bcl-2-Associated X Protein
Trans-Activators
Hepatitis B virus
Hepatitis B Antigens
Carcinoma, Hepatocellular
Proto-Oncogene Proteins c-bcl-2
Bornaviridae
Hepatocytes
Transcriptional Activation
Hep G2 Cells
Apoptosis
Transfection
Fragile X Mental Retardation Protein
Hepatitis B Virus, Woodchuck
Gene Expression Regulation, Viral
DNA-Binding Proteins
Hepatitis B
Marmota
Base Sequence
Transcription, Genetic
Molecular Sequence Data
Borna disease virus
Hepadnaviridae
Promoter Regions, Genetic
Chloramphenicol O-Acetyltransferase
Transcription Factors
X Chromosome
Tumor Suppressor Protein p53
Mutation
Protein Binding
Liver
Group X Phospholipases A2
Blotting, Western
Plasmids
RNA, Messenger
Signal Transduction
Viral Regulatory and Accessory Proteins
Tumor Cells, Cultured
NF-kappa B
Virus Replication
Mice, Transgenic
Amino Acid Sequence
Precipitin Tests
Gene Expression Regulation
Mitochondria
Proto-Oncogene Proteins
Genes, bcl-2
Cell Nucleus
Hepatitis B, Chronic
Binding Sites
Reverse Transcriptase Polymerase Chain Reaction
Hepatitis B Core Antigens
Proteasome Endopeptidase Complex
bcl-X Protein
Up-Regulation
Hepatocyte Nuclear Factor 1
Down-Regulation
Nuclear Proteins
RNA, Small Interfering
CARD Signaling Adaptor Proteins
Two-Hybrid System Techniques
Translocation, Genetic
Cell Survival
Gene Expression Regulation, Neoplastic
RNA Interference
Lymphoma, B-Cell
Caspase 3
Caspases
Enhancer Elements, Genetic
Fragile X Syndrome
Chromosomes, Human, Pair 14
Gene Expression
HeLa Cells
Genes, Reporter
Phosphorylation
Hepatocyte Nuclear Factor 1-alpha
Lymphoma, Large B-Cell, Diffuse
Luciferases
BH3 Interacting Domain Death Agonist Protein
Germinal Center
Recombinant Fusion Proteins
DNA, Complementary
Cyclic AMP Response Element-Binding Protein
Chromosomes, Human, Pair 18
Immunohistochemistry
Factor X
Polymerase Chain Reaction
Real-Time Polymerase Chain Reaction
Cloning, Molecular
DNA Primers
Carrier Proteins
Cell Transformation, Neoplastic
Cell Line, Transformed
Cysteine Endopeptidases
Dietary Proteins
Flow Cytometry
Gene Expression Profiling
Cell Cycle
Cells, Cultured
Restriction Mapping
Multienzyme Complexes
Cytoplasm
Protein Structure, Tertiary
Sequence Homology, Amino Acid
Mice, Knockout
Protein-Serine-Threonine Kinases
Simian virus 40
RNA-Binding Proteins
Drosophila Proteins
Mice, Nude
Protein Biosynthesis
Disease Models, Animal
Repetitive Sequences, Nucleic Acid
Enzyme Activation
Models, Biological
Cell Death
Adaptor Proteins, Signal Transducing
Cell Division
Neoplasm Proteins
Lymphoma, Follicular
Repressor Proteins
B-Lymphocytes
Gene Rearrangement
gamma-Globins
In Situ Hybridization, Fluorescence
Retinoid X Receptors
Lymphoma, B-Cell, Marginal Zone
Chromosomes, Human, Pair 3
Myeloid Cell Leukemia Sequence 1 Protein
Genes, Immunoglobulin Heavy Chain
Precursor Cells, B-Lymphoid
Immunoglobulin Heavy Chains
Proto-Oncogenes
Bacteriophage phi X 174
Genes, myc
Reticulocytosis
Cell Differentiation
Precursor Cells, T-Lymphoid
Neprilysin
Leukemia, Lymphocytic, Chronic, B-Cell
Receptors, Purinergic P2
Fetal Hemoglobin
Sperm Midpiece
Tumor Suppressor Proteins
Cyclin D2
Proto-Oncogene Proteins c-myc
Chromosome Breakage
Gene Rearrangement, B-Lymphocyte
Caspases, Effector
Oligonucleotide Array Sequence Analysis
Interferon Regulatory Factors
Chromosomes, Human, Pair 11
Prognosis
Tumor Markers, Biological
Chromosomal Puffs
Immunophenotyping
Factor X Deficiency
Nuclear Receptor Co-Repressor 2
Antibodies, Monoclonal, Murine-Derived
HEK293 Cells
Jurkat Cells
Genes, Immunoglobulin
Gene Rearrangement, B-Lymphocyte, Heavy Chain
Phenotype
delta-Globins
I-kappa B Kinase
Oncogene Proteins, Fusion
Membrane Proteins
Lymphoma, Non-Hodgkin
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
bcl-2 Homologous Antagonist-Killer Protein
beta-Globins
Polymorphism, Single Nucleotide
Oncogenes
Chromatin Immunoprecipitation
Caspase 7
T-Lymphocytes
Zinc Fingers
Receptors, CXCR5
Bcl-2 regulates amplification of caspase activation by cytochrome c. (1/2563)
