AnatomyOrganismsChemicals and DrugsPhenomena and Processes
Killer Factors, Yeastbcl-2 Homologous Antagonist-Killer ProteinMycotoxinsKiller Cells, NaturalWhale, KillerKiller Cells, Lymphokine-ActivatedHormone AntagonistsNatural Killer T-CellsDopamine AntagonistsCytotoxicity, ImmunologicExcitatory Amino Acid AntagonistsNeurokinin-1 Receptor AntagonistsNarcotic AntagonistsHistamine H2 AntagonistsInterleukin 1 Receptor Antagonist ProteinDose-Response Relationship, DrugMuscarinic AntagonistsReceptors, Natural Killer Cell
Killer Factors, Yeast
Protein factors released from one species of YEAST that are selectively toxic to another species of yeast.
bcl-2 Homologous Antagonist-Killer Protein
A multi-domain mitochondrial membrane protein and member of the bcl-2 Protein family. Bak protein interacts with TUMOR SUPPRESSOR PROTEIN P53 and promotes APOPTOSIS.
Mycotoxins
Toxic compounds produced by FUNGI.
Killer Cells, Natural
Bone marrow-derived lymphocytes that possess cytotoxic properties, classically directed against transformed and virus-infected cells. Unlike T CELLS; and B CELLS; NK CELLS are not antigen specific. The cytotoxicity of natural killer cells is determined by the collective signaling of an array of inhibitory and stimulatory CELL SURFACE RECEPTORS. A subset of T-LYMPHOCYTES referred to as NATURAL KILLER T CELLS shares some of the properties of this cell type.
Whale, Killer
The species Orcinus orca, in the family Delphinidae, characterized by its black and white coloration, and huge triangular dorsal fin. It is the largest member of the DOLPHINS and derives its name from the fact that it is a fearsome predator.
Killer Cells, Lymphokine-Activated
Cytolytic lymphocytes with the unique capacity of killing natural killer (NK)-resistant fresh tumor cells. They are INTERLEUKIN-2-activated NK cells that have no MAJOR HISTOCOMPATIBILITY COMPLEX restriction or need for antigen stimulation. LAK cells are used for ADOPTIVE IMMUNOTHERAPY in cancer patients.
Hormone Antagonists
Chemical substances which inhibit the function of the endocrine glands, the biosynthesis of their secreted hormones, or the action of hormones upon their specific sites.
Natural Killer T-Cells
A specialized subset of T-LYMPHOCYTES that exhibit features of INNATE IMMUNITY similar to that of NATURAL KILLER CELLS. They are reactive to glycolipids presented in the context of the major histocompatibility complex (MHC) class I-like molecule, CD1D ANTIGEN.
Dopamine Antagonists
Drugs that bind to but do not activate DOPAMINE RECEPTORS, thereby blocking the actions of dopamine or exogenous agonists. Many drugs used in the treatment of psychotic disorders (ANTIPSYCHOTIC AGENTS) are dopamine antagonists, although their therapeutic effects may be due to long-term adjustments of the brain rather than to the acute effects of blocking dopamine receptors. Dopamine antagonists have been used for several other clinical purposes including as ANTIEMETICS, in the treatment of Tourette syndrome, and for hiccup. Dopamine receptor blockade is associated with NEUROLEPTIC MALIGNANT SYNDROME.
Cytotoxicity, Immunologic
The phenomenon of target cell destruction by immunologically active effector cells. It may be brought about directly by sensitized T-lymphocytes or by lymphoid or myeloid "killer" cells, or it may be mediated by cytotoxic antibody, cytotoxic factor released by lymphoid cells, or complement.
Excitatory Amino Acid Antagonists
Drugs that bind to but do not activate excitatory amino acid receptors, thereby blocking the actions of agonists.
Neurokinin-1 Receptor Antagonists
Compounds that inhibit or block the activity of NEUROKININ-1 RECEPTORS.
Narcotic Antagonists
Agents inhibiting the effect of narcotics on the central nervous system.
Histamine H2 Antagonists
Drugs that selectively bind to but do not activate histamine H2 receptors, thereby blocking the actions of histamine. Their clinically most important action is the inhibition of acid secretion in the treatment of gastrointestinal ulcers. Smooth muscle may also be affected. Some drugs in this class have strong effects in the central nervous system, but these actions are not well understood.
Interleukin 1 Receptor Antagonist Protein
A ligand that binds to but fails to activate the INTERLEUKIN 1 RECEPTOR. It plays an inhibitory role in the regulation of INFLAMMATION and FEVER. Several isoforms of the protein exist due to multiple ALTERNATIVE SPLICING of its mRNA.
Dose-Response Relationship, Drug
The relationship between the dose of an administered drug and the response of the organism to the drug.
Muscarinic Antagonists
Drugs that bind to but do not activate MUSCARINIC RECEPTORS, thereby blocking the actions of endogenous ACETYLCHOLINE or exogenous agonists. Muscarinic antagonists have widespread effects including actions on the iris and ciliary muscle of the eye, the heart and blood vessels, secretions of the respiratory tract, GI system, and salivary glands, GI motility, urinary bladder tone, and the central nervous system.
Receptors, Natural Killer Cell
Receptors that are specifically found on the surface of NATURAL KILLER CELLS. They play an important role in regulating the cellular component of INNATE IMMUNITY.

Expression of apoptosis regulatory proteins of the Bcl-2 family and p53 in primary resected non-small-cell lung cancer. (1/716)

Proteins of the Bcl-2 family as well as p53 are important regulators of apoptosis. Alterations in the expression of these proteins can contribute to the formation of cancer, as well as influence tumour response to chemo- and radiotherapy. We used antibodies specific for the human Bcl-2, Mcl-1, Bax, Bak and p53 proteins to examine the expression of these apoptosis-regulating genes in 49 archival specimens of patients with radically resected non-small-cell lung cancer (NSCLC). Tumour cells containing immunostaining for the antiapoptotic proteins Bcl-2 and Mcl-1 were present in 31% and 58% of the cases evaluated, respectively, whereas immunopositivity for the proapoptotic proteins Bax and Bak was found in 47% and 58% of the samples. p53 immunopositivity was detected in 61% of the samples. The expression of Bcl-2 and p53 and the expression of Mcl-1 and Bax showed a positive association (P = 0.02 and P = 0.06 respectively), whereas the expression of Bax was inversely related to p53 (P = 0.008). The expression of Bcl-2 had a negative influence on relapse-free survival in this population of primary resected NSCLC patients (P = 0.02). The expression of p53 and Bcl-2 was significantly associated with metastasis-free survival (P < 0.01). Only patients with p53-positive tumours developed metastases during the follow-up period. Our results establish the frequent expression of the Bcl-2 family proteins Bcl-2, Mcl-1, Bax and Bak in NSCLC. It can be expected that Bcl-2 family members have no straightforward impact on clinical outcome in this disease because their interactions in the regulation of apoptosis are complex.  (+info)

Cell damage-induced conformational changes of the pro-apoptotic protein Bak in vivo precede the onset of apoptosis. (2/716)

