching to Bcl-2 and blocking its actions, venetoclax causes the death of cancer cells and thereby slows down progression ... Overexpression of Bcl-2 in some lymphoid malignancies has been linked to increased resistance to chemotherapy. The maximum ...
BNIP3
... is a member of the apoptotic Bcl-2 protein family. It can induce cell death while also assisting with cell survival. Like ... January 2000). "BNIP3 heterodimerizes with Bcl-2/Bcl-X(L) and induces cell death independent of a Bcl-2 homology 3 (BH3) domain ... January 2000). "BNIP3 heterodimerizes with Bcl-2/Bcl-X(L) and induces cell death independent of a Bcl-2 homology 3 (BH3) domain ... Protein families, Membrane proteins, Transmembrane proteins, Transmembrane transporters, Transport proteins, Integral membrane ...
MCL1
Bcl-2-related ovarian death gene) is an ovarian BH3 domain-containing proapoptotic Bcl-2 protein capable of dimerization with ... June 2005). "Proapoptotic Bak is sequestered by Mcl-1 and Bcl-xL, but not Bcl-2, until displaced by BH3-only proteins". Genes ... The protein encoded by this gene belongs to the Bcl-2 family. Alternative splicing occurs at this locus and two transcript ... February 2005). "Differential targeting of prosurvival Bcl-2 proteins by their BH3-only ligands allows complementary apoptotic ...
Bcl-2 homologous antagonist killer
... mediates cell death and protein binding functions". The EMBO Journal. 14 (22): 5589-96. doi:10.1002/j.1460-2075.1995.tb00246.x ... Bcl-2 homologous antagonist/killer is a protein that in humans is encoded by the BAK1 gene on chromosome 6. The protein encoded ... BAK1 is a pro-apoptotic Bcl-2 protein containing four Bcl-2 homology (BH) domains: BH1, BH2, BH3, and BH4. These domains are ... binds the BH3 domain of other BCL-2 proteins in its active form. As a member of the BCL2 protein family, BAK1 functions as a ...
Bcl-2-interacting killer
This protein shares a critical BH3 domain with other death-promoting proteins, BAX and BAK. Bcl-2-interacting killer has been ... a novel death-inducing protein shares a distinct sequence motif with Bcl-2 family proteins and interacts with viral and ... a BH3-containing mouse protein that interacts with Bcl-2 and Bcl-xL, is a potent death agonist". J. Biol. Chem. 273 (14): 7783- ... encodes a protein that activates apoptosis and interacts selectively with survival-promoting proteins Bcl-2 and Bcl-X(L)". EMBO ...
BNIP2
"Adenovirus E1B 19 kDa and Bcl-2 proteins interact with a common set of cellular proteins". Cell. 79 (2): 341-51. doi:10.1016/ ... it interacts with the E1B 19 kDa protein which is responsible for the protection of virally induced cell death, as well as E1B ... BCL2/adenovirus E1B 19 kDa protein-interacting protein 2 is a protein that in humans is encoded by the BNIP2 gene. This gene is ... Low BC, Lim YP, Lim J, Wong ES, Guy GR (November 1999). "Tyrosine phosphorylation of the Bcl-2-associated protein BNIP-2 by ...
Primary pigmented nodular adrenocortical disease
"Loss of Prkar1a leads to Bcl-2 family protein induction and cachexia in mice". Cell Death and Differentiation. 21 (11): 1815-24 ... CNC patients have also been discovered with an unusually shortened PRKAR1α protein, detected in tumours and leukocytes, ... "Mutations of the gene encoding the protein kinase a type I-alpha regulatory subunit in patients with the Carney complex". ... which is the gene encoding the regulatory R1α subunit of protein kinase A. Germline heterozygous PRKAR1α inactivation mutations ...
BCLAF1
... a Novel Death-Promoting Transcriptional Repressor That Interacts with Bcl-2-Related Proteins". Mol Cell Biol. 19 (6): 4390-404 ... Bcl-2-associated transcription factor 1 is a Bcl-2 family protein in humans that is encoded by the BCLAF1 gene. This gene ... Overexpression of this protein induces apoptosis, which can be suppressed by co-expression of BCL2 proteins. The protein ... "Protein Kinase C δ Induces Transcription of the TP53 Tumor Suppressor Gene by Controlling Death-Promoting Factor Btf in the ...
Sanford Burnham Prebys Medical Discovery Institute
Nature 388:300-304 (1997). Reed, J.C. Bcl-2-family proteins and hematologic malignancies: history and future prospects. Blood ... Cell (1997). Deveraux, Q.L., Takahashi, R, Salvesen, G.S., and Reed, J.C. X-linked IAP is a direct inhibitor of cell-death ... and anti-apoptotic proteins, namely caspases, IAPs, and Bcl-2 family members. The demonstration by Institute scientists that ... The common trend is discovery of proteins that are linked to the development of a disease and identification of chemical ...
TARBP2
... a novel death-promoting transcriptional repressor that interacts with Bcl-2-related proteins". Molecular and Cellular Biology. ... "Double-stranded-RNA-dependent protein kinase and TAR RNA-binding protein form homo- and heterodimers in vivo". Proceedings of ... "Double-stranded-RNA-dependent protein kinase and TAR RNA-binding protein form homo- and heterodimers in vivo". Proceedings of ... "Two dimerization domains in the trans-activation response RNA-binding protein (TRBP) individually reverse the protein kinase R ...
Chandrima Shaha
Host-parasite interaction studies show the involvement of Bcl-2 proteins in parasite survival. Other studies with cells having ... Understanding of how parasite death occurs is important as successful killing of the parasite would reduce disease burden. The ... Shaha's research programme is geared towards the understanding of cell death pathways and cellular defense processes in ... research demonstrated the ability of the Leishmania parasite to execute death phenotypes similar to metazoans and experimental ...
Apoptosome
Members of the Bcl-2 family of pro-apoptotic proteins can induce the opening of the VDAC (12). This will cause the same release ... Mutations of the cell pathway can either promote cell death or disallow cell death creating a huge amount of disease in the ... Scientists have found that binding depressors to Bcl-2 anti-apoptotic proteins inhibits them and leaves direct activators free ... The term Apoptosome was first introduced in Yoshihide Tsujimoto's 1998 paper "Role of Bcl-2 family proteins in apoptosis: ...
Bcl-xL
Other Bcl-2 proteins include Bcl-2, Bcl-w, Bcl-xs, and Mcl-1. Korsmeyer SJ (March 1995). "Regulators of cell death". Trends in ... and anti-survival Bcl-2 family of proteins determine whether the cell will undergo cell death; if more Bcl-xL is present, then ... Small molecule Bcl-xL inhibitor that directly binds to Bcl-xL and releases their partner such as Bax, a proapoptotic protein, ... It is a member of the Bcl-2 family of proteins, and acts as an anti-apoptotic protein by preventing the release of ...
BAG3
... a Bcl-2-binding protein that synergizes with Bcl-2 in preventing cell death". Oncogene. 18 (46): 6183-90. doi:10.1038/sj.onc. ... "Isolation of Bcl-2 binding proteins that exhibit homology with BAG-1 and suppressor of death domains protein". Biochemical and ... BAG3 balances protein synthesis and protein degradation under mechanical stress. PLCG1 has been shown to interact with: FGFR1, ... Suzuki H, Fukunishi Y, Kagawa I, Saito R, Oda H, Endo T, Kondo S, Bono H, Okazaki Y, Hayashizaki Y (Oct 2001). "Protein-protein ...
XIAP
"Human IAP-like protein regulates programmed cell death downstream of Bcl-xL and cytochrome c". Molecular and Cellular Biology. ... and baculoviral IAP repeat-containing protein 4 (BIRC4), is a protein that stops apoptotic cell death. In humans, this protein ... two death-signaling proteins released into the cytoplasm by the mitochondria. Smac/DIABLO, a mitochondrial protein and negative ... The protein is also called human IAP-like Protein (hILP), because it is not as well conserved as the human IAPS: hIAP-1 and ...
Phorbol-12-myristate-13-acetate-induced protein 1
Apoptosis Apoptosome Bcl-2 Bcl-2-associated X protein (BAX) BH3 interacting domain death agonist (BID) Caspases Cytochrome c ... Noxa (Latin for damage) is a pro-apoptotic member of the Bcl-2 protein family. Bcl-2 family members can form hetero- or ... "Proapoptotic Bak is sequestered by Mcl-1 and Bcl-xL, but not Bcl-2, until displaced by BH3-only proteins". Genes Dev. 19 (11): ... "Proapoptotic Bak is sequestered by Mcl-1 and Bcl-xL, but not Bcl-2, until displaced by BH3-only proteins". Genes Dev. 19 (11): ...