Caspases, a family of specific proteases, have central roles in apoptosis [1]. Caspase activation in response to diverse apoptotic stimuli involves the relocalisation of cytochrome c from mitochondria to the cytoplasm where it stimulates the proteolytic processing of caspase precursors. Cytochrome c release is controlled by members of the Bcl-2 family of apoptosis regulators [2] [3]. The anti-apoptotic members Bcl-2 and Bcl-xL may also control caspase activation independently of cytochrome c relocalisation or may inhibit a positive feedback mechanism [4] [5] [6] [7]. Here, we investigate the role of Bcl-2 family proteins in the regulation of caspase activation using a model cell-free system. We found that Bcl-2 and Bcl-xL set a threshold in the amount of cytochrome c required to activate caspases, even in soluble extracts lacking mitochondria. Addition of dATP (which stimulates the procaspase-processing factor Apaf-1 [8] [9]) overcame inhibition of caspase activation by Bcl-2, but did not prevent the control of cytochrome c release from mitochondria by Bcl-2. Cytochrome c release was accelerated by active caspase-3 and this positive feedback was negatively regulated by Bcl-2. These results provide evidence for a mechanism to amplify caspase activation that is suppressed at several distinct steps by Bcl-2, even after cytochrome c is released from mitochondria. (+info)Bcl-2 and Bcl-XL serve an anti-inflammatory function in endothelial cells through inhibition of NF-kappaB. (2/2563)
To maintain the integrity of the vascular barrier, endothelial cells (EC) are resistant to cell death. The molecular basis of this resistance may be explained by the function of antiapoptotic genes such as bcl family members. Overexpression of Bcl-2 or Bcl-XL protects EC from tumor necrosis factor (TNF)-mediated apoptosis. In addition, Bcl-2 or Bcl-XL inhibits activation of NF-kappaB and thus upregulation of proinflammatory genes. Bcl-2-mediated inhibition of NF-kappaB in EC occurs upstream of IkappaBalpha degradation without affecting p65-mediated transactivation. Overexpression of bcl genes in EC does not affect other transcription factors. Using deletion mutants of Bcl-2, the NF-kappaB inhibitory function of Bcl-2 was mapped to bcl homology domains BH2 and BH4, whereas all BH domains were required for the antiapoptotic function. These data suggest that Bcl-2 and Bcl-XL belong to a cytoprotective response that counteracts proapoptotic and proinflammatory insults and restores the physiological anti-inflammatory phenotype to the EC. By inhibiting NF-kappaB without sensitizing the cells (as with IkappaBalpha) to TNF-mediated apoptosis, Bcl-2 and Bcl-XL are prime candidates for genetic engineering of EC in pathological conditions where EC loss and unfettered activation are undesirable. (+info)Constitutive activation of Stat3 signaling confers resistance to apoptosis in human U266 myeloma cells. (3/2563)
Interleukin 6 (IL-6) is the major survival factor for myeloma tumor cells and induces signaling through the STAT proteins. We report that one STAT family member, Stat3, is constitutively activated in bone marrow mononuclear cells from patients with multiple myeloma and in the IL-6-dependent human myeloma cell line U266. Moreover, U266 cells are inherently resistant to Fas-mediated apoptosis and express high levels of the antiapoptotic protein Bcl-xL. Blocking IL-6 receptor signaling from Janus kinases to the Stat3 protein inhibits Bcl-xL expression and induces apoptosis, demonstrating that Stat3 signaling is essential for the survival of myeloma tumor cells. These findings provide evidence that constitutively activated Stat3 signaling contributes to the pathogenesis of multiple myeloma by preventing apoptosis. (+info)In vitro induction of activation-induced cell death in lymphocytes from chronic periodontal lesions by exogenous Fas ligand. (4/2563)
Periodontitis is a chronic inflammatory disease which gradually destroys the supporting tissues of the teeth, leading to tooth loss in adults. The lesions are characterized by a persistence of inflammatory cells in gingival and periodontal connective tissues. To understand what mechanisms are involved in the establishment of chronic lesions, we hypothesized that infiltrating lymphocytes might be resistant to apoptosis. However, both Bcl-2 and Bcl-xL were weakly detected in lymphocytes from the lesions, compared with those from peripheral blood, suggesting that these cells are susceptible to apoptosis. Nevertheless, very few apoptotic cells were observed in tissue sections from the lesions. Lymphocytes from the lesions expressed mRNA encoding Fas, whereas Fas-ligand mRNA was very weakly expressed in lymphocytes from the lesions and in periodontal tissues. Since the results indicated that lymphocytes in the lesions might be susceptible to Fas-mediated apoptosis but lack the death signal, we next investigated if these lymphocytes actually undergo apoptosis by the addition of anti-Fas antibodies in vitro. Fas-positive lymphocytes from the lesions underwent apoptosis by these antibodies, but Fas-negative lymphocytes and Fas-positive peripheral lymphocytes did not undergo apoptosis by these antibodies. These results indicate that lymphocytes in the lesions are susceptible to activation-induced cell death and are induced to die by apoptosis after the addition of exogenous Fas ligand. (+info)Control of apoptosis in Epstein Barr virus-positive nasopharyngeal carcinoma cells: opposite effects of CD95 and CD40 stimulation. (5/2563)