Investigation of events committing cells to death revealed that a concealed NH2-terminal epitope of the pro-apoptotic protein Bak became exposed in vivo before apoptosis. This occurred after treatment of human Jurkat or CEM-C7A T-lymphoma cells with the mechanistically disparate agents staurosporine, etoposide or dexamethasone. The rapid, up to 10-fold increase in Bak-associated immunofluorescence was measured with epitope-specific monoclonal antibodies using flow cytometry and microscopy. In contrast, using a polyclonal antibody to Bak, immunofluorescence was detected both before and after treatment. There were no differences in Bak protein content nor in subcellular location before or after treatment. Immunofluorescence showed Bcl-xL and Bak were largely associated with mitochondria and in untreated cells they coimmunoprecipitated in the presence of nonioinic detergent. This association was significantly decreased after cell perturbation suggesting that Bcl-xL dissociation from Bak occurred on exposure of Bak's NH2 terminus. Multiple forms of Bak protein were observed by two dimensional electrophoresis but these were unchanged by inducers of apoptosis. This indicated that integration of cellular damage signals did not take place directly on the Bak protein. Release of proteins, including Bcl-xL, from Bak is suggested to be an important event in commitment to death.  (+info)

Developmental expression patterns of Bcl-2, Bcl-x, Bax, and Bak in teeth. (3/716)

The ontogenic profile of expression of four members of the Bcl-2 family (Bcl-2, Bcl-x, Bax and Bak) was examined in the mouse by immunohistochemistry using paraffin sections. All four members were expressed in changing patterns during critical stages of tooth morphogenesis. Expression was detected in epithelial cell populations including the dental lamina, internal dental epithelium (IDE; differentiating ameloblasts), stratum intermedium and stellate reticulum cells, as well as in the condensed dental mesenchyme. The temporo-spatial localization of the various members of the Bcl-2 family in dental epithelium and mesenchyme showed striking overlapping areas but often their expression patterns differed. In general, contemporaneous co-expression of the Bcl-2 and Bax proteins, and of the Bcl-x and Bak proteins was noted in various types of cells during the developmental process, with the intensity of Bcl-2>Bax and of Bak>Bcl-x. Expression was pronounced at sites where interaction between surface ectoderm and induced mesenchyme takes place, and at the enamel knot, which is regarded as organization/regulating center for tooth development. Around birth, after the structural maturation was accomplished, the expression was down-regulated. The absence of elevated expression of each of these four members of the Bcl-2 family after birth in the teeth suggests that these proteins are relevant during the accomplishment of the basic architecture but not once the structure of the tooth is established.  (+info)

Bak BH3 peptides antagonize Bcl-xL function and induce apoptosis through cytochrome c-independent activation of caspases. (4/716)

The Bcl-2 homology 3 (BH3) domain is crucial for the death-inducing and dimerization properties of pro-apoptotic members of the Bcl-2 protein family, including Bak, Bax, and Bad. Here we report that synthetic peptides corresponding to the BH3 domain of Bak bind to Bcl-xL, antagonize its anti-apoptotic function, and rapidly induce apoptosis when delivered into intact cells via fusion to the Antennapedia homeoprotein internalization domain. Treatment of HeLa cells with the Antennapedia-BH3 fusion peptide resulted in peptide internalization and induction of apoptosis within 2-3 h, as indicated by caspase activation and subsequent poly(ADP-ribose) polymerase cleavage, as well as morphological characteristics of apoptosis. A point mutation within the BH3 peptide that blocks its ability to bind to Bcl-xL abolished its apoptotic activity, suggesting that interaction of the BH3 peptide with Bcl-2-related death suppressors, such as Bcl-xL, may be critical for its activity in cells. While overexpression of Bcl-xL can block BH3-induced apoptosis, treatment with BH3 peptides resensitized Bcl-xL-expressing cells to Fas-mediated apoptosis. BH3-induced apoptosis was blocked by caspase inhibitors, demonstrating a dependence on caspase activation, but was not accompanied by a dramatic early loss of mitochondrial membrane potential or detectable translocation of cytochrome c from mitochondria to cytosol. These findings demonstrate that the BH3 domain itself is capable of inducing apoptosis in whole cells, possibly by antagonizing the function of Bcl-2-related death suppressors.  (+info)

Epstein-Barr virus encodes a novel homolog of the bcl-2 oncogene that inhibits apoptosis and associates with Bax and Bak. (5/716)

The sequenced gammaherpesviruses each contain a single viral bcl-2 homolog (v-bcl-2) which may encode a protein that functions in preventing the apoptotic death of virus-infected cells. Epstein-Barr virus (EBV), a gammaherpesvirus associated with several lymphoid and epithelial malignancies, encodes the v-Bcl-2 homolog BHRF1. In this report the previously uncharacterized BALF1 open reading frame in EBV is identified as having significant sequence similarity to other v-bcl-2 homologs and cellular bcl-2. Transfection of cells with a BALF1 cDNA conferred apoptosis resistance. Furthermore, a recombinant green fluorescent protein-BALF1 fusion protein suppressed apoptosis and associated with Bax and Bak. These results indicate that EBV encodes a second functional v-bcl-2.  (+info)

Developmental regulation of Bcl-2 family protein expression in the involuting mammary gland. (6/716)

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)

Tumor necrosis factor-alpha and lipopolysaccharide induce apoptotic cell death in bovine glomerular endothelial cells. (7/716)

BACKGROUND: The glomerular endothelial cell is a specialized microvascular cell type involved in the regulation of glomerular ultrafiltration. During gram-negative sepsis, glomerulonephritis, and acute renal failure, bacterial lipopolysaccharide (LPS) and tumor necrosis factor-alpha (TNF-alpha) may cause severe cell damage. Our aim was to study and compare the direct effects of TNF-alpha and LPS on the induction of apoptosis in bovine glomerular endothelial cells. METHODS: Primary bovine glomerular endothelial cells were stimulated with TNF-alpha or LPS, and apoptotic cell death was investigated by DNA fragmentation analysis, morphological studies, measurement of cytochrome c efflux and mitochondrial permeability transition, Bak, Bad, Bax, Bcl-2, Bcl-xL protein expression, and caspase-3-like protease activity. RESULTS: TNF-alpha, as well as LPS, elicited apoptotic cell death both time and concentration dependently. Along with DNA ladder formation, we detected the formation of 50 kbp high molecular weight DNA fragments, nuclear condensation, and mitochondrial permeability transition. Concerning all parameters, LPS signaling proved to be more rapid than TNF-alpha. Mechanistically, TNF-alpha-induced cell death was preceded by an efflux of mitochondrial cytochrome c into the cytosol and, subsequently, by a marked increase in the proapoptotic protein Bak and a decrease in the anti-apoptotic Bcl-xL protein content. Comparable but more pronounced effects were seen with LPS. Later, caspase-3-like protease activity was first detectable after 10 hours and was continuously increased up to 24 hours in both TNF-alpha- and LPS-stimulated cells. Correspondingly, we detected an extended cleavage of the nuclear enzyme poly(ADP-ribose) polymerase. Caspase inhibitors Z-Asp-CH2-DCB and Z-VAD-fmk blocked both TNF-alpha- and LPS-induced apoptosis in a comparable manner. Only Z-Asp-CH2-DCB was able to block apoptotic cell death completely. CONCLUSION: Both bacterial LPS and TNF-alpha potently induced apoptotic cell death in glomerular endothelial cells. Direct endotoxin-induced apoptosis may therefore be relevant in the progression of acute renal failure, which is a frequent complication of gram-negative sepsis.  (+info)