HRK (gene)
Activator of apoptosis Hrk regulates apoptosis through interaction with death-repressor proteins Bcl-2 and Bcl-X(L). The HRK ... encodes a protein that activates apoptosis and interacts selectively with survival-promoting proteins Bcl-2 and Bcl-X(L)". EMBO ... "Physical and functional interaction between BH3-only protein Hrk and mitochondrial pore-forming protein p32". Cell Death Differ ... HRK interacts with BCL2 and BCLXL via the BH3 domain, but not with the death-promoting BCL2-related proteins BAX, BAK, or BCLXS ...
Ebola viral protein 24
STAT1 has also been shown to regulate cell death by the inhibition of anti-apoptotic proteins Bcl-2 and Bcl-xL. STAT1 also ... "Opposing actions of STAT-1 and STAT-3 on the Bcl-2 and Bcl-x promoters". Cell Death and Differentiation. 7 (3): 329-30. doi: ... Ebola viral protein 24 (eVP24) is considered a multifunctional secondary matrix protein present in viral particles. The broad ... It has been noted that eVP24 function can overlap with that of two other viral proteins; eVP40 matrix protein which functions ...
Major facilitator superfamily
... a transmembrane protein interacting with Bcl-2/Bcl-xL, induces a caspase-independent autophagic cell death". Cell Death and ... Protein domains, Transmembrane proteins, Articles containing video clips, Protein superfamilies, Transport proteins). ... The two halves of the protein pack against each other in a clam-shell fashion, sealing via interactions at the ends of the ... There are several MFS proteins in humans, where they are known as solute carriers (SLCs) and Atypical SLCs. There are today 52 ...
Neuroprotection
Oxidative stress can directly cause neuron cell death or it can trigger a cascade of events that leads to protein misfolding, ... Bcl-2), heat shock protein 70 (HSP-70)), and concomitantly downregulates pro-apoptotic factors. Lithium has been shown to ... Glutamate excitotoxicity is one of the most important mechanisms known to trigger cell death in CNS disorders. Over-excitation ... Not only can oxidative stress and excitotoxicity trigger neuron cell death but when combined they have synergistic effects that ...
BAG1
... a novel Bcl-2-binding protein with anti-cell death activity". Cell. 80 (2): 279-84. doi:10.1016/0092-8674(95)90410-7. PMID ... The oncogene BCL2 is a membrane protein that blocks a step in a pathway leading to apoptosis or programmed cell death. The ... Wang HG, Takayama S, Rapp UR, Reed JC (July 1996). "Bcl-2 interacting protein, BAG-1, binds to and activates the kinase Raf-1 ... Wang HG, Takayama S, Rapp UR, Reed JC (1996). "Bcl-2 interacting protein, BAG-1, binds to and activates the kinase Raf-1". Proc ...
DAD1
Yulug IG, See CG, Fisher EM, Ylug IG (1995). "The DAD1 protein, whose defect causes apoptotic cell death, maps to human ... one of the bcl-2 protein family". J. Biochem. 128 (3): 399-405. doi:10.1093/oxfordjournals.jbchem.a022767. PMID 10965038. ... DAD1, the defender against apoptotic cell death, was initially identified as a negative regulator of programmed cell death in ... one of the bcl-2 protein family". J. Biochem. 128 (3): 399-405. doi:10.1093/oxfordjournals.jbchem.a022767. PMID 10965038. ...
HSPA1A
"Isolation of Bcl-2 binding proteins that exhibit homology with BAG-1 and suppressor of death domains protein". Biochem. Biophys ... This protein is a member of the Hsp70 family. In conjunction with other heat shock proteins, this protein stabilizes existing ... In order to properly fold non-native proteins, this protein interacts with the hydrophobic peptide segments of proteins in an ... As a Hsp70 protein, it has a C-terminal protein substrate-binding domain and an N-terminal ATP-binding domain. The substrate- ...
P53 upregulated modulator of apoptosis
Apoptosis Apoptosome Bcl-2 Bcl-2-associated X protein (BAX) BH3 interacting domain death agonist (BID) Caspases Cytochrome c ... is a pro-apoptotic protein, member of the Bcl-2 protein family. In humans, the Bcl-2-binding component 3 protein is encoded by ... The PUMA protein is part of the BH3-only subgroup of Bcl-2 family proteins. This group of proteins only share sequence ... such as Bcl-2 and Bcl-xL. Structural analysis has shown that PUMA directly binds to antiapoptotic Bcl-2 family proteins via an ...
Caspase-activated DNase
2007). "Large-scale mapping of human protein-protein interactions by mass spectrometry". Molecular Systems Biology. 3 (1): 89. ... Cell apoptotic death is a process executed by cysteine proteases that allows the animals to keep their homeostasis, also ... "Apoptosis initiated by Bcl-2-regulated caspase activation independently of the cytochrome c/Apaf-1/caspase-9 apoptosome". ... It also depends on the activity of a protein or a common signal. The factor that seems to induce more cell differentiation is ...
Galectin-9
... factor-related apoptosis-inducing ligand activates a lysosomal pathway of apoptosis that is regulated by Bcl-2 proteins". The ... an interaction with CD40 on T-cells induced their proliferation inhibition and cell death. Galectin-9 also has important ... The protein has N- and C- terminal carbohydrate-binding domains connected by a link peptide. Multiple alternatively spliced ... Galectin-9 was first isolated from mouse embryonic kidney in 1997 as a 36 kDa beta-galactoside lectin protein. Human galectin-9 ...
GLI2
The anti-apoptotic protein BCL-2 is up regulated by Gli2 and, to a lesser extent, Gli1 - but not Gli3, which may lead to ... This phenotype includes failure to thrive, early death, and a distended gut although no tumors form in transgenic Gli1-/- and ... Zinc finger protein GLI2 also known as GLI family zinc finger 2 is a protein that in humans is encoded by the GLI2 gene. The ... Gli2+protein at the US National Library of Medicine Medical Subject Headings (MeSH) GLI2+protein,+human at the US National ...
Erinna Lee
Lee's research focuses on cell death and survival, and in particular the role of the BCL-2 protein and its associated homolog ... This is typically via characterising protein-protein interactions in the BCL-2 signalling pathway via structural ... It was during this PhD where she began research on programmed cell death, which would form a large part of her subsequent ... She then applies this information to animal models to understand the contributions of these proteins to normal physiology and ...
BCL2L13
Bcl-rambo is a member of the Bcl-2 family of proteins that regulate apoptosis. In cells, Bcl-rambo is localized to the ... death receptor' (FLIP, FADD-DN) or the 'mitochondrial' pro-apoptotic pathway (Bcl-x(L)) had no effect. Bcl-rambo mediates ... such as Bcl-rambo beta. As a member of the Bcl-2 protein family, Bcl-rambo comprises four conserved BH domains and a ... This gene encodes a mitochondrially-localized protein which is classified under the Bcl-2 protein family. Overexpression of the ...
Prostate cancer
In 2010, prostate cancer resulted in 256,000 deaths, up from 156,000 deaths in 1990. Rates of prostate cancer vary widely. ... Transport protein ZIP1 is responsible for the transport of zinc into prostate cells. One of zinc's important roles is to change ... The upregulation of BCL-2 after androgen ablation in prostate carcinoma cell lines and in a castrated-male rat model further ... The lower death rates reported with surgery appear to occur because surgery is more likely to be offered to younger men with ...
AP-1 transcription factor
"Protein kinase C-theta-mediated signals enhance CD4+ T cell survival by up-regulating Bcl-xL". Journal of Immunology. 176 (11 ... Shaulian E, Karin M (May 2002). "AP-1 as a regulator of cell life and death". Nature Cell Biology. 4 (5): E131-6. doi:10.1038/ ... Masuda A, Yoshikai Y, Kume H, Matsuguchi T (November 2004). "The interaction between GATA proteins and activator protein-1 ... "Human cytomegalovirus IE1 protein activates AP-1 through a cellular protein kinase(s)". The Journal of General Virology. 80 ( ...
Belimumab
... who jointly published a paper detailing their findings in May 1999 and named the protein TALL-1. The same protein was named ... Because belimumab is an immunosuppressant, more serious infections and deaths were reported among patients treated with the ... levels of Bcl-2, a survival factor, are increased. When all three BAFF receptors are stimulated, levels of NF kappa B, which ... BR3-Fc, a recombinant fusion protein built with the extracellular ligand-binding portion of BAFF-R, blocks activation of this ...
Nuclear receptor 4A1
In addition, subcellular localization of the NR4A1 protein appears to play a key role in the survival and death of cells. ... Nuclear receptor 4A1 has been shown to interact with: AKT1, Bcl-2, HIF1A, Nuclear receptor co-repressor 2, Promyelocytic ... Lee MO, Kang HJ, Cho H, Shin EC, Park JH, Kim SJ (November 2001). "Hepatitis B virus X protein induced expression of the Nur77 ... 2000). "TR3 death receptor expression in the normal and ischaemic brain". Neuroscience. 96 (1): 147-160. doi:10.1016/S0306-4522 ...