The expression and function of CD95 and CD40 were investigated in malignant cells from EBV-positive undifferentiated nasopharyngeal carcinomas (NPCs). Large amounts of CD95 and CD40 expression were detected in 15 of 16 EBV-positive NPC specimens. In contrast, CD95 was not detected in two biopsies from patients with EBV-negative differentiated NPCs. We tested whether the CD95 apoptotic pathway was functional in NPC cells by treating two EBV-positive NPC tumor lines in vitro with a CD95 agonist. In both cases, NPC cells were extremely susceptible to CD95-mediated apoptosis, despite strong constitutive expression of Bcl-x. Combined CD40 and CD95 stimulation was used to investigate the possible anti-apoptotic activity mediated by CD40. The CD40 receptor was activated by incubating NPC cells with murine L cells producing CD154, the CD40 ligand. This treatment resulted in a strong inhibition of CD95-related cytotoxicity. Such an anti-apoptotic effect of CD40 is well known for B lymphocytes, but has not previously been reported for epithelial cells. These data suggest that NPC tumor-infiltrating lymphocytes, which often produce the CD40 ligand in situ, may increase the survival of malignant cells, thereby enhancing tumor growth in patients. (+info)Role of cytokine signaling molecules in erythroid differentiation of mouse fetal liver hematopoietic cells: functional analysis of signaling molecules by retrovirus-mediated expression. (6/2563)
Erythropoietin (EPO) and its cell surface receptor (EPOR) play a central role in proliferation, differentiation, and survival of erythroid progenitors. Signals induced by EPO have been studied extensively by using erythroid as well as nonerythroid cell lines, and various controversial results have been reported as to the role of signaling molecules in erythroid differentiation. Here we describe a novel approach to analyze the EPO signaling by using primary mouse fetal liver hematopoietic cells to avoid possible artifacts due to established cell lines. Our strategy is based on high-titer retrovirus vectors with a bicistronic expression system consisting of an internal ribosome entry site (IRES) and green fluorescent protein (GFP). By placing the cDNA for a signaling molecule in front of IRES-GFP, virus-infected cells can be viably sorted by fluorescence-activated cell sorter, and the effect of expression of the signaling molecule can be assessed. By using this system, expression of cell-survival genes such as Bcl-2 and Bcl-XL was found to enhance erythroid colony formation from colony-forming unit-erythroid (CFU-E) in response to EPO. However, their expression was not sufficient for erythroid colony formation from CFU-E alone, indicating that EPO induces signals for erythroid differentiation. To examine the role of EPOR tyrosine residues in erythroid differentiation, we introduced a chimeric EGFR-EPOR receptor, which has the extracellular domain of the EGF receptor and the intracellular domain of the EPOR, as well as a mutant EGFR-EPOR in which all the cytoplasmic tyrosine residues are replaced with phenylalanine, and found that tyrosine residues of EPOR are essential for erythroid colony formation from CFU-E. We further analyzed the function of the downstream signaling molecules by expressing modified signaling molecules and found that both JAK2/STAT5 and Ras, two major signaling pathways activated by EPOR, are involved in full erythroid differentiation. (+info)Rubella virus-induced apoptosis varies among cell lines and is modulated by Bcl-XL and caspase inhibitors. (7/2563)