Human right and left colon differ in epithelial cell apoptosis and in expression of Bak, a pro-apoptotic Bcl-2 homologue. (8/716)

BACKGROUND: Propensity to colonic neoplasia differs between the right and left colon. AIMS: To examine whether this difference may be related to regional differences in epithelial apoptosis, in expression of a proapoptotic regulatory protein, Bak, and in proliferation. PATIENTS: Individuals with no history of colorectal neoplasia. METHODS: Archival blocks of colorectal tissues were immunostained for proliferating cells (antibody to Ki-67 antigen), and Bak expression (polyclonal antiserum). Cells containing DNA strand breaks, a marker of apoptosis, were identified by terminal deoxyuridine nucleotidyl nick end labelling (TUNEL). RESULTS: There were fewer TUNEL positive epithelial cells in the right colon (mean 1.2 (SE 0.1)% of all epithelial cells) than the left colon (2.2 (0.1)%, p<0.0001) or rectum (2.2 (0.3)%, p<0.05). Bak expression was less common in the right colon (mean 46 (2.3)% of epithelial cells immunoreactive) than the left colon (66 (2.7)%, p<0.0001), or rectum (67 (2.3)%, p<0.001). Bak expression and TUNEL positivity were highly positively correlated (p<0.0001). In contrast to apoptosis, mean whole crypt proliferation labelling index was similar throughout the colorectum (right colon: 15.6 (3.2)%; left colon: 13. 5 (1.2)%; rectum: 13.3 (2.3)%). CONCLUSION: The percentage of proliferating colonic epithelial cells is constant throughout the colon, but fewer epithelial cells undergo Bak mediated apoptosis in the right than in the left colon or rectum. This suggests that colonocytes may be lost by methods other than apoptosis in the right colon.  (+info)

"Killer factors in yeast refer to the ability of certain strains of yeast to produce and release proteins that are lethal to sensitive competing strains of yeast, providing a competitive advantage in their environment."

I cannot find a specific medical term called "killer factors" in the context of yeast. However, there is a phenomenon known as "killer yeasts," where certain strains of yeast produce proteins that can kill other strains of yeast. These proteins are referred to as "killer toxins."

Killer yeasts have been found in various species, including Saccharomyces cerevisiae and Saccharomyces bayanus. The killer toxin produced by these yeasts targets specific receptors on the cell membrane of sensitive yeast cells, leading to ion imbalance, disruption of cellular processes, and eventually cell death.

Therefore, "killer factors" in the context of yeast may refer to the genetic elements or proteins that enable certain strains of yeast to produce killer toxins and kill other sensitive yeast cells.

BAK (Bcl-2 Homologous Antagonist-Killer) protein is a BCL-2 family member, acting as a pro-apoptotic factor that forms oligomers and permeabilizes the mitochondrial outer membrane, thereby facilitating the release of cytochrome c and other apoptogenic factors during programmed cell death.

BAK (Bcl-2 Homologous Antagonist-Killer) protein is a member of the Bcl-2 family, which consists of proteins that regulate programmed cell death, also known as apoptosis. The Bcl-2 family includes both pro-apoptotic and anti-apoptotic members, and their interactions play a crucial role in determining whether a cell lives or dies.

BAK is a pro-apoptotic protein that forms oligomers and creates pores in the outer mitochondrial membrane, leading to the release of cytochrome c and other pro-apoptotic factors into the cytosol. This triggers a cascade of events that ultimately results in cell death.

BAK is kept in an inactive state under normal conditions by binding to anti-apoptotic Bcl-2 family members, such as Bcl-xL and Mcl-1. However, when cells receive signals to undergo apoptosis, the interactions between pro- and anti-apoptotic proteins are disrupted, allowing BAK to become activated and initiate the cell death process.

In summary, BAK is a crucial protein involved in regulating programmed cell death, and its dysregulation has been implicated in various diseases, including cancer and neurodegenerative disorders.

Mycotoxins are toxic secondary metabolites produced by certain types of fungi, which can contaminate food and feed crops, potentially leading to serious health issues in both humans and animals when ingested.

Mycotoxins are toxic secondary metabolites produced by certain types of fungi (molds) that can contaminate food and feed crops, both during growth and storage. These toxins can cause a variety of adverse health effects in humans and animals, ranging from acute poisoning to long-term chronic exposure, which may lead to immune suppression, cancer, and other diseases. Mycotoxin-producing fungi mainly belong to the genera Aspergillus, Penicillium, Fusarium, and Alternaria. Common mycotoxins include aflatoxins, ochratoxins, fumonisins, zearalenone, patulin, and citrinin. The presence of mycotoxins in food and feed is a significant public health concern and requires stringent monitoring and control measures to ensure safety.

Natural Killer cells are a type of lymphocytes that constitute the innate immune system and are capable of mediating spontaneous cytotoxicity against virus-infected or malignantly transformed cells without needing prior immunization.

Natural Killer (NK) cells are a type of lymphocyte, which are large granular innate immune cells that play a crucial role in the host's defense against viral infections and malignant transformations. They do not require prior sensitization to target and destroy abnormal cells, such as virus-infected cells or tumor cells. NK cells recognize their targets through an array of germline-encoded activating and inhibitory receptors that detect the alterations in the cell surface molecules of potential targets. Upon activation, NK cells release cytotoxic granules containing perforins and granzymes to induce target cell apoptosis, and they also produce a variety of cytokines and chemokines to modulate immune responses. Overall, natural killer cells serve as a critical component of the innate immune system, providing rapid and effective responses against infected or malignant cells.

*Orcinus orca*, also known as the killer whale, is a large marine mammal and the largest species of the dolphin family, characterized by its distinctive black and white body markings, prominent dorsal fin, and intellectual complexity, inhabiting various oceanic regions and known for its hierarchical social structure and predatory behavior towards diverse marine life including fish and other cetaceans.

The term "Killer Whale" is used in medical literature to describe an unusual and very rare phenomenon where a live newborn calf becomes lodged in the birth canal of a female whale (usually a species of baleen whale), leading to potential serious complications such as infection, injury, or even death for the mother if not resolved. This condition is also known as "whale entrapment" or "cesarean delivery candidate." It is not to be confused with the common name of the species Orcinus orca, which are actually the largest species of dolphin and not whales, but are often called "killer whales" due to their size and predatory behavior.

Lymphokine-Activated Killer (LAK) cells are a type of immune cell, specifically natural killer cells, that have been activated and expanded in vitro through exposure to lymphokines, such as interleukin-2, demonstrating enhanced cytotoxicity against various tumor cells.

Lymphokine-activated killer (LAK) cells are a type of immune cell that has been activated to kill certain types of cells, including cancer cells and virus-infected cells. They are called "lymphokine-activated" because they are activated through the action of lymphokines, which are proteins secreted by other immune cells. LAK cells are a type of natural killer (NK) cell, which are a type of white blood cell that plays a role in the body's defense against viruses and cancer.