Calcineurin
"Association of protein kinase A and protein phosphatase 2B with a common anchoring protein". Science. 267 (5194): 108-11. ... Shibasaki F, McKeon F (1995). "Calcineurin functions in Ca(2+)-activated cell death in mammalian cells". J. Cell Biol. 131 (3 ... "Suppression of signalling through transcription factor NF-AT by interactions between calcineurin and Bcl-2". Nature. 386 (6626 ... Calcineurin (CaN) is a calcium and calmodulin dependent serine/threonine protein phosphatase (also known as protein phosphatase ...
Anticancer gene
E4orf4 partners mainly with protein phosphatase 2A (PP2A) and Src kinases to induce cell death. Modeling of this protein ... Noxa, isolated from mice, is a member of the Bcl-2 family and is able to regulate cell death through a variety of intracellular ... This protein binds to anti-apoptotic proteins resulting in these proteins' inhibition. As a p53 inducible gene, NOXA is ... NS1 is considered a regulatory protein due to its activity in transcription, translation, and protein-protein interactions, ...
Unfolded protein response
CHOP causes downregulation of the anti-apoptotic mitochondrial protein Bcl-2, favouring a pro-apoptotic drive at the ... March 2016). "Dengue-induced autophagy, virus replication and protection from cell death require ER stress (PERK) pathway ... An important example is that the proapoptotic protein CHOP (CCAAT/-enhancer-binding protein homologous protein), is upregulated ... exposed hydrophobic residues of the misfolded protein are bound by the protein glucose regulate protein 78 (Grp78), a heat ...
Chronic lymphocytic leukemia
It represents less than 1% of deaths from cancer. Most people are diagnosed as having CLL based on the result of a routine ... Smudge cells are due to cancer cells lacking in vimentin, a type of cytoskeleton proteins which is a structural component in a ... Targeted drugs used in CLL include venetoclax (a Bcl-2 inhibitor), ibrutinib (a Bruton's tyrosine kinase inhibitor), idelalisib ... In 2021, the estimated incidence of CLL in the United States is 21,250 new cases and 4,320 deaths. The disease most commonly ...
MicroRNA 148a
Zhang H, Li Y, Huang Q, Ren X, Hu H, Sheng H, Lai M (2011). "MiR-148a promotes apoptosis by targeting Bcl-2 in colorectal ... that can be either protein-coding or non-coding. The primary transcript is cleaved by the Drosha ribonuclease III enzyme to ... cancer". Cell Death Differ. 18 (11): 1702-10. doi:10.1038/cdd.2011.28. PMC 3190106. PMID 21455217. Kulkarni S, Savan R, Qi Y, ...
Tyrosine-protein kinase BLK
1998). "Blk, a BH3-containing mouse protein that interacts with Bcl-2 and Bcl-xL, is a potent death agonist". J. Biol. Chem. ... "The protein product of the c-cbl protooncogene is the 120-kDa tyrosine-phosphorylated protein in Jurkat cells activated via the ... microtubule-associated protein kinase, GTPase-activating protein, and phosphatidylinositol 3-kinase". Mol. Cell. Biol. 13 (9): ... Tyrosine-protein kinase BLK, also known as B lymphocyte kinase, is a non-receptor tyrosine kinase that in humans is encoded by ...
DLC1
... is responsible for inducing programmed cell death by at least two mechanisms: caspase-3-mediated apoptosis and Bcl-2 ... DLC1 also performs a second pro-apoptotic function: it reduces cellular levels of the anti-apoptotic protein Bcl-2. ... In tumor cells which are not expressing DLC1, Bcl-2 levels remain high and the ratio of Bax/Bcl-2 low, so apoptosis is ... Deleted in Liver Cancer 1 also known as DLC1 and StAR-related lipid transfer protein 12 (STARD12) is a protein which in humans ...
Fas ligand
BH-3 only members of the Bcl-2 family engage exclusively anti-apoptotic members of the family (Bcl-2, Bcl-xL), allowing Bak and ... This allows the adaptor molecule Fas-associated death domain (FADD) to bind the death domain of Fas through its own death ... Fas ligand (FasL or CD95L or CD178) is a type-II transmembrane protein that belongs to the tumor necrosis factor (TNF) family. ... namely Bcl-2 and Bcl-xL) to protect from Fas-mediated apoptosis. Characterized Type 1 cells include H9, CH1, SKW6.4, and SW480 ...
AIFM2
... also known as apoptosis-inducing factor-homologous mitochondrion-associated inducer of death (AMID), is a protein that in ... AIFM2 is not inhibited by Bcl-2. AIFM2 can also bind the following coenzymes: 6-hydroxy-FAD, Flavin adenine dinucleotide (FAD ... The expression of this gene is also found to be induced by tumor suppressor protein p53 in colon cancer cells. The protein ... This protein is a flavoprotein that functions as an NAD(P)H-dependent oxidoreductase and induces caspase- and p53-independent ...
S100A10
Hsu SY, Kaipia A, Zhu L, Hsueh AJ (Nov 1997). "Interference of BAD (Bcl-xL/Bcl-2-associated death promoter)-induced apoptosis ... S100 calcium-binding protein A10 (S100A10), also known as p11, is a protein that is encoded by the S100A10 gene in humans and ... Hsu SY, Kaipia A, Zhu L, Hsueh AJ (Nov 1997). "Interference of BAD (Bcl-xL/Bcl-2-associated death promoter)-induced apoptosis ... The S100 protein is implicated in exocytosis and endocytosis by reorganization of F-actin. The p11 protein is linked with the ...
Beth Levine (physician)
... and later went on to directly associate this gene with the protein Bcl-2. This association provided significant implications in ... 2020 deaths, Women microbiologists, 20th-century American women scientists, 21st-century American women scientists, Weill ... showing how the herpes simplex virus type-1 expressed a protein that blocked Beclin 1 activity. She was also able to show a ... of internal medicine and microbiology at the University of Texas Southwestern Medical Center up until the time of her death. ...
Forkhead box protein O1
Additionally, FOXO1 trans-activate Bim protein, which a member of the Bcl-2 family that promotes apoptosis and plays a role in ... Further, it was revealed that DNA damage-induced cell death in p53-deficient and p53-proficient cells was reduced when human ... Forkhead box protein O1 (FOXO1), also known as forkhead in rhabdomyosarcoma (FKHR), is a protein that in humans is encoded by ... "DAF-16 recruits the CREB-binding protein coactivator complex to the insulin-like growth factor binding protein 1 promoter in ...
MOAP1
This protein contains a Bcl-2 homology 3 (BH3)-like motif, which is required for the association with BAX. When overexpressed, ... 2005). "The tumor suppressor RASSF1A and MAP-1 link death receptor signaling to Bax conformational change and cell death". Mol ... Modulator of apoptosis 1 is a protein that in humans is encoded by the MOAP1 gene. The protein encoded by this gene was ... 2006). "A protein-protein interaction network for human inherited ataxias and disorders of Purkinje cell degeneration". Cell. ...
CDKN1B
Because hair cell death in the human cochlea is a major cause of hearing loss, the CDKN1B protein could be an important factor ... Youn CK, Cho HJ, Kim SH, Kim HB, Kim MH, Chang IY, Lee JS, Chung MH, Hahm KS, You HJ (2005). "Bcl-2 expression suppresses ... It encodes a protein which belongs to the Cip/Kip family of cyclin dependent kinase (Cdk) inhibitor proteins. The encoded ... Degradation of the p27 protein occurs as cells exit quiescence and enter G1. Protein levels continue to fall rapidly as the ...
Giardiasis
... substantial downregulation of the anti-apoptotic protein Bcl-2 and upregulation of the proapoptotic protein Bax. These ... Arginine starvation is known to be a cause of programmed cell death, and local removal is a strong apoptotic agent. Host ... They are targeting: recombinant proteins, DNA vaccine, variant-specific surface proteins (VSP), cyst wall proteins (CWP), ... This occurs after the disruption of proteins that connect brush border endothelial cells to one another. The result is ...
BAG domain
The proteins have anti-apoptotic activity and increase the anti-cell death function of BCL-2 induced by various stimuli. BAG-1 ... BAG domains are protein domains found in proteins which are modulators of chaperone activity, they bind to HSP70/HSC70 proteins ... The BAG domain is a conserved region located at the C terminus of the BAG-family proteins that binds the ATPase domain of Hsc70 ... Doong H, Vrailas A, Kohn EC (December 2002). "What's in the 'BAG'?--A functional domain analysis of the BAG-family proteins". ...