Rubella virus (RV) causes multisystem birth defects in the fetuses of infected women. To investigate the cellular basis of this pathology, we examined the cytopathic effect of RV in three permissive cell lines: Vero 76, RK13, and BHK21. Electron microscopy and the TUNEL assay showed that the cytopathic effect resulted from RV-induced programmed cell death (apoptosis) in all three cell lines, but the extent of apoptosis varied among these cells. At 48 h postinfection, the RK13 cell line showed the greatest number of apoptotic cells, the Vero 76 cell line was approximately 3-fold less, and BHK21 had very few. An increased multiplicity of infection and longer time postinfection were required for the BHK21 cell line to reach the level of apoptotic cells in Vero 76 at 48 h. Purified RV induced apoptosis in a dose-dependent fashion, but not UV-inactivated RV or virus-depleted culture supernatant. Specific inhibitors of the apoptosis-specific proteases caspases reduced RV-induced apoptosis and led to higher levels of RV components in infected cells. To address the role of regulatory proteins in RV-induced apoptosis, the antiapoptotic gene Bcl-2 or Bcl-XL was transfected into RK13 cells. Although a high level of Bcl-2 family proteins was expressed, no protection was observed from apoptosis induced by RV, Sindbis virus, or staurosporine in RK13 cells. In BHK21 cells, however, increased expression of Bcl-XL protected cells from apoptosis. The observed variability in apoptotic response to RV of these cell lines demonstrates that programmed cell death is dependent on the unique properties of each cell and may be indicative of how selective organ damage occurs in a congenital rubella syndrome fetus. (+info)Bcl-2 overexpression results in reciprocal downregulation of Bcl-X(L) and sensitizes human testicular germ cell tumours to chemotherapy-induced apoptosis. (8/2563)
Testicular germ cell tumours are hypersentive to chemotherapy and cell lines derived from these tumours are chemosensitive in vitro. We have previously shown that these cell lines express undetectable levels of the suppressor of apoptosis Bcl-2 and relatively high levels of the apoptosis inducer Bax (Chresta et al., 1996). To determine whether the absence of Bcl-2 in these cell lines makes them highly susceptible to drug-induced apoptosis, Bcl-2 was expressed ectopically in the 833K testicular germ cell tumour cell line. Stable overexpressing clones were isolated and three clones were studied further. Surprisingly, Bcl-2 overexpressing cells were sensitized to chemotherapy-induced apoptosis compared to the parental and vector control cells. Analysis of potential mechanisms of sensitization revealed there was a reciprocal downregulation of the endogenously expressed Bcl-X(L) in the Bcl-2 overexpressing clones. Downregulation of Bcl-X(L) to the same extent using antisense oligonucleotides enhanced etoposide-induced apoptosis by twofold. Our results indicate that Bcl-2 and Bcl-X(L) have different abilities to protect against chemotherapy-induced apoptosis in testicular germ cell tumours. In contrast to findings in some tumour cell types, Bcl-2 did not act as a gatekeeper to prevent entry of p53 to the nucleus. (+info)There are several risk factors for developing HCC, including:
* Cirrhosis, which can be caused by heavy alcohol consumption, viral hepatitis (such as hepatitis B and C), or fatty liver disease
* Family history of liver disease
* Chronic obstructive pulmonary disease (COPD)
* Diabetes
* Obesity
HCC can be challenging to diagnose, as the symptoms are non-specific and can be similar to those of other conditions. However, some common symptoms of HCC include:
* Yellowing of the skin and eyes (jaundice)
* Fatigue
* Loss of appetite
* Abdominal pain or discomfort
* Weight loss
If HCC is suspected, a doctor may perform several tests to confirm the diagnosis, including:
* Imaging tests, such as ultrasound, CT scan, or MRI, to look for tumors in the liver
* Blood tests to check for liver function and detect certain substances that are produced by the liver
* Biopsy, which involves removing a small sample of tissue from the liver to examine under a microscope
Once HCC is diagnosed, treatment options will depend on several factors, including the stage and location of the cancer, the patient's overall health, and their personal preferences. Treatment options may include:
* Surgery to remove the tumor or parts of the liver
* Ablation, which involves destroying the cancer cells using heat or cold
* Chemoembolization, which involves injecting chemotherapy drugs into the hepatic artery to reach the cancer cells
* Targeted therapy, which uses drugs or other substances to target specific molecules that are involved in the growth and spread of the cancer
Overall, the prognosis for HCC is poor, with a 5-year survival rate of approximately 20%. However, early detection and treatment can improve outcomes. It is important for individuals at high risk for HCC to be monitored regularly by a healthcare provider, and to seek medical attention if they experience any symptoms.