LAK cells are generated in the laboratory by incubating peripheral blood mononuclear cells (PBMCs), which include lymphocytes and monocytes, with high concentrations of interleukin-2 (IL-2) for several days. This process activates and expands the population of NK cells, resulting in the formation of LAK cells. These activated cells are then able to recognize and kill a wide range of tumor cells and virus-infected cells, regardless of whether they express specific antigens or not.

LAK cell therapy is an experimental form of cancer treatment that involves infusing patients with large numbers of LAK cells in order to enhance their immune response against cancer. While some studies have shown promising results, more research is needed to determine the safety and effectiveness of this approach.

Hormone antagonists are medications that block the action of hormones by binding to their receptors, preventing the hormones from exerting their physiological effects.

Hormone antagonists are substances or drugs that block the action of hormones by binding to their receptors without activating them, thereby preventing the hormones from exerting their effects. They can be classified into two types: receptor antagonists and enzyme inhibitors. Receptor antagonists bind directly to hormone receptors and prevent the hormone from binding, while enzyme inhibitors block the production or breakdown of hormones by inhibiting specific enzymes involved in their metabolism. Hormone antagonists are used in the treatment of various medical conditions, such as cancer, hormonal disorders, and cardiovascular diseases.

Natural Killer T-cells are a type of unconventional T-cells that recognize and respond to lipid antigens presented by CD1d molecules, bridging the innate and adaptive immune responses.

Natural Killer T-cells (NKT cells) are a type of unconventional T-cell that express both T-cell receptors and natural killer cell receptors. They recognize lipid antigens presented by CD1d molecules, which are mainly expressed on the surface of antigen-presenting cells. NKT cells play a crucial role in the immune response against certain infections, cancer cells, and autoimmune diseases. They can quickly produce large amounts of cytokines, such as interferon-gamma and tumor necrosis factor-alpha, upon activation, thereby modulating the immune response and exerting cytotoxic effects on target cells.

Dopamine antagonists are a class of drugs that block the action of dopamine, a neurotransmitter, at various receptor sites in the brain and other parts of the body, used primarily to treat conditions such as psychosis, gastroesophageal reflux disease (GERD), and vomiting.

Dopamine antagonists are a class of drugs that block the action of dopamine, a neurotransmitter in the brain associated with various functions including movement, motivation, and emotion. These drugs work by binding to dopamine receptors and preventing dopamine from attaching to them, which can help to reduce the symptoms of certain medical conditions such as schizophrenia, bipolar disorder, and gastroesophageal reflux disease (GERD).

There are several types of dopamine antagonists, including:

1. Typical antipsychotics: These drugs are primarily used to treat psychosis, including schizophrenia and delusional disorders. Examples include haloperidol, chlorpromazine, and fluphenazine.
2. Atypical antipsychotics: These drugs are also used to treat psychosis but have fewer side effects than typical antipsychotics. They may also be used to treat bipolar disorder and depression. Examples include risperidone, olanzapine, and quetiapine.
3. Antiemetics: These drugs are used to treat nausea and vomiting. Examples include metoclopramide and prochlorperazine.
4. Dopamine agonists: While not technically dopamine antagonists, these drugs work by stimulating dopamine receptors and can be used to treat conditions such as Parkinson's disease. However, they can also have the opposite effect and block dopamine receptors in high doses, making them functionally similar to dopamine antagonists.

Common side effects of dopamine antagonists include sedation, weight gain, and movement disorders such as tardive dyskinesia. It's important to use these drugs under the close supervision of a healthcare provider to monitor for side effects and adjust the dosage as needed.

Immunologic cytotoxicity refers to the damage or destruction of cells, specifically targeted by the immune system, through the action of immune effector mechanisms such as antibody-dependent cellular cytotoxicity (ADCC), complement-mediated lysis, or direct T-cell mediated cytolysis.

Immunologic cytotoxicity refers to the damage or destruction of cells that occurs as a result of an immune response. This process involves the activation of immune cells, such as cytotoxic T cells and natural killer (NK) cells, which release toxic substances, such as perforins and granzymes, that can kill target cells.

In addition, antibodies produced by B cells can also contribute to immunologic cytotoxicity by binding to antigens on the surface of target cells and triggering complement-mediated lysis or antibody-dependent cellular cytotoxicity (ADCC) by activating immune effector cells.

Immunologic cytotoxicity plays an important role in the body's defense against viral infections, cancer cells, and other foreign substances. However, it can also contribute to tissue damage and autoimmune diseases if the immune system mistakenly targets healthy cells or tissues.

Excitatory Amino Acid Antagonists are a class of pharmaceutical compounds that block the actions of excitatory amino acids, such as glutamate and aspartate, at their respective receptor sites, thus inhibiting neurotransmission and reducing neuronal activity in the central nervous system.

Excitatory amino acid antagonists are a class of drugs that block the action of excitatory neurotransmitters, particularly glutamate and aspartate, in the brain. These drugs work by binding to and blocking the receptors for these neurotransmitters, thereby reducing their ability to stimulate neurons and produce an excitatory response.

Excitatory amino acid antagonists have been studied for their potential therapeutic benefits in a variety of neurological conditions, including stroke, epilepsy, traumatic brain injury, and neurodegenerative disorders such as Alzheimer's disease and Parkinson's disease. However, their use is limited by the fact that blocking excitatory neurotransmission can also have negative effects on cognitive function and memory.

There are several types of excitatory amino acid receptors, including N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), and kainite receptors. Different excitatory amino acid antagonists may target one or more of these receptor subtypes, depending on their specific mechanism of action.

Examples of excitatory amino acid antagonists include ketamine, memantine, and dextromethorphan. These drugs have been used in clinical practice for various indications, such as anesthesia, sedation, and treatment of neurological disorders. However, their use must be carefully monitored due to potential side effects and risks associated with blocking excitatory neurotransmission.

Neurokinin-1 Receptor Antagonists are a class of pharmaceutical compounds that block the binding of substance P to its receptor, Neurokinin-1, thereby inhibiting neurogenic inflammation and pain transmission in the nervous system.

Neurokinin-1 (NK-1) receptor antagonists are a class of drugs that block the action of substance P, a neuropeptide involved in pain transmission and inflammation. These drugs work by binding to NK-1 receptors found on nerve cells, preventing substance P from activating them and transmitting pain signals. NK-1 receptor antagonists have been studied for their potential use in treating various conditions associated with pain and inflammation, such as migraine headaches, depression, and irritable bowel syndrome. Some examples of NK-1 receptor antagonists include aprepitant, fosaprepitant, and rolapitant.

Narcotic antagonists are a class of drugs that bind to opioid receptors without activating them, thereby blocking the effects of opioids and reversing or preventing opioid overdose.

Narcotic antagonists are a class of medications that block the effects of opioids, a type of narcotic pain reliever, by binding to opioid receptors in the brain and blocking the activation of these receptors by opioids. This results in the prevention or reversal of opioid-induced effects such as respiratory depression, sedation, and euphoria. Narcotic antagonists are used for a variety of medical purposes, including the treatment of opioid overdose, the management of opioid dependence, and the prevention of opioid-induced side effects in certain clinical situations. Examples of narcotic antagonists include naloxone, naltrexone, and methylnaltrexone.