P21
"Towards a proteome-scale map of the human protein-protein interaction network". Nature. 437 (7062): 1173-8. Bibcode:2005Natur. ... However p21 may inhibit apoptosis and does not induce cell death on its own. The ability of p21 to inhibit apoptosis in ... role of bcl-2, and the cyclin dependent kinase inhibitors P27 and P21". Leuk. Lymphoma. 43 (1): 51-7. doi:10.1080/ ... This protein is encoded by the CDKN1A gene located on chromosome 6 (6p21.2) in humans. p21 is a potent cyclin-dependent kinase ...
Glucocorticoid
... and phosphorylates a protein that in turn displaces an adaptor protein from a receptor important in inflammation, epidermal ... The exact mechanism regulating this glucocorticoid sensitivity lies in the Bcl-2 gene. Glucocorticoids also suppress the ... ISBN 978-0-205-23939-9. Sapolsky RM (October 1994). "Glucocorticoids, stress and exacerbation of excitotoxic neuron death". ... and proteins (i.e., adhesion proteins) that promote the immune response. Inhibition of this transcription factor, therefore, ...
BAD-dependent regulation of fuel metabolism and K(ATP) channel activity confers resistance to epileptic seizures
We provide genetic evidence that BAD, a protein with dual functions in apoptosis and glucose metabol … ... bcl-Associated Death Protein Grant support * R01 NS055031-01A1/NS/NINDS NIH HHS/United States ... We provide genetic evidence that BAD, a protein with dual functions in apoptosis and glucose metabolism, imparts reciprocal ...
The discovery from the TRAIL protein and its own death receptors - New dimension in therapeutic targeting of BCL-2 family
The discovery from the TRAIL protein and its own death receptors. * Post author By colinsbraincancer ... The discovery from the TRAIL protein and its own death receptors DR4/5 changed the horizon of cancer research because TRAIL ... Presently, inhibitors from the apoptosis protein, mobile FLICE-like R935788 inhibitory proteins (c-FLIP) and inhibitors of ... The protein kinase mammalian target of rapamycin (mTOR) regulates the phosphorylation → Because of the enhanced metabolic ...
FITC anti-Bcl-2 Antibody anti-Bcl-2 - BCL/10C4
Bcl-2 (B-cell leukemia 2) is an apoptotic protein and a member of the Bcl-2 family containing BH1-4 domains. ... This protein blocks apoptotic death by controlling mitochondrial membrane permeability. Cleavage of Bcl-2 can convert to pro- ... The Bcl-2 protein forms homo- or hetero-dimers with other Bcl-2 family members. Bcl-2 is distributed in the outer mitochondrial ... View All Bcl-2 Reagents Request Custom Conjugation Description. Clone. Applications. Purified anti-Bcl-2. BCL/10C4. WB,IP,ICC, ...
Potent, p53-independent induction of NOXA sensitizes MLL-rearranged B-cell acute lymphoblastic leukemia cells to venetoclax |...
... drugs resulted from auranofin-mediated upregulation of NOXA pro-apoptotic protein and potent induction of apoptotic cell death ... we observed that auranofin orchestrates upregulation of the NOXA-encoding gene Phorbol-12-Myristate-13-Acetate-Induced Protein ... long-term exposure to venetoclax in vivo in a patient-derived xenograft model leads to downregulation of several tumor protein ... Inhibition of anti-apoptotic protein BCL-2 with venetoclax emerged as a promising strategy for this subtype of BCP-ALL, however ...
Plus it
1990) Bcl-2 is an inner mitochondrial membrane protein that blocks programmed cell death. Nature 348:334-336. ... 1992) Prevention of programmed cell death of sympathetic neurons by the bcl-2 proto-oncogene. Science 258:302-304. ... 1995) Cytoskeletal and calcium-binding proteins in the mammalian organ of Corti: cell type-specific proteins displaying ... Although the exact function of these proteins is still unclear, high levels of calcium-binding proteins in neurons and hair ...
Publication Detail
... bcl-2-Associated X Protein; bcl-Associated Death Protein ... Proto-Oncogene Proteins c-bcl-2/genetics; Proto-Oncogene ... Carrier Proteins/genetics; Carrier Proteins/metabolism*; Cerebellum/cytology; Cerebellum/drug effects*; Cerebellum/physiology; ... Proteins c-bcl-2/metabolism*; RNA, Messenger/metabolism*; Rats; Rats, Sprague-Dawley; Research Support, Non-U.S. Govt; ... Doses greater than 1.5 g/kg produced significant decreases in Bcl(2) and significant increases in Bad and Bax mRNA during the 8 ...
Structural Biophysics | NHLBI, NIH
One is the Bcl-2 protein Bax, which is a critical component in programmed cell death. As cell death is activated under a ... can be modulated by other regulatory proteins. The goal is to understand how protein-protein interactions involving CP can ... The proteins that form viral particles are another area of interest for Dr. Tjandra. During viral replication, these proteins ... Bax transforms from a soluble protein in the cytoplasm to a membrane-associated protein that irreversibly promotes cell death. ...
Figure 1 - Immune Cell Apoptosis Prevention as Potential Therapy for Severe Infections - Volume 13, Number 2-February 2007 -...
Fas-associated death domain; FLIP, Fas-associated death domain-like interleukin-1β converting enzyme-like inhibitory protein. ... Trail, tumor necrosis factor-α-related apoptosis-inducing ligand; Bim/Puma, Bcl-2 interacting mediator of cell death/p53- ... Apoptotic pathways of cell death. The extrinsic pathway is mediated by a variety of death receptor ligands, including tumor ... Communication between the pathways exists through cleavage of Bcl-2 interacting domain (Bid) by active caspase-8 to form ...
Ultrasonic Nanoemulsification of Cuminum cyminum Essential Oil and Its | IJN
Bcl-2-family proteins and the role of mitochondria in apoptosis. Curr Opin Cell Biol. 2003;15:691-699. ... 53 Cancer cells have been suppressing apoptosis as exemplified by a few proteins and between cell death and cell proliferation. ... Accelerating progress in the field of cancer treatment has brought down the rate of deaths.19 Optimal therapeutic methods for ... Apoptosis, necrosis, autophagy and cell cycle arrest are diverse pathways through which cells enter the death phase.62 In order ...
New compound shows promise in treating multiple human cancers | WEHI
... has been shown by researchers at the Walter and Eliza Hall Institute and Servier to block a protein that is essential for the ... "BH3 mimetics inhibit a group of proteins known as the pro-survival BCL-2 proteins," he said. "MCL1 is a member of this ... Exploiting cell death pathways in regulatory T cells for cancer immunotherapy. *Exploiting the cell death pathway to fight ... Targeting cell death pathways in tissue Tregs to treat inflammatory diseases. *The cellular and molecular calculation of life ...
Biomarkers Search
3. Critical role of anti-apoptotic Bcl-2 protein phosphorylation in mitotic death.. Eichhorn JM; Sakurikar N; Alford SE; Chu R ... Role of cyclin B1/Cdc2 in mediating Bcl-XL phosphorylation and apoptotic cell death following nocodazole-induced mitotic arrest ... 2. CDK1 switches mitotic arrest to apoptosis by phosphorylating Bcl-2/Bax family proteins during treatment with microtubule ... Mitotic cell death induction by targeting the mitotic spindle with tubulin-inhibitory indole derivative molecules.. Di Cesare E ...
Pathology Research Laboratories | Pathology
We use a multidisciplinary approach to study select pro-apoptotic BCL-2 family proteins. ... Samuel Katz Laboratory. The goal of the Katz Laboratory is to selectively control the cell death machinery for therapeutic ... In particular, we focus on the roles and regulatory mechanisms of histone demethylases from the JARID1/KDM5 protein family. ...
NIOSHTIC-2 Search Results - Full View
Fas-associated protein with death domain (FADD), caspase-8, death receptor 3 (DR3) and BID in apoptotic cells induced by ... In addition, activation of antiapoptotic factors including phospho-Akt (protein kinase B) and Bcl-2 was detected. Further ... Apoptotic cell death induced by metallic nickel particles in JB6 cells is through a caspase-8/AIF mediated cytochrome c- ... Activation of Akt and Bcl-2 may play an important role in preventing cytochrome c release from mitochondria to the cytoplasm ...
Exploring the anti-cancer and anti-inflammatory properties of isothiocyanates, News, University of Otago, Christchurch,...
One of the isothiocyanates was able to trigger apoptosis in cells overexpressing Bcl-2, a protein that is present at high ... and to trigger apoptotic cell death. Some isothiocyanates inhibited MIF at low micromolar concentrations and have therapeutic ... The isothiocyanate had a greater effect on mitochondrial function in cells with Bcl-2, suggesting a mechanism for how it ... bypasses Bcl-2 action. Understanding exactly how this happens could be valuable for the design of new anti-cancer compounds. ...