Liver neoplasms, also known as liver tumors or hepatic tumors, are abnormal growths of tissue in the liver. These growths can be benign (non-cancerous) or malignant (cancerous). Malignant liver tumors can be primary, meaning they originate in the liver, or metastatic, meaning they spread to the liver from another part of the body.
There are several types of liver neoplasms, including:
1. Hepatocellular carcinoma (HCC): This is the most common type of primary liver cancer and arises from the main cells of the liver (hepatocytes). HCC is often associated with cirrhosis and can be caused by viral hepatitis or alcohol abuse.
2. Cholangiocarcinoma: This type of cancer arises from the cells lining the bile ducts within the liver (cholangiocytes). Cholangiocarcinoma is rare and often diagnosed at an advanced stage.
3. Hemangiosarcoma: This is a rare type of cancer that originates in the blood vessels of the liver. It is most commonly seen in dogs but can also occur in humans.
4. Fibromas: These are benign tumors that arise from the connective tissue of the liver (fibrocytes). Fibromas are usually small and do not spread to other parts of the body.
5. Adenomas: These are benign tumors that arise from the glandular cells of the liver (hepatocytes). Adenomas are usually small and do not spread to other parts of the body.
The symptoms of liver neoplasms vary depending on their size, location, and whether they are benign or malignant. Common symptoms include abdominal pain, fatigue, weight loss, and jaundice (yellowing of the skin and eyes). Diagnosis is typically made through a combination of imaging tests such as CT scans, MRI scans, and ultrasound, and a biopsy to confirm the presence of cancer cells.
Treatment options for liver neoplasms depend on the type, size, location, and stage of the tumor, as well as the patient's overall health. Surgery may be an option for some patients with small, localized tumors, while others may require chemotherapy or radiation therapy to shrink the tumor before surgery can be performed. In some cases, liver transplantation may be necessary.
Prognosis for liver neoplasms varies depending on the type and stage of the cancer. In general, early detection and treatment improve the prognosis, while advanced-stage disease is associated with a poorer prognosis.
The symptoms of hepatitis B can range from mild to severe and may include fatigue, loss of appetite, nausea, vomiting, abdominal pain, dark urine, pale stools, joint pain, and jaundice (yellowing of the skin and eyes). In some cases, hepatitis B can be asymptomatic, meaning that individuals may not experience any symptoms at all.
Hepatitis B is diagnosed through blood tests that detect the presence of HBV antigens or antibodies in the body. Treatment for acute hepatitis B typically involves rest, hydration, and medication to manage symptoms, while chronic hepatitis B may require ongoing therapy with antiviral drugs to suppress the virus and prevent liver damage.
Preventive measures for hepatitis B include vaccination, which is recommended for individuals at high risk of infection, such as healthcare workers, sexually active individuals, and those traveling to areas where HBV is common. In addition, safe sex practices, avoiding sharing of needles or other bodily fluids, and proper sterilization of medical equipment can help reduce the risk of transmission.
Overall, hepatitis B is a serious infection that can have long-term consequences for liver health, and it is important to take preventive measures and seek medical attention if symptoms persist or worsen over time.
A persistent infection with the hepatitis B virus (HBV) that can lead to liver cirrhosis and hepatocellular carcinoma. HBV is a bloodborne pathogen and can be spread through contact with infected blood, sexual contact, or vertical transmission from mother to child during childbirth.
Chronic hepatitis B is characterized by the presence of HBsAg in the blood for more than 6 months, indicating that the virus is still present in the liver. The disease can be asymptomatic or symptomatic, with symptoms such as fatigue, malaise, loss of appetite, nausea, vomiting, joint pain, and jaundice.
Chronic hepatitis B is diagnosed through serological tests such as HBsAg, anti-HBc, and HBV DNA. Treatment options include interferon alpha and nucleos(t)ide analogues, which can slow the progression of the disease but do not cure it.