Histamine H2 Antagonists are a class of medications that block the action of histamine at the H2 receptors, which are primarily found in the stomach and heart, thereby inhibiting gastric acid secretion and reducing symptoms of gastroesophageal reflux disease (GERD) and peptic ulcers.

Histamine H2 antagonists, also known as H2 blockers, are a class of medications that work by blocking the action of histamine on the H2 receptors in the stomach. Histamine is a chemical that is released by the body during an allergic reaction and can also be released by certain cells in the stomach in response to food or other stimuli. When histamine binds to the H2 receptors in the stomach, it triggers the release of acid. By blocking the action of histamine on these receptors, H2 antagonists reduce the amount of acid produced by the stomach, which can help to relieve symptoms such as heartburn, indigestion, and stomach ulcers. Examples of H2 antagonists include ranitidine (Zantac), famotidine (Pepcid), and cimetidine (Tagamet).

Interleukin 1 Receptor Antagonist Protein (IL-1Ra) is a naturally occurring anti-inflammatory cytokine that binds to the interleukin-1 receptor, preventing the binding of IL-1α and IL-1β, thereby inhibiting their pro-inflammatory effects.

Interleukin-1 Receptor Antagonist Protein (IL-1Ra) is a naturally occurring protein that acts as a competitive inhibitor of the interleukin-1 (IL-1) receptor. IL-1 is a pro-inflammatory cytokine involved in various physiological processes, including the immune response and inflammation. The binding of IL-1 to its receptor triggers a signaling cascade that leads to the activation of inflammatory genes and cellular responses.

IL-1Ra shares structural similarities with IL-1 but does not initiate the downstream signaling pathway. Instead, it binds to the same receptor site as IL-1, preventing IL-1 from interacting with its receptor and thus inhibiting the inflammatory response.

Increased levels of IL-1Ra have been found in various inflammatory conditions, such as rheumatoid arthritis, inflammatory bowel disease, and sepsis, where it acts to counterbalance the pro-inflammatory effects of IL-1. Recombinant IL-1Ra (Anakinra) is used clinically as a therapeutic agent for the treatment of rheumatoid arthritis and other inflammatory diseases.

In pharmacology, a dose-response relationship for a drug refers to the correlation between the dosage of a medication administered and the resulting therapeutic or adverse effects, typically depicted as a curve that illustrates the increase in response with escalating doses while also highlighting the potential toxicity at higher dosages.

A dose-response relationship in the context of drugs refers to the changes in the effects or symptoms that occur as the dose of a drug is increased or decreased. Generally, as the dose of a drug is increased, the severity or intensity of its effects also increases. Conversely, as the dose is decreased, the effects of the drug become less severe or may disappear altogether.

The dose-response relationship is an important concept in pharmacology and toxicology because it helps to establish the safe and effective dosage range for a drug. By understanding how changes in the dose of a drug affect its therapeutic and adverse effects, healthcare providers can optimize treatment plans for their patients while minimizing the risk of harm.

The dose-response relationship is typically depicted as a curve that shows the relationship between the dose of a drug and its effect. The shape of the curve may vary depending on the drug and the specific effect being measured. Some drugs may have a steep dose-response curve, meaning that small changes in the dose can result in large differences in the effect. Other drugs may have a more gradual dose-response curve, where larger changes in the dose are needed to produce significant effects.

In addition to helping establish safe and effective dosages, the dose-response relationship is also used to evaluate the potential therapeutic benefits and risks of new drugs during clinical trials. By systematically testing different doses of a drug in controlled studies, researchers can identify the optimal dosage range for the drug and assess its safety and efficacy.

Muscarinic antagonists are a class of drugs that block the action of acetylcholine at muscarinic receptors, which can result in a variety of effects including decreased heart rate, relaxation of smooth muscles, and decreased secretions from exocrine glands.

Muscarinic antagonists, also known as muscarinic receptor antagonists or parasympatholytics, are a class of drugs that block the action of acetylcholine at muscarinic receptors. Acetylcholine is a neurotransmitter that plays an important role in the parasympathetic nervous system, which helps to regulate various bodily functions such as heart rate, digestion, and respiration.

Muscarinic antagonists work by binding to muscarinic receptors, which are found in various organs throughout the body, including the eyes, lungs, heart, and gastrointestinal tract. By blocking the action of acetylcholine at these receptors, muscarinic antagonists can produce a range of effects depending on the specific receptor subtype that is affected.

For example, muscarinic antagonists may be used to treat conditions such as chronic obstructive pulmonary disease (COPD) and asthma by relaxing the smooth muscle in the airways and reducing bronchoconstriction. They may also be used to treat conditions such as urinary incontinence or overactive bladder by reducing bladder contractions.

Some common muscarinic antagonists include atropine, scopolamine, ipratropium, and tiotropium. It's important to note that these drugs can have significant side effects, including dry mouth, blurred vision, constipation, and confusion, especially when used in high doses or for prolonged periods of time.

Natural Killer (NK) cell receptors are germline-encoded surface molecules that play a crucial role in the innate immune system by recognizing and triggering responses against virus-infected or malignantly transformed cells, maintaining homeostasis and surveillance through activating and inhibitory signals.

Natural Killer (NK) cell receptors are a type of cell surface receptors expressed by natural killer cells, which are a crucial component of the innate immune system. These receptors play an essential role in the recognition and elimination of abnormal cells, such as virus-infected or malignantly transformed cells.

There are two major types of NK cell receptors: activating receptors and inhibitory receptors. Activating receptors bind to ligands on the surface of target cells, triggering a signaling cascade that leads to the cytotoxic killing of the abnormal cell. In contrast, inhibitory receptors recognize major histocompatibility complex (MHC) class I molecules on healthy cells and transmit an inhibitory signal, preventing NK cells from attacking normal cells.

The balance between activating and inhibitory signals received by NK cells determines their response to target cells. When the activating signals outweigh the inhibitory ones, NK cells become activated and initiate cytotoxic responses or release cytokines to help coordinate the immune response. Dysregulation of NK cell receptors has been implicated in various diseases, including cancer and autoimmune disorders.