Frontiers | IL-1β and TNFα Differentially Influence NF-κB Activity and FasL-Induced Apoptosis in Primary Murine Hepatocytes...
These results give first insights into the complex interplay between macrophages and hepatocytes which may influence life/death ... sensitized to FasL-induced caspase-3 activation and cell death. However, when TNFα action was blocked by neutralizing ... sensitized to FasL-induced caspase-3 activation and cell death. However, when TNFα action was blocked by neutralizing ... Whereas TNFα preincubation leads to elevated levels of caspase-3 activity and cell death, pretreatment with IL-1β induces ...
Venetoclax: First Global Approval - PubMed
... is an oral selective inhibitor of the prosurvival protein BCL-2 and therefore restores the apoptotic ability of malignant cells ... BCL-G: 20 years of research on a non-typical protein from the BCL-2 family. Hartman ML, Czyz M. Hartman ML, et al. Cell Death ... Venetoclax (Venclexta™) is an oral selective inhibitor of the prosurvival protein BCL-2 and therefore restores the apoptotic ... Therapeutics targeting Bcl-2 in hematological malignancies. Ruefli-Brasse A, Reed JC. Ruefli-Brasse A, et al. Biochem J. 2017 ...
MeSH Browser
Unphosphorylated Bad protein inhibits the activity of BCL-XL PROTEIN.. Terms. bcl-Associated Death Protein Preferred Term Term ... Proteins [D12.776] * Phosphoproteins [D12.776.744] * bcl-Associated Death Protein [D12.776.744.049] * BRCA1 Protein [D12.776. ... Unphosphorylated Bad protein inhibits the activity of BCL-XL PROTEIN.. Entry Term(s). Bad Protein bcl2-Antagonist of Cell Death ... Apoptosis Regulatory Proteins [D12.644.360.075] * Proto-Oncogene Proteins c-bcl-2 [D12.644.360.075.718] * bcl-Associated Death ...
Pediatric Posttransplant Lymphoproliferative Disease: Overview, Incidence, Risk Factors
... an intracellular protein of the bcl group of proteins that are involved in passive cell death pathways. Polymorphisms in 2 key ... 107] The latent membrane proteins LMP1 and LMP2 are believed to act as oncogenes, allowing B cells to escape cell death and ... Monoclonal proteins, particularly IgM-related proteins, have been reported to appear with greater frequency in serum and urine ... The EBV genome adopts an episomal configuration and expresses proteins such as BCRF1, BARF1 and viral IL-10 that help avoid ...
Venetoclax - LiverTox - NCBI Bookshelf
Venetoclax is an oral selective BCL-2 inhibitor and antineoplastic agent used in the therapy of refractory chronic lymphocytic ... Venetoclax (ven et oh klax) is a small molecule inhibitor of BCL-2, an intracellular protein that inhibits apoptosis. BCL2 is ... Venetoclax binds directly to BCL2 and blocks its antiapoptotic activity, leading to programmed cell death in the malignant B ... Venetoclax is an oral selective BCL-2 inhibitor and antineoplastic agent used in the therapy of refractory chronic lymphocytic ...
2003 NIH Research Festival
Visualizing Signaling by Bcl-2 Family Proteins in vivo. Mariusz Karbowski, Ph.D.. Research Fellow, Biochemistry Section, ... Receptors that signal for cell death (death receptors) may have other. non-apoptotic functions as well. Techniques for ... Death Receptor Signaling: Paradigms and Paradoxes. Richard Siegel, M.D., Ph.D.. Head, Immunoregulation Unit and Investigator, ... Caspase-independent Non-apoptotic HIV-1 Induced Cell Death in CD4+ T Cells. Diane L. Bolton. Predoctoral IRTA, Laboratory of ...
NIMH » Macrophage Infection by HIV: Implications for Pathogenesis and Cure: Day One
... specifically looking at the roles of Bcl-2 family proteins on mitrofusions, both of which are upregulated by TREM1 signaling ... will targeted inhibition or removal of these proteins result in the death of the infected cell? ... Based on the list of all the proteins, we performed network analysis to see how these proteins would actually interact. This ... We previously demonstrated that silencing TREM1 in HIV-infected macrophages will add to a decrease in Bcl-2 and Bcl-XL ...
Advances in Understanding the Role of Aloe Emodin and Targeted Drug Delivery Systems in Cancer
Cancer is one of the important causes of death worldwide. Despite remarkable improvements in cancer research in the past few ... Besides, a significant reduction in Bcl-2 protein levels and proform caspase-3 and caspase-7 protein expression levels and ... When the cycle works properly, the cycle regulatory proteins control cell growth and induce the death of damaged cells, thus ... upregulation of caspase-3 and Bax protein levels and downregulation of Bcl-2 protein levels in oral mucosa cancer (KB) cells ...
cell death<...
... interest to our group are the mechanisms by which Bcl-2 family proteins and other factors regulate programmed cell death, ... We have shown that anti-apoptotic Bcl-2 family proteins can be converted into killer molecules (Science 278:1966-8, 1997), that ... Defective cell death programs cause disease states. Insufficient cell death underlies human cancer and autoimmune disease, ... Interestingly, cell death regulators also regulate many other cellular processes prior to a death stimulus, including neuronal ...
NIH Director's New Innovator Award Program - 2014 Award Recipients | NIH Common Fund
His Ph.D. work at Harvard Medical School focused on the role of BCL-2 family proteins in regulating cell death in the ... Project Title: Life, Death, and Function: The Primate-Specific Long Non-Coding RNA Transcriptome. Grant ID: DP2-CA196375 ... Her lab utilizes tools from systems biology and tissue engineering to determine how variations in protein expression interact ... At Berkeley Gabriel also collaborated with Andreas Martin to decipher the mechanisms of protein degradation by the 26S ...
Mapping of Structure-Function Peptide Sites on the Human Alpha-fetoprotein Amino Acid Sequence
... or binding of AFP to a Bcl-2 protein could block the rescue/survival signal, resulting in the induction of cell death. A fetal ... Protein-protein and protein-DNA interactions of the nuclear oncoproteins are often mediated through helix-loop-helix and ... protein existing in monomeric, filamentous, and protein-complexed forms. Profilin, also a major intracellular protein, binds ... One could speculate that dimerization or binding of AFP to these signal proteins could blunt the cell-death signal resulting in ...
Nanoparticles of Titanium and Zinc Oxides as Novel Agents in Tumor Treatment: a Review | SpringerLink
Bcl-2, Bcl-xL) proteins, as well as death ligands (FasL), thus promoting the cell apoptosis. Likewise, ERKs promote the cell ... JNK1/2 and p38 MAPKs lead to AP-1-mediated inactivation of anti-apoptotic proteins (Bcl-2 and Bcl-xL), the result of which is ... Cory S, Adams JM (2002) The Bcl-2 family: regulators of the cellular life-or-death switch. Nat Rev Cancer 2(9):647-656 ... Consequently, the dissociation of Beclin 1/Bcl-2 complex, hence the activation of Beclin 1, a pro-autophagic protein, takes ...
A C177536 GDC Property Terminology C104674 Genome-Wide DNA Copy Number The number of DNA sequence copies found over the entire...
... this agent targets and hybridizes with Bcl-2 mRNA and inhibits the expression of Bcl-2 protein. This may induce tumor cell ... blocking its binding to and activation of its receptor programmed cell death protein 1 (PD-1; PDCD1; CD279; programmed death-1 ... Bcl2, a protein involved in regulating programmed cell death, is overexpressed in a wide variety of tumors. It promotes ... p53-HDM2 Protein-protein Interaction Inhibitor APG-115 , therapeutic_agents C1909 therapeutic_agents A C177537 GDC Value ...
Publications - Institute for Bioengineering of Catalonia
Evaluation of the death decision circuits controlled by the BCL-2 family of proteins revealed that FASN inhibition is ... JTD Keywords: activation, apoptosis, bh3 mimetics, cytochrome-c, death, inhibition, metabolism, pathways, venetoclax, Bcl-2 ... We focused on studying the use of BH3 mimetics to specifically inhibit pro-survival BCL-2 family proteins, overwhelm resistance ... accompanied by the upregulation of the pro-death BH3-only proteins BIM, PUMA, and NOXA. Cell death triggered by FASN inhibition ...
Huperzine A ameliorates damage induced by acute myocardial infarction in rats through antioxidant, anti-apoptotic and anti...
In addition, proteins of the Bcl-2 family, such as Bcl-2 and Bax, are considered to play a pivotal role in the regulation of ... Bcl-2 itself acts as a repressor of apoptosis, while another member of the family, Bax, functions as a promoter of cell death ( ... proteins of the Bcl-2 family have been shown to play a central role in the regulation of cellular apoptosis. Bcl-2 is a ... functions as a pro-apoptotic protein (6). These findings suggest that the regulation of caspase-3, Bcl-2 and Bax proteins may ...