Prevention strategies for chronic hepatitis B include vaccination with hepatitis B vaccine, which is effective in preventing acute and chronic HBV infection, as well as avoidance of risky behaviors such as unprotected sex and sharing of needles.
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.
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.
People with Fragile X syndrome may have intellectual disability, developmental delays, and various physical characteristics such as large ears, long face, and joint hypermobility. They may also experience behavioral problems such as anxiety, hyperactivity, and sensory sensitivities. In addition, they are at increased risk for seizures, sleep disturbances, and other health issues.
Fragile X syndrome is usually diagnosed through a combination of clinical evaluation, genetic testing, and molecular analysis. There is no cure for the condition, but various interventions such as behavioral therapy, speech and language therapy, occupational therapy, and medications can help manage its symptoms.
Prevention of Fragile X syndrome is not possible, as it is a genetic disorder caused by an expansion of CGG repeats in the FMR1 gene. However, early identification and intervention can improve outcomes for individuals with the condition.
Overall, Fragile X syndrome is a complex and multifaceted condition that requires comprehensive and individualized care to help individuals with the condition reach their full potential.
DLBCL is characterized by the rapid growth of malignant B cells in the lymph nodes, spleen, bone marrow, and other organs. These cells can also spread to other parts of the body through the bloodstream or lymphatic system. The disease is often aggressive and can progress quickly without treatment.
The symptoms of DLBCL vary depending on the location and extent of the disease, but they may include:
* Swollen lymph nodes in the neck, underarm, or groin
* Fever
* Fatigue
* Night sweats
* Weight loss
* Abdominal pain or discomfort
* Itching
The diagnosis of DLBCL is based on a combination of physical examination findings, imaging studies (such as CT scans or PET scans), and biopsy results. Treatment typically involves a combination of chemotherapy, radiation therapy, and in some cases, immunotherapy or targeted therapy. The prognosis for DLBCL has improved significantly over the past few decades, with overall survival rates ranging from 60% to 80%, depending on the stage and other factors.
Explanation: Neoplastic cell transformation is a complex process that involves multiple steps and can occur as a result of genetic mutations, environmental factors, or a combination of both. The process typically begins with a series of subtle changes in the DNA of individual cells, which can lead to the loss of normal cellular functions and the acquisition of abnormal growth and reproduction patterns.
Over time, these transformed cells can accumulate further mutations that allow them to survive and proliferate despite adverse conditions. As the transformed cells continue to divide and grow, they can eventually form a tumor, which is a mass of abnormal cells that can invade and damage surrounding tissues.
In some cases, cancer cells can also break away from the primary tumor and travel through the bloodstream or lymphatic system to other parts of the body, where they can establish new tumors. This process, known as metastasis, is a major cause of death in many types of cancer.
It's worth noting that not all transformed cells will become cancerous. Some forms of cellular transformation, such as those that occur during embryonic development or tissue regeneration, are normal and necessary for the proper functioning of the body. However, when these transformations occur in adult tissues, they can be a sign of cancer.
See also: Cancer, Tumor
Word count: 190
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
Source: National Cancer Institute (www.cancer.gov)
The above definition is given by the National Cancer Institute, which is an authoritative source of information on cancer and lymphoma. It provides a concise overview of follicular lymphoma, including its characteristics, diagnosis, treatment options, and prognosis. The definition includes key terms such as "slow-growing," "B cells," "lymph nodes," and "five-year survival rate," which are important to understand when discussing this type of cancer.
Symptoms of this type of cancer can include swelling of the lymph nodes, fatigue, fever, night sweats, and weight loss. Treatment options for marginal zone B-cell lymphoma depend on the stage and location of the cancer and may involve a combination of chemotherapy, immunotherapy, and/or targeted therapy.
The prognosis for this type of cancer is generally good if it is diagnosed early and treated appropriately. However, in some cases, it can be more aggressive and difficult to treat, and the prognosis may be poorer.
There are several subtypes of B-cell leukemia, including:
1. Chronic lymphocytic leukemia (CLL): This is the most common type of B-cell leukemia, and it typically affects older adults. CLL is a slow-growing cancer that can progress over time.
2. Acute lymphoblastic leukemia (ALL): This is a fast-growing and aggressive form of B-cell leukemia that can affect people of all ages. ALL is often treated with chemotherapy and sometimes with bone marrow transplantation.
3. Burkitt lymphoma: This is an aggressive form of B-cell leukemia that typically affects older adults in Africa and Asia. Burkitt lymphoma can be treated with chemotherapy and sometimes with bone marrow transplantation.