Anti-apoptoticBCL2LymphomaMitochondrialBAK1Proto-oncogene proteinInhibitorsRegulatorKinaseOverexpressionDomain-containInhibitionIntracellular SignalinAccumulation of misfoldedInhibitEndoplasmic reticulumFamilyPeptidesMitochondriaAmino AcidsCaspaseInteractInteractsProteaseMeSHCytoplasmicCytoskeletalInductionSubstancesLeukemiaBindsReceptorInhibitorPathwayCaspasesSurvivalRNAsAntibodiesSerumCellIsoformsOxidationAgonistCells
Anti-apoptotic10
  • The inactive form of BAK1 is maintained by the protein's interactions with VDAC2, Mtx2, and other anti-apoptotic members of the BCL2 protein family. (wikipedia.org)
  • NOXA is able to interact with the anti-apoptotic Bcl-2 protein induced myeloid leukemia cell differentiation protein Mcl-1 (Mcl-1), interfering with the polymerization of apoptosis regulator BAX and Bcl-2 homologous antagonist/killer to trigger the mitochondrial apoptosis pathway ( 14 ). (spandidos-publications.com)
  • Innate Conformational Dynamics Drive Binding Specificity in Anti-Apoptotic Proteins Mcl-1 and Bcl-2. (uchicago.edu)
  • All anti-apoptotic Bcl-2 protein had been targeted via RNA disturbance only or in mixtures of two in major human fibroblasts. (biosemiotics2013.org)
  • These results claim for auto-activation of Bak in the lack of anti-apoptotic Bcl-2 protein and provide proof profound variations in the activation of Bax and Bak. (biosemiotics2013.org)
  • The anti-apoptotic Bcl-2 proteins consist of Bcl-2 Bcl-XL (B-cell lymphoma-extra huge) Bcl-w (Bcl-2-like proteins 2) Mcl-1 (myeloid cell leukemia series 1) and A1 (Bcl-2-related proteins SP-420 A1). (biosemiotics2013.org)
  • Nevertheless these peptides can bind to anti-apoptotic Bcl-2 protein with varying choices.4 As this might neutralize a combined mix of anti-apoptotic protein it could facilitate Bax/Bak activation by activator BH3-only protein. (biosemiotics2013.org)
  • BH3-just protein can bind to anti-apoptotic Bcl-2 protein and upon apoptotic excitement could cause the displacement of the protein from Bax and Bak which might result in the activation of effectors. (biosemiotics2013.org)
  • BH3-peptides produced from Bim and Puma can bind to all or any anti-apoptotic Bcl-2 proteins and its own related proteins exert eliminating upon overexpression whereas Poor Bmf Bet Bik Hrk and Noxa screen binding patterns limited to particular anti-apoptotic Bcl-2 proteins.4 It had been therefore recommended that Bax/Bak activation needs the neutralization/displacement of several anti-apoptotic proteins which might be. (biosemiotics2013.org)
  • IAP proteins interact with and inhibit CASPASES , and they function as ANTI-APOPTOTIC PROTEINS . (lookformedical.com)
BCL26
  • The protein encoded by this gene belongs to the BCL2 protein family. (wikipedia.org)
  • As a member of the BCL2 protein family, BAK1 functions as a pro-apoptotic regulator involved in a wide variety of cellular activities. (wikipedia.org)
  • The Ki67 and BCL2 proteins are known prognostic markers for different types of cancer. (karger.com)
  • A Ki67/BCL2 index based on the relative expression of each protein was divided into low- and high-risk groups using receiver operating characteristic curves. (karger.com)
  • Several isoforms of BCL2-associated X protein occur due to ALTERNATIVE SPLICING of the mRNA for this protein. (lookformedical.com)
  • BCL2 family antagonists, CDK inhibitors) are promising new approaches. (springermedizin.de)
Lymphoma6
  • Activation of AMPK inhibits cell proliferation and induces apoptosis through the inhibition of phosphorylated (p)‑Akt and control of B‑cell lymphoma 2 (Bcl‑2) family members. (nih.gov)
  • The intrinsic pathway is regulated by B-cell lymphoma-2 (Bcl-2) protein family which include proapoptotic effector proteins, proapoptotic BH3-only proteins, and antiapoptotic Bcl-2 proteins. (biomedcentral.com)
  • Additionally, TRPV1 deficiency-induced CREB activation increases the antiapoptotic factor B-cell lymphoma 2 (Bcl-2) gene, which consequently downregulates Bcl-2-associated X (Bax) expression and decreases cleaved caspase-3 and cleaved poly (ADP-ribose) polymerase (PARP), which leads to the prevention of hippocampal apoptosis. (molcells.org)
  • Overexpression of bcl-2 proteins, due to a translocation of the gene, is associated with follicular lymphoma. (uchicago.edu)
  • B-cell lymphoma-2 downregulation is a useful feature supporting a neoplastic phenotype in mature T-cell lymphomas. (uchicago.edu)
  • Mitochondrial apoptosis can be characterized by CALN lack of mitochondrial external membrane integrity as well as the launch of mitochondrial intermembrane space protein especially cytochrome can be governed by protein from the B-cell lymphoma 2 (Bcl-2) family members.2 The Bcl-2 family includes three organizations whose interaction and expression determine cell SP-420 survival. (biosemiotics2013.org)
Mitochondrial5
  • A multi-domain mitochondrial membrane protein and member of the bcl-2 Protein family. (nih.gov)
  • The proteins are found on mitochondrial, microsomal, and NUCLEAR MEMBRANE sites within many cell types. (uchicago.edu)
  • Upon activation Bax and Bak type oligomers in the external mitochondrial membrane and trigger the discharge of cytochrome systems that's isolated mitochondria or liposomes where peptides encompassing the BH3-domains of Bim or Bet ('activator' BH3-just protein) could actually activate Bax. (biosemiotics2013.org)
  • In this cycle, carbonyl pressure can harm mitochondrial proteins and drive further endogenous production of ROS (69).Enhanced mtROS has been demonstrated in a quantity of fibrotic issues, such as pulmonary fibrosis. (namptinhibitor.com)
  • Permeabilization on the outer mitochondrial membrane through apoptosis regulator Bcl-2 linked X (BAX) and/or Bcl-2 homologous antagonist/killer (BAK), or the opening on the mitochondrial permeability transition pore (mPTP) inside the inner mitochondrial membrane top for the release of intrinsic apoptosis-induced elements, for instance cytochrome c, is described to initiate the mitochondrial apoptotic pathway (93, 94). (namptinhibitor.com)
BAK13
  • Bcl-2 antagonist killer 1 (BAK1) is a Bcl-2 family proapoptotic member suggested as a candidate gene for autoimmune diseases. (nih.gov)
  • Bcl-2 homologous antagonist/killer is a protein that in humans is encoded by the BAK1 gene on chromosome 6. (wikipedia.org)
  • BAK1 is a pro-apoptotic Bcl-2 protein containing four Bcl-2 homology (BH) domains: BH1, BH2, BH3, and BH4. (wikipedia.org)
Proto-oncogene protein1
  • A member of the Bcl-2 protein family and homologous partner of C-BCL-2 PROTO-ONCOGENE PROTEIN. (lookformedical.com)
Inhibitors2
  • Matrix metalloproteinases and their tissue inhibitors in comparison to other inflammatory proteins in gastric cancer (GC). (edu.pl)
  • Membrane proteins encoded by the BCL-2 GENES and serving as potent inhibitors of cell death by APOPTOSIS. (uchicago.edu)
Regulator2