ApoptosisAnti-apoptotic proteinsPhosphorylationApoptotic deathMRNAInhibitsVenetoclaxLymphomaMitochondrialCellsReceptorsFamilyOverexpressionBcl21997KinaseTherapeuticIntracellularCleavageAminoInhibitoryRegulationCytoskeletalSerineCellularPathwaysInteractCaspaseCytoplasmActivationGeneReceptorDegradationRatioTumorCheckpointCriticalSurvivalGenesRegulateInductionSuppressionDefectiveDomainCancerTriggerComplexesSuggestsHeterogeneous
Apoptosis26
- We provide genetic evidence that BAD, a protein with dual functions in apoptosis and glucose metabolism, imparts reciprocal effects on metabolism of glucose and ketone bodies in brain cells. (nih.gov)
- Presently, inhibitors from the apoptosis protein, mobile FLICE-like R935788 inhibitory proteins (c-FLIP) and inhibitors of apoptosis proteins (IAPs, including XIAP) are believed to lead to cellular Path resistance. (colinsbraincancer.com)
- Apoptosis regulator proteins, Bcl-2 family, BH1-4 domains. (biolegend.com)
- The extrinsic pathway is mediated by a variety of death receptor ligands, including tumor necrosis factor (TNF) and Fas ligand (FaSL), that trigger apoptosis by binding to cell surface receptors. (cdc.gov)
- 3 Besides, drug resistance due to suppression of apoptosis and expressive levels of anti-apoptotic proteins has intensified in cancer treatment. (dovepress.com)
- 2. CDK1 switches mitotic arrest to apoptosis by phosphorylating Bcl-2/Bax family proteins during treatment with microtubule interfering agents. (nih.gov)
- 10. A novel BH3 mimetic efficiently induces apoptosis in melanoma cells through direct binding to anti-apoptotic Bcl-2 family proteins, including phosphorylated Mcl-1. (nih.gov)
- 13. MJ-29 inhibits tubulin polymerization, induces mitotic arrest, and triggers apoptosis via cyclin-dependent kinase 1-mediated Bcl-2 phosphorylation in human leukemia U937 cells. (nih.gov)
- One of the isothiocyanates was able to trigger apoptosis in cells overexpressing Bcl-2, a protein that is present at high levels in many cancers. (otago.ac.nz)
- Venetoclax (ven et' oh klax) is a small molecule inhibitor of BCL-2, an intracellular protein that inhibits apoptosis. (nih.gov)
- Recently it has become apparent that there are multiple pathways leading to cell death besides classical caspase-mediated apoptosis. (nih.gov)
- Apoptosis and other forms of cell death are required for trimming excess, expired and damaged cells. (hopkinsmedicine.org)
- We are also investigating the contribution of neuronal/glial apoptosis and necrosis as cell death pathways in animal (including transgenic mice) models of acute and progressive neurodegeneration. (hopkinsmedicine.org)
- We also investigate several discrete mechanisms involved in cell death , including the role of nitric oxide as an endogenous messenger, the function of poly (ADP-ribose) polymerase-1 and apoptosis inducing factor in cell death , and how endogenous cell survival mechanisms protect neurons from death. (hopkinsmedicine.org)
- Emphasis is further placed upon homeodomain and apoptosis AA sequence identities given that AFP serves as a fetal, phase-specific protein throughout embryogenesis, histogenesis, and organogenesis. (atlasgeneticsoncology.org)
- In addition, proteins of the Bcl-2 family have been shown to play a central role in the regulation of cellular apoptosis. (spandidos-publications.com)
- DISCUSSION: The higher Bax: Bcl-2 ratio in preterm placenta suggests the sensitivity to apoptosis. (bvsalud.org)
- Bcl-XL is an anti-apoptotic protein which is a member of the Bcl-2 family which are able to form heterodimers, and this is an significant event in the regulation of apoptosis. (neobiolab.com)
- Bcl-xL is the leading monitor of apoptosis/active cell suicide. (neobiolab.com)
- Apoptosis is an evolutionarily conserved form of programmed cell death. (cnrs.fr)
- The ubiquitin-proteasome system plays an important role in the regulation of apoptosis by controlling the level or function of many regulatory proteins. (cnrs.fr)
- TRIM17 induces neuronal apoptosis by promoting the degradation of the anti-apoptotic protein Mcl-1 and by inhibiting the survival factor NFATc4, but also by inhibiting the degradation of pro-apoptotic proteins mediated by other E3 ubiquitin-ligases from the TRIM family: ZSCAN21 by TRIM41 and NFATc3 by TRIM39. (cnrs.fr)
- It is currently unclear whether BCL-2 inhibits autophagy as well as apoptosis in follicular lymphoma (FL) and diffuse large B-cell lymphoma (DLBCL) which frequently express BCL-2 at high levels. (bl.uk)
- We initially found that the BCL-2 inhibitor ABT-737 concurrently induced autophagy and apoptosis in BCL-2HIGH DLBCL cell lines. (bl.uk)
- These results suggest that inhibition of BCL-2 can induce cytoprotective autophagy, but overexpression of BCL-2 alone may increase basal level autophagy by inhibiting apoptosis. (bl.uk)
- DLBCL patients with lower p62 or LC3 expression and higher levels of BCL-2, i.e. active autophagy and inhibited apoptosis, had the worst prognosis. (bl.uk)
Anti-apoptotic proteins2
- Cisplatin upregulated the expression of both death and decoy TRAIL receptors, as well as of TRAF5 and -6, downregulated the anti-apoptotic proteins, Bcl-2, and induced activation of caspases-3, -8 and -9. (nih.gov)
- Cisplatin/Apo2L/TRAIL combination resulted in further downregulation of expression of anti-apoptotic proteins, Bcl-2 and Bcl-xL, as well as an increase in mitochondrial permeability transition and activation of caspases-3, -8, and -10. (nih.gov)
Phosphorylation6
- This protein is modified by ASK1/JNK1, PKC, ERKs, and stress-activated kinase phosphorylation and can be ubiquitinated. (biolegend.com)
- 3. Critical role of anti-apoptotic Bcl-2 protein phosphorylation in mitotic death. (nih.gov)
- 6. Proteomic analysis of annexin A2 phosphorylation induced by microtubule interfering agents and kinesin spindle protein inhibitors. (nih.gov)
- 16. Role of cyclin B1/Cdc2 in mediating Bcl-XL phosphorylation and apoptotic cell death following nocodazole-induced mitotic arrest. (nih.gov)
- A pro-apoptotic protein and member of the Bcl-2 protein family that is regulated by PHOSPHORYLATION . (nih.gov)
- Upon oral administration,gartisertib selectively inhibits ATR activity and blocks the downstream phosphorylation of the serine/threonine protein kinase CHK1. (nih.gov)
Apoptotic death1
- This protein blocks apoptotic death by controlling mitochondrial membrane permeability. (biolegend.com)
MRNA2
- Semi-quantitative reverse transcriptase with polymerase chain reaction (PCR) techniques were used to determine the expression levels of pro-apoptotic factors Bad and Bax, and anti-apoptotic Bcl(2) mRNA. (nih.gov)
- The mRNA and protein expression of Bcl-2, Bax, Cyclin D1, VEGF-A and VEGFR2 was measured by RT-PCR and IHS, respectively. (biomedcentral.com)
Inhibits4
- Unphosphorylated Bad protein inhibits the activity of BCL-XL PROTEIN . (nih.gov)
- SDX7539 binds to and inhibits MetAP2, which prevents MetAP2-mediated signal transduction pathways and results in tumor cell death. (nih.gov)
- For example, we showed that TRIM17 inhibits TRIM28-mediated ubiquitination and degradation of the anti-apoptotic protein BCL2A1, thereby promoting the survival of BCL2A1-dependent cells, including chemotherapy-resistant melanoma cells (Lionnard et al. (cnrs.fr)
- TRIM17 overexpression in Neuro2A cells inhibits the interaction between the endogenous proteins TRIM39 and NFATc3 assessed by proximity ligation assay. (cnrs.fr)
Venetoclax6
- Inhibition of anti-apoptotic protein BCL-2 with venetoclax emerged as a promising strategy for this subtype of BCP-ALL, however, lack of sufficient responses in preclinical models and the possibility of developing resistance exclude using venetoclax as monotherapy. (nature.com)
- Using RNA-seq, we observed that long-term exposure to venetoclax in vivo in a patient-derived xenograft model leads to downregulation of several tumor protein 53 ( TP53 )-related genes. (nature.com)
- Venetoclax (Venclexta™) is an oral selective inhibitor of the prosurvival protein BCL-2 and therefore restores the apoptotic ability of malignant cells. (nih.gov)
- Venetoclax: Bcl-2 inhibition for the treatment of chronic lymphocytic leukemia. (nih.gov)
- Venetoclax is an oral selective BCL-2 inhibitor and antineoplastic agent used in the therapy of refractory chronic lymphocytic leukemia (CLL). (nih.gov)
- Venetoclax binds directly to BCL2 and blocks its antiapoptotic activity, leading to programmed cell death in the malignant B cells. (nih.gov)
Lymphoma2