4. Hairy cell leukemia: This is a rare type of B-cell leukemia that is characterized by the presence of hair-like projections on the surface of cancer cells. Hairy cell leukemia can be treated with chemotherapy and sometimes with bone marrow transplantation.
The diagnosis of B-cell leukemia is based on a combination of physical examination, medical history, laboratory tests, and biopsies. Treatment options for B-cell leukemia include chemotherapy, bone marrow transplantation, and in some cases, targeted therapy with drugs that specifically target cancer cells. The prognosis for B-cell leukemia varies depending on the subtype of the disease and the patient's overall health.
The term "reticulocytosis" is derived from the Latin words "reticulum," meaning net-like, and "cytosis," meaning the condition of cells. This refers to the characteristic net-like appearance of reticulocytes under a microscope.
There are several possible causes of reticulocytosis, including:
1. Inherited disorders such as hereditary elliptocytosis, hereditary spherocytosis, and pyruvate kinase (PK) deficiency.
2. Acquired disorders such as hemolytic anemia, thalassemia, and sickle cell disease.
3. Infections such as malaria, dengue fever, and babesiosis.
4. Medications such as antibiotics, chemotherapy drugs, and anti-inflammatory medications.
5. Other conditions such as chronic kidney disease, liver disease, and autoimmune disorders.
Reticulocytosis can be diagnosed through a blood test called a complete blood count (CBC) or a reticulocyte count. Treatment depends on the underlying cause of the condition. In some cases, no treatment may be necessary, while in other cases, medication or blood transfusions may be required.
In LLCB, the B cells undergo a mutation that causes them to become cancerous and multiply rapidly. This can lead to an overproduction of these cells in the bone marrow, causing the bone marrow to become crowded and unable to produce healthy red blood cells, platelets, and white blood cells.
LLCB is typically a slow-growing cancer, and it can take years for symptoms to develop. However, as the cancer progresses, it can lead to a range of symptoms including fatigue, weakness, weight loss, fever, night sweats, and swollen lymph nodes.
LLCB is typically diagnosed through a combination of physical examination, blood tests, bone marrow biopsy, and imaging studies such as X-rays or CT scans. Treatment options for LLCB include chemotherapy, radiation therapy, and in some cases, stem cell transplantation.
Overall, while LLCB is a serious condition, it is typically slow-growing and can be managed with appropriate treatment. With current treatments, many people with LLCB can achieve long-term remission and a good quality of life.
When a chromosome breaks, it can lead to genetic instability and potentially contribute to the development of diseases such as cancer. Chromosome breakage can also result in the loss or gain of genetic material, which can further disrupt normal cellular function and increase the risk of disease.
There are several types of chromosome breakage, including:
1. Chromosomal aberrations: These occur when there is a change in the number or structure of the chromosomes, such as an extra copy of a chromosome (aneuploidy) or a break in a chromosome.
2. Genomic instability: This refers to the presence of errors in the genetic material that can lead to changes in the function of cells and tissues.
3. Chromosomal fragile sites: These are specific regions of the chromosomes that are more prone to breakage than other regions.
4. Telomere shortening: Telomeres are the protective caps at the ends of the chromosomes, and their shortening can lead to chromosome breakage and genetic instability.
Chromosome breakage can be detected through cytogenetic analysis, which involves staining the cells with dyes to visualize the chromosomes and look for any abnormalities. The detection of chromosome breakage can help diagnose certain diseases, such as cancer, and can also provide information about the risk of disease progression.
In summary, chromosome breakage is a type of genetic alteration that can occur as a result of various factors, including exposure to radiation or chemicals, errors during cell division, or aging. It can lead to genetic instability and increase the risk of diseases such as cancer. Detection of chromosome breakage through cytogenetic analysis can help diagnose certain diseases and provide information about the risk of disease progression.
Factor X deficiency can be inherited or acquired, and it can have mild to severe effects on the body. People with factor X deficiency may experience prolonged bleeding after an injury or surgery, easy bruising, and frequent nosebleeds. In severe cases, factor X deficiency can lead to spontaneous bleeding, especially in the joints and internal organs.
There are two types of factor X deficiency:
1. Classic factor X deficiency: This is the most common type of factor X deficiency and is caused by a mutation in the gene that codes for factor X. It is usually inherited in an autosomal recessive pattern, which means that the child must inherit two copies of the mutated gene, one from each parent, to develop the condition.