  • Adenosine monophosphate‑activated protein kinase (AMPK), the major regulator of energy metabolism, is activated by metabolic stress, including hypoxia and glucose deprivation. (nih.gov)
  • Members of the apoptosis regulator Bcl-2 (Bcl-2) family serve crucial roles in the regulation of apoptotic processes in various cancer cells ( 12 ). (spandidos-publications.com)
Kinase4
  • Ligation of tumor necrosis factor receptor 1 (TNFR1) can cause cell death by caspase 8 or receptor-interacting protein kinase 1 (RIPK1)- and RIPK3-dependent mechanisms. (ox.ac.uk)
  • Epidermal growth factor receptor (EGFR) and B-RAF play a role in regulating the mitogen-activated protein (MAP) kinase pathway which affects cell division, differentiation, and could lead to abnormal cell proliferation [ 14 ]. (biomedcentral.com)
  • The results show that TRPV1 deficiency leads to CREB activation by increasing BDNF levels and promoting phosphorylation of tyrosine receptor kinase B (TrkB), extracellular signal-regulated kinase (ERK), protein kinase B (Akt), and CREB in the hippocampus. (molcells.org)
  • Microvesicles loaded with MCs encoding a thymidine kinase (TK)/nitroreductase (NTR) fusion protein produced prolonged TK-NTR expression in mammary carcinoma cells. (regenerativemedicine.net)
Overexpression1
  • Usually, the predominant methods of apoptosis evasion include inhibition of intrinsic pathway and caspase function, overexpression of antiapoptotic Bcl-2 proteins, and loss of BAX and/or BAK [ 12 ]. (biomedcentral.com)
Domain-contain2
  • In the present work, by mining the transcriptome, we identified a single transcript codifying for a protein, member of the C1q-domain-containing protein family, with a signal peptide followed by two globular C1q (gC1q) domains. (unimore.it)
  • Our gC1q domain-containing protein, called BsC1qDC, is actively transcribed by immunocytes. (unimore.it)
Inhibition2
  • The present study demonstrated that CME induced the release of LDH and apoptosis through its inhibition of p‑Akt to control Bcl‑2 and activate Bax and Bak. (nih.gov)
  • We expected these scaffolds to display anticancer activity via inhibition of BRAF, EGFR, and Bcl-2 and induction of apoptosis through activation of caspases. (biomedcentral.com)
Intracellular Signalin1
  • This family of proteins includes many ONCOGENE PROTEINS as well as a wide variety of classes of INTRACELLULAR SIGNALING PEPTIDES AND PROTEINS such as CASPASES . (lookformedical.com)
Accumulation of misfolded2
  • At the cellular and molecular levels, we found that 18β-GA could significantly reduce the accumulation of misfolded protein in rat lung tissue, inhibit ERS activation, reduce the expression of GRP78, p-PERK, p-eIF2α, and p-NF-κB p65, and increase IκB protein expression. (cjphysiology.org)
  • S1R activation results in reduced toxic accumulation of misfolded proteins, as well as lesser dysfunction in mitochondria (a cell's "powerhouse"), oxidative stress and neuroinflammation, all involved in Rett syndrome. (epiphanyasd.com)
Inhibit1
  • BH3-only proteins inhibit the antiapoptotic Bcl-2 proteins [ 11 ]. (biomedcentral.com)
Endoplasmic reticulum1
  • The protein expression of endoplasmic reticulum stress markers inositol‑requiring enzyme 1α, binding immunoglobulin protein and CCAAT‑enhancer‑binding protein homologous protein were upregulated following treatment with pemetrexed. (spandidos-publications.com)
Family6
  • HN - 2006(1981) BX - Actin-Capping Proteins MH - Actin Depolymerizing Factors UI - D051339 MN - D5.750.78.730.212 MN - D12.776.220.525.212 MS - A family of low MOLECULAR WEIGHT actin-binding proteins found throughout eukaryotes. (nih.gov)
  • Phorbol-12-myristate-13-acetate-induced protein 1 (NOXA), a crucial pro-apoptotic protein in the Bcl-2 family, has been reported to be involved in chemotherapeutic agent-induced apoptosis ( 13 ). (spandidos-publications.com)
  • Loss of BIM in T cells results in BCL-2 family BH3-member compensation but incomplete cell death sensitivity normalization. (uchicago.edu)
  • A member of the myeloid leukemia factor (MLF) protein family with multiple alternatively spliced transcript variants encoding different protein isoforms. (nih.gov)
  • In mammalian cells AIF is released in response to pro-apoptotic protein members of the bcl-2 protein family. (lookformedical.com)
  • It shares a similar domain organisation with C1q/TNF-related proteins 4, the only vertebrate protein family with two gC1q domains. (unimore.it)
Peptides2
  • Peptides produced from the BH3-only protein Poor Bik Hrk Puma or Noxa didn't activate Bax directly. (biosemiotics2013.org)
  • Consequently this band of BH3-just protein has been called 'sensitizer' or 'derepressor' BH3-just protein.3 5 6 7 The immediate activation magic size has received latest support by structural research of activator BH3-domains destined to Bax.8 That study also discovered that the BH3-only peptides used previously lacked a residue that's important in the activation of Bax and the prior results may need to be reconsidered. (biosemiotics2013.org)
Mitochondria3
  • The pro‑apoptotic proteins Bcl‑2‑associated X protein (Bax) and Bcl‑2‑homologous antagonist killer (Bak), are activated by their translocation to mitochondria from the cytosol. (nih.gov)
  • In the present study, the apoptotic effects and influence on mitochondria‑mediated apoptotic proteins of CME in HCT116 cells were assessed. (nih.gov)
  • This protein localizes to mitochondria, and functions to induce apoptosis. (wikipedia.org)
Amino Acids1
  • use AMINO ACIDS, BRANCHED-CHAIN 1979, & KETO ACIDS & VALERATES 1973-1979 MH - 3-Hydroxyanthranilate 3,4-Dioxygenase UI - D050561 MN - D8.811.682.690.416.328 MS - An enzyme that catalyzes the conversion of 3-hydroxyanthranilate to 2-amino-3-carboxymuconate semialdehyde. (nih.gov)
Caspase2
  • An APOPTOSIS-regulating protein that is structurally related to CASPASE 8 and competes with CASPASE 8 for binding to FAS ASSOCIATED DEATH DOMAIN PROTEIN. (lookformedical.com)
  • Two forms of CASP8 and FADD-like apoptosis regulating protein exist, a long form containing a caspase-like enzymatically inactive domain and a short form which lacks the caspase-like domain. (lookformedical.com)
Interact2
  • Third, specific viral proteins interact with other cell proteins or directly transactivate other cell genes to provide additional functions necessary for cell proliferation and immortalization. (clinicalgate.com)
  • Several EBV proteins interact with cellular proteins to activate transcription of viral and cellular genes or to engage signal transduction pathways in the cell. (clinicalgate.com)
Interacts2
  • This protein also interacts with the tumor suppressor P53 after exposure to cell stress. (wikipedia.org)
  • Bak protein interacts with TUMOR SUPPRESSOR PROTEIN P53 and promotes APOPTOSIS . (nih.gov)
Protease1
  • Protein Z/protein Z-dependent protease inhibitor system in loco in human gastric cancer. (edu.pl)
MeSH1
  • Proto-Oncogene Proteins c-bcl-2" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (uchicago.edu)
Cytoplasmic1