- Analysis of apoptotic signalling pathways reveals that TL-77 down-regulates expression of B-cell lymphoma 2 (Bcl-2) family proteins [Bid (BH3 interacting-domain death agonist), Bcl-xl (B-cell lymphoma-extra large) and Mcl-1 (induced myeloid leukaemia cell differentiation protein)] and stimulates caspase activation. (nottingham.ac.uk)
- In summary, this study demonstrates that FL, characterised by overexpression of BCL-2, shows increased autophagy activity, indicating that BCL-2 may not inhibit basal level autophagy in this indolent lymphoma. (bl.uk)
Mitochondrial5
- Bcl-2 is distributed in the outer mitochondrial membrane, the nuclear envelope, and the endoplasmic reticulum. (biolegend.com)
- The isothiocyanate had a greater effect on mitochondrial function in cells with Bcl-2, suggesting a mechanism for how it bypasses Bcl-2 action. (otago.ac.nz)
- Interestingly, cell death regulators also regulate many other cellular processes prior to a death stimulus, including neuronal activity, mitochondrial dynamics and energetics. (hopkinsmedicine.org)
- In addition, Bcl-2 family proteins have normal physiological roles in regulating mitochondrial fission/fusion and mitochondrial energetics to facilitate neuronal activity in healthy brains. (hopkinsmedicine.org)
- Bcl-XL is a transmembrane protein located in the mitochondrial membranes of cells that are long-lived and postmitotic, such as adult brain cells. (neobiolab.com)
Cells17
- The discovery from the TRAIL protein and its own death receptors DR4/5 changed the horizon of cancer research because TRAIL specifically kills cancer cells. (colinsbraincancer.com)
- PN9) would not be expected to demonstrate alterations in these apoptotic proteins since the Purkinje cells no longer demonstrate vulnerability to ethanol. (nih.gov)
- Of many epithelial, neuronal, and glial markers, we found that calcium-binding protein antibodies recognizing calretinin, calmodulin, or parvalbumin labeled immature hair cells in rat vestibular end organs. (jneurosci.org)
- The Servier compound - S63845 - targets a protein of the BCL2 family, called MCL1, which is essential for the sustained survival of these cancer cells. (edu.au)
- MCL1 is important for many cancers because it is a pro-survival protein that allows the cancerous cells to evade the process of programmed cell death that normally removes cancer cells from the body," Associate Professor Lessene said. (edu.au)
- Walter and Eliza Hall Institute researchers revealed the role of BCL-2 in cancer more than 28 years ago and the essential role of MCL1 for the survival of malignant cells four years ago. (edu.au)
- 5. 6,7-Dimethoxy-3-(3-methoxyphenyl)isoquinolin-1-amine induces mitotic arrest and apoptotic cell death through the activation of spindle assembly checkpoint in human cervical cancer cells. (nih.gov)
- Western-blot analysis showed an activation of proapoptotic factors including Fas (CD95), Fas-associated protein with death domain (FADD), caspase-8, death receptor 3 (DR3) and BID in apoptotic cells induced by metallic nickel particles. (cdc.gov)
- Apoptotic cell death induced by metallic nickel particles in JB6 cells is through a caspase-8/AIF mediated cytochrome c-independent pathway. (cdc.gov)
- Whereas TNFα preincubation leads to elevated levels of caspase-3 activity and cell death, pretreatment with IL-1β induces increased caspase-3 activity but keeps cells alive. (frontiersin.org)
- Techniques for visualizing cell death signaling in real-time in living cells has enhanced our understanding of these pathways. (nih.gov)
- Due to the rapid and active growth processes of tumor cells, cancer ranks second among the diseases that cause death worldwide [ 4 ]. (hindawi.com)
- We have reported that many insults can trigger cells to activate a cellular death pathway (Nature, 361:739-742, 1993), that several viruses encode proteins to block attempted cell suicide (Proc. (hopkinsmedicine.org)
- BCL-XL is involved in the survival of cancer cells. (neobiolab.com)
- In addition, in melanoma cells, TRIM17 favors cell survival and chemotherapy resistance by inhibiting TRIM28-mediated degradation of the anti-apoptotic and oncogenic protein BCL2A1. (cnrs.fr)
- Blocking autophagy degradation with chloroquine sensitised BCL-2HIGH cells to ABT-737-induced cell death, indicating that acquired autophagy acts as a cytoprotective mechanism in these cells. (bl.uk)
- It interacts with the E1B 19 kDa protein, which protects cells from virally-induced cell death. (nih.gov)
Receptors4
- Receptors that signal for cell death (death receptors) may have other non-apoptotic functions as well. (nih.gov)
- We believe it is mediated by excitotoxic cell death resulting from abnormalities in excitatory glutamatergic signal transduction pathways, including glutamate transporters and glutamate receptors as well as their downstream intracellular signaling molecules. (hopkinsmedicine.org)
- The multiple molecular variant forms of AFP are discussed in relation to published reports of AFP binding proteins and cell surface receptors. (atlasgeneticsoncology.org)
- AFP AA sequences are further presented as peptide identification sites for growth factors, receptors, cytoskeletal proteins, and chemokines. (atlasgeneticsoncology.org)
Family11
- Bcl-2 (B-cell leukemia 2) is an apoptotic protein and a member of the Bcl-2 family containing BH1-4 domains. (biolegend.com)
- The Bcl-2 protein forms homo- or hetero-dimers with other Bcl-2 family members. (biolegend.com)
- Furthermore, ethanol acts to prevent the reception of this trophic signaling resulting in the execution of the apoptotic pathway that includes specific alterations of proteins in the Bcl2 gene family. (nih.gov)
- MCL1 is a member of this protein family, and inhibiting it activates the process of programmed cell death. (edu.au)
- We use a multidisciplinary approach to study select pro-apoptotic BCL-2 family proteins. (yale.edu)
- Of particular interest to our group are the mechanisms by which Bcl-2 family proteins and other factors regulate programmed cell death , particularly in the nervous system, in cancer and in virus infections. (hopkinsmedicine.org)
- We have shown that anti-apoptotic Bcl-2 family proteins can be converted into killer molecules (Science 278:1966-8, 1997), that Bcl-2 family proteins interact with regulators of caspases and regulators of cell cycle check point activation (Molecular Cell 6:31-40, 2000). (hopkinsmedicine.org)
- Bcl-2 is a cytosolic protein and serves as an anti-apoptotic molecule, whereas another member of the family, Bax, functions as a pro-apoptotic protein ( 6 ). (spandidos-publications.com)
- 2013). This anti-apoptotic Bcl-2 family protein plays a critical role in the survival of a myriad of cell types and contributes to tumorigenesis and chemoresistance in a large number of cancers (Mojsa et al. (cnrs.fr)
- 2015). In addition, a series of studies on other TRIM17 partners led us to discribe a novel mode of action: TRIM17 can modulate the level of certain proteins by inhibiting other E3 ubiquitin-ligases of the TRIM family (Figure 1). (cnrs.fr)
- This gene is a member of the BCL2/adenovirus E1B 19 kd-interacting protein (BNIP) family. (nih.gov)
Overexpression1
- 12. Cyclin B1 overexpression induces cell death independent of mitotic arrest. (nih.gov)
Bcl21
- The encoded protein also interacts with E1B 19 kDa-like sequences of BCL2, another apoptotic protector. (nih.gov)
19971
- 94: 690-694, 1997), that cellular anti-death genes can alter the pathogenesis of virus infections (Nature Med. (hopkinsmedicine.org)
Kinase1
- In addition, activation of antiapoptotic factors including phospho-Akt (protein kinase B) and Bcl-2 was detected. (cdc.gov)
Therapeutic1
- The goal of the Katz Laboratory is to selectively control the cell death machinery for therapeutic benefit. (yale.edu)
Intracellular1
- C57BL/6 splenocytes intracellular stained with BCL/10C4 FITC. (biolegend.com)
Cleavage2
- Cleavage of Bcl-2 can convert to pro-apoptotic (by cleavage of BH4 domain). (biolegend.com)
- Communication between the pathways exists through cleavage of Bcl-2 interacting domain (Bid) by active caspase-8 to form truncated Bid (tBid). (cdc.gov)
Amino2
- The atlas further shows AFP as a protein consisting of multiple peptide-cassettes consisting of amino acid (AA) sequence stretches matched to peptide segments on prohormones and biological response modifier proteins. (atlasgeneticsoncology.org)
- Bcl-XL Human Recombinant produced in E.Coli is a single, non-glycosylated polypeptide chain containing amino acids 1-210.The Bcl-XL is expressed as GST-Tag fusion protein and purified by proprietary chromatographic techniques. (neobiolab.com)