  • Beta actins are cytoplasmic proteins ubuquitously expressed in all eukaryotic cells. (thermofisher.com)
Cytoskeletal2
  • AN - coordinate IM with ADENOMA (IM) HN - 2006 BX - Corticotroph Adenoma BX - Pituitary Adenoma, ACTH-Secreting BX - Pituitary Corticotropin-Secreting Adenoma MH - Actin Capping Proteins UI - D051344 MN - D5.750.78.730.32 MN - D12.776.220.525.32 MS - Actin capping proteins are cytoskeletal proteins that bind to the ends of ACTIN FILAMENTS to regulate actin polymerization. (nih.gov)
  • Beta actin is a non-muscle cytoskeletal protein in all human cell types and is involved in cell motility, structure, and integrity. (thermofisher.com)
Induction1
  • Activator BH3-just protein were not necessary for apoptosis induction as apoptosis was unaltered in the lack of all BH3-just protein recognized to activate Bax or Bak straight Bcl-2-interacting mediator of cell loss of life BH3-interacting SP-420 domain loss of life agonist and p53-upregulated modulator of apoptosis. (biosemiotics2013.org)
Substances1
Leukemia1
  • Furthermore, the results demonstrated that the phorbol‑12‑myristate‑13‑acetate‑induced protein 1/induced myeloid leukemia cell differentiation protein Mcl‑1 axis is involved in intrinsic apoptosis induced by pemetrexed. (spandidos-publications.com)
Binds3
  • A hydrophobic groove formed along the C-terminal of α2 to the N-terminal of α5, and some residues from α8, binds the BH3 domain of other BCL-2 proteins in its active form. (wikipedia.org)
  • Arp2-3 complex binds WASP PROTEIN and existing ACTIN FILAMENTS, and it nucleates the formation of new branch point filaments. (nih.gov)
  • HN - 2006 BX - Arp2-3 Complex MH - Actin-Related Protein 3 UI - D051378 MN - D5.750.78.730.246.750 MN - D12.776.220.525.246.750 MS - A component of the Arp2-3 complex that is related in sequence and structure to ACTIN and that binds ATP. (nih.gov)
Receptor6
  • These cell surface receptors include Fas receptor (also known as APO-1 receptor or CD95), TNF-α receptor 1, TNF-related apoptosis-inducing ligand (TRAIL) receptor 1 or 2 and TGF-ß receptor 1 or 2. (medscape.com)
  • Transient receptor potential vanilloid 1 (TRPV1) protein is a Ca 2+ -permeable non-selective cation channel known for its pain modulation pathway. (molcells.org)
  • 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 . (lookformedical.com)
  • Others, such as retinoic acid, renin-angiotensin-aldosterone system, TLR2 (Toll-Like Receptor 2) and leptin, are also important in this process. (preprints.org)
  • JV-1-38), growth hormone receptor antagonists (e.g. pegvisomant), IGF-1R antibodies (e.g. (crenolanibinhibitor.com)
  • Anavex 2-73 (blarcamesine) is an oral investigational therapy developed by Anavex Life Sciences that works by activating the sigma-1 receptor (S1R), a protein involved in the correct folding of other proteins. (epiphanyasd.com)
Inhibitor3
  • The protein class is defined by an approximately 80-amino acid motif called the baculoviral inhibitor of apoptosis repeat. (lookformedical.com)
  • An inhibitor of apoptosis protein that is translated by a rare cap-independent mechanism. (lookformedical.com)
  • Takeda announced that the FDA approved fruquintinib (Fruzaqla)-the only selective inhibitor of VEGF-1, -2, and -3-for adults with previously treated metastatic colorectal cancer regardless of biomarker status. (aacrjournals.org)
Pathway1
  • The expression of proteins in the brain-derived neurotrophic factor (BDNF)/cAMP response element binding protein (CREB) pathway in a 3xTg-AD/TRPV1 transgenic mice model was investigated to better understand the AD regulatory effect of TRPV1 deficiency. (molcells.org)
Caspases1
  • Furthermore, Compounds 7k, 7l, and 7m increased Caspases 3,8 & 9, Cytochrome C and Bax levels and decreased Bcl-2 protein levels. (biomedcentral.com)
Survival1
  • Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer. (uchicago.edu)
RNAs1
  • Eight EBV proteins and several nontranslated RNAs are expressed in latently infected B lymphocytes that have been growth transformed by EBV in vitro ( Table 1 ). (clinicalgate.com)
Antibodies1
  • A total of 26,717 blood samples were collected and tested for SARs-CoV-2 antibodies (anti-S IgG) using a qualitative immunoassay. (bvsalud.org)
Serum1
  • [email protected] high serum insulin-like growth factor 2 (IGF-2) have been particularly found in colorectal cancer, with levels appearing to correlate with tumour load, being higher in metastatic disease [13]. (crenolanibinhibitor.com)
Cell4
  • The cell cycle and apoptosis were evaluated using flow cytometry analysis, and proteins were detected using western blotting. (spandidos-publications.com)
  • Western blot analysis was performed on whole cell extracts (30µg lysate) of A-431 (Lane 1), COS-7 (Lane 2), MDCK (Lane 3), C2C12 (Lane 4), PC-3 (Lane 5), L6 (Lane 6), RSC96 (Lane 7), tissue extracts (30µg lysate) of Mouse Lung (Lane 8), Rat Stomach (Lane 9), Mouse Pancreas (Lane 10) and Rat Brain (Lane 11). (thermofisher.com)
  • Actins are highly conserved proteins that are involved in cell motility, structure and integrity. (thermofisher.com)
  • Although genetic and epigenetic aberrations that occur in components of the central dogma clearly elicit disease development in humans, recent findings also point to a prominent role for non-protein-coding regions of the genome in regulating cell and tissue homeostasis, as well as in contributing to the formation of human tumors. (biomedcentral.com)
Isoforms1
  • Isoforms of this protein exist due to multiple alternative splicing of its MESSENGER RNA. (lookformedical.com)
Oxidation3
  • HN - 2006(1983) MH - 2-Oxoisovalerate Dehydrogenase (Acylating) UI - D050645 MN - D8.811.682.657.350.825 MS - An NAD+ dependent enzyme that catalyzes the oxidation 3-methyl-2-oxobutanoate to 2-methylpropanoyl-CoA. (nih.gov)
  • use ANTHRANILIC ACID 1974-1979 MH - 3-Isopropylmalate Dehydrogenase UI - D050539 MN - D8.811.682.47.500 MS - An NAD+ dependent enzyme that catalyzes the oxidation of 3-carboxy-2-hydroxy-4-methylpentanoate to 3-carboxy-4-methyl-2-oxopentanoate. (nih.gov)
  • mtROS also causes oxidation of lipids and proteins identified in bleomycininduced mouse models of pulmonary fibrosis and in sufferers with IPF (80, 81). (namptinhibitor.com)
Agonist1
  • Hundreds of millions of dollars are being spent in the US to develop a safe sigma-1R agonist (Anavex 2-73). (epiphanyasd.com)
Cells3
  • Each of these viruses encodes proteins important for establishment of latency, transforming cells, and evading the immune system. (clinicalgate.com)
  • Because beta actin is ubiquitously expressed in all eukaryotic cells, it is frequently used as a loading control for assays involving protein detection, such as Western blotting. (thermofisher.com)
  • The central dogma of molecular biology states that the transfer of genetic information within cells transpires sequentially from DNA to RNA to proteins, whose coding sequences comprise a paltry 1.5-2% of the human genome [ 2 , 3 ]. (biomedcentral.com)