Inhibitory3
- FLIP, Fas-associated death domain-like interleukin-1β converting enzyme-like inhibitory protein. (cdc.gov)
- 19. Mitotic cell death induction by targeting the mitotic spindle with tubulin-inhibitory indole derivative molecules. (nih.gov)
- Consequently, the inhibitory effect of EESP on STAT3 activation resulted in an increase in the pro-apoptotic Bax/Bcl-2 ratio, decrease in the expression of the pro-proliferative Cyclin D1 and CDK4, as well as down-regulation of pro-angiogenic VEGF-A and VEGFR-2 expression. (biomedcentral.com)
Regulation4
- These findings suggest that the regulation of caspase-3, Bcl-2 and Bax proteins may attenuate the cardiac damage occuring in myocardial infarction. (spandidos-publications.com)
- In recent years, we have been interested in the regulation of α-synuclein, a protein whose accumulation plays a crucial role in the death of dopaminergic neurons and the pathogenesis of Parkinson's disease. (cnrs.fr)
- Our current projects focus on this protein, notably the regulation of its expression in various models. (cnrs.fr)
- The BCL-2HIGH cell line Su-DHL4 showed up-regulation of more autophagy machinery genes at both the basal level and following starvation-induced autophagy compared with the BCL-2LOW cell line. (bl.uk)
Cytoskeletal1
- Additionally, in collaboration with colleagues, Dr. Tjandra is studying how the assembly of the cytoskeletal protein actin is regulated. (nih.gov)
Serine1
- A discussion follows in which peptide epitopes, extracellular matrix proteins, serine proteases, extracellular matrix, and cellular adhesion AA identity sites on AFP are considered. (atlasgeneticsoncology.org)
Cellular3
- The goal is to understand how protein-protein interactions involving CP can manage a relatively fast actin polymerization response to cellular stimuli. (nih.gov)
- His lab uses a number of unbiased approaches, including single cell and bulk RNA-Seq and proteomics, in both cell and animal models, as well as cellular imaging to understand how mutations affect protein function. (nih.gov)
- More specifically, they investigate the RNA-binding proteins and noncoding RNAs (lncRNAs, circRNAs, and microRNAs) that govern aging-relevant processes including cellular senescence, myogenesis, and the response to cell damage. (nih.gov)
Pathways2
Interact1
- During viral replication, these proteins assemble and interact with the host membrane to bud off forming infectious particles. (nih.gov)
Caspase3
- Furthermore, Path recruits the adaptor Fas-associated loss of life domain name (FADD) and procaspase-8 to create death-inducing signaling complexes (Disk), which leads to the activation from the initiator caspase-8, resulting in the activation of extrinsic and intrinsic apoptotic signaling downstream of caspase-3 (4,8). (colinsbraincancer.com)
- The treatment of hepatocytes with the BMDM supernatant, which contains both IL-1β and TNFα, sensitized to FasL-induced caspase-3 activation and cell death. (frontiersin.org)
- Furthermore, decreased protein levels of caspase-3 and Bax, and increased levels of Bcl-2 were observed in the infarcted hearts of the rats treated with various concentrations of HupA. (spandidos-publications.com)
Cytoplasm3
- Dr. Tjandra is studying how Bax transforms from a soluble protein in the cytoplasm to a membrane-associated protein that irreversibly promotes cell death. (nih.gov)
- Activation of Akt and Bcl-2 may play an important role in preventing cytochrome c release from mitochondria to the cytoplasm and may also be important in the carcinogenicity of metallic nickel particles. (cdc.gov)
- Phosphorylated STAT3 proteins in the cytoplasm dimerize and translocate to the nucleus where they regulate the expression of genes containing STAT3-binding sites in their promoters [ 12 ]. (biomedcentral.com)
Activation1
- Humanin selectively prevents the activation of pro-apoptotic protein BID by sequestering it into fibers. (nih.gov)
Gene2
- More specifically, we observed that auranofin orchestrates upregulation of the NOXA-encoding gene Phorbol-12-Myristate-13-Acetate-Induced Protein 1 ( PMAIP1 ) associated with chromatin remodeling and increased transcriptional accessibility. (nature.com)
- The hazard ratio (HR) for risk of death was 0.51 and statistically significant only when KRAS and BRAF wild-type pts were compared with pts harboring mutations in one gene. (biomedcentral.com)
Receptor2
- Las vitelogeninas son segregadas en la HEMOLINFA e incorporadas a los OVOCITOS por ENDOCITOSIS mediada por receptor, para formar las principales proteinas de la yema, las VITELINAS. (bvsalud.org)
- Vitellogenins are secreted into the HEMOLYMPH, and taken into the OOCYTES by receptor-mediated ENDOCYTOSIS to form the major yolk proteins, VITELLINS. (bvsalud.org)
Degradation1
- This post-translational modification can have various consequences on protein function, localization, interactions with partners or degradation by the proteasome. (cnrs.fr)
Ratio1
- We further compared the levels of pro-protein convertase, furin between samples having high and low proNGF: mature NGF ratio. (bvsalud.org)
Tumor1
- In order to investigate mechanisms of anti-tumor activity of cisplatin/Apo2L/TRAIL combination, we assessed in detail the molecular effects of cisplatin and Apo2L/TRAIL-activated cell death in two ovarian carcinoma cell lines, OVCAR3 and SKOV3, using cDNA array hybridization, Western blot and flow cytometry. (nih.gov)
Checkpoint1
- The checkpoint proteins p53 and ATM (ataxia telangiectasia mutated) are designed to block DNA replication of damaged DNA until repair of the DNA has been accomplished (Weinert, 1998), and ATM deficiency results in the lack of p53 induction by ionizing radiation, a DNA damaging agent (Barlow et al. (nih.gov)
Critical2
- One is the Bcl-2 protein Bax, which is a critical component in programmed cell death. (nih.gov)
- Like cell division and differentiation, cell death is also critical for normal development and maintenance of healthy tissues. (hopkinsmedicine.org)
Survival3
- BH3 mimetics inhibit a group of proteins known as the 'pro-survival BCL-2 proteins'," he said. (edu.au)
- Bcl-xL has cell death repressor activity and therefore acts as a survival protein. (neobiolab.com)
- High levels of BCL-2 and active autophagy did not affect the clinical outcome of FL, but significantly shortened the survival rates of DLBCL patients. (bl.uk)
Genes1
- In particular, more autophagy machinery genes showed significantly increased expression in both purified and un-purified FL samples, indicating that despite frequently overexpressing BCL-2, FL appears to have increased basal level autophagy activity. (bl.uk)
Regulate2
- Bcl-2 has been reported to regulate cell cycle progression via ROS. (biolegend.com)
- For more than 15 years, our team has been interested in the molecular mechanisms that regulate cell death in neurons. (cnrs.fr)
Induction2
- Synergistic activity of these drugs resulted from auranofin-mediated upregulation of NOXA pro-apoptotic protein and potent induction of apoptotic cell death. (nature.com)
- Autophagy can be inhibited by the anti-apoptotic protein BCL-2 which binds and sequesters the autophagy essential protein Beclin-1, therefore preventing autophagy induction. (bl.uk)
Suppression1
- Implicated in the suppression of cell death. (nih.gov)
Defective1
- Defective cell death programs cause disease states. (hopkinsmedicine.org)
Domain1
- TRIM proteins represent one of the largest classes of E3 ubiquitin-ligases with a RING domain. (cnrs.fr)
Cancer2
- Cancer is one of the important causes of death worldwide. (hindawi.com)
- Insufficient cell death underlies human cancer and autoimmune disease, while excessive cell death underlies human neurological disorders and aging. (hopkinsmedicine.org)
Trigger1
- Emma examined the ability of a library of synthetic isothiocyanates to inhibit the pro-inflammatory cytokine MIF, and to trigger apoptotic cell death. (otago.ac.nz)
Complexes1
- In particular, he wants to improve the ability of NMR to study protein complexes in their proper context, i.e. as part of multi-component systems in complex lipid environments. (nih.gov)
Suggests1
- This work also suggests that calcium-binding proteins are useful markers for studies on inner ear hair cell differentiation and regeneration. (jneurosci.org)
Heterogeneous1
- DLBCL samples (n=109) showed a heterogeneous expression pattern of these four proteins. (bl.uk)