2. Acquired factor X deficiency: This type of factor X deficiency can occur due to certain medical conditions, such as liver disease, vitamin K deficiency, or exposure to certain medications. It can also occur in people who have a high risk of bleeding, such as those with hemophilia.
Treatment for factor X deficiency typically involves replacing the missing clotting factor through infusions of factor X concentrate. In some cases, medications that help the body produce more factor X may also be used. People with factor X deficiency may need to receive regular infusions to maintain adequate levels of factor X in their blood.
Overall, factor X deficiency is a rare but potentially serious condition that can affect the body's ability to form blood clots and stop bleeding. With proper diagnosis and treatment, however, most people with factor X deficiency can lead normal lives.
There are several types of lymphoma, including:
1. Hodgkin lymphoma: This is a type of lymphoma that originates in the white blood cells called Reed-Sternberg cells. It is characterized by the presence of giant cells with multiple nucleoli.
2. Non-Hodgkin lymphoma (NHL): This is a type of lymphoma that does not meet the criteria for Hodgkin lymphoma. There are many subtypes of NHL, each with its own unique characteristics and behaviors.
3. Cutaneous lymphoma: This type of lymphoma affects the skin and can take several forms, including cutaneous B-cell lymphoma and cutaneous T-cell lymphoma.
4. Primary central nervous system (CNS) lymphoma: This is a rare type of lymphoma that develops in the brain or spinal cord.
5. Post-transplantation lymphoproliferative disorder (PTLD): This is a type of lymphoma that develops in people who have undergone an organ transplant, often as a result of immunosuppressive therapy.
The symptoms of lymphoma can vary depending on the type and location of the cancer. Some common symptoms include:
* Swollen lymph nodes
* Fever
* Fatigue
* Weight loss
* Night sweats
* Itching
Lymphoma is diagnosed through a combination of physical examination, imaging tests (such as CT scans or PET scans), and biopsies. Treatment options for lymphoma depend on the type and stage of the cancer, and may include chemotherapy, radiation therapy, immunotherapy, or stem cell transplantation.
Overall, lymphoma is a complex and diverse group of cancers that can affect people of all ages and backgrounds. While it can be challenging to diagnose and treat, advances in medical technology and research have improved the outlook for many patients with lymphoma.
There are several subtypes of NHL, including:
1. B-cell lymphomas (such as diffuse large B-cell lymphoma and follicular lymphoma)
2. T-cell lymphomas (such as peripheral T-cell lymphoma and mycosis fungoides)
3. Natural killer cell lymphomas (such as nasal NK/T-cell lymphoma)
4. Histiocyte-rich B-cell lymphoma
5. Primary mediastinal B-cell lymphoma
6. Mantle cell lymphoma
7. Waldenström macroglobulinemia
8. Lymphoplasmacytoid lymphoma
9. Myelodysplastic syndrome/myeloproliferative neoplasms (MDS/MPN) related lymphoma
These subtypes can be further divided into other categories based on the specific characteristics of the cancer cells.
Symptoms of NHL can vary depending on the location and size of the tumor, but may include:
* Swollen lymph nodes in the neck, underarm, or groin
* Fever
* Fatigue
* Weight loss
* Night sweats
* Itching
* Abdominal pain
* Swollen spleen
Treatment for NHL typically involves a combination of chemotherapy, radiation therapy, and in some cases, targeted therapy or immunotherapy. The specific treatment plan will depend on the subtype of NHL, the stage of the cancer, and other individual factors.
Overall, NHL is a complex and diverse group of cancers that require specialized care from a team of medical professionals, including hematologists, oncologists, radiation therapists, and other support staff. With advances in technology and treatment options, many people with NHL can achieve long-term remission or a cure.
T-ALL typically occurs in children and young adults, although it can also occur in older adults. The symptoms of T-ALL can include fever, fatigue, loss of appetite, weight loss, swollen lymph nodes, and an enlarged spleen. If left untreated, T-ALL can progress rapidly and lead to life-threatening complications such as infection, bleeding, and organ failure.
The exact cause of T-ALL is not known, but it is believed to be linked to genetic mutations that occur in the T cells. The diagnosis of T-ALL typically involves a combination of physical examination, blood tests, bone marrow biopsy, and imaging studies such as CT scans or PET scans.
Treatment for T-ALL usually involves a combination of chemotherapy and/or radiation therapy to kill the abnormal T cells. In some cases, bone marrow transplantation may also be recommended. The prognosis for T-ALL depends on several factors, including the age of the patient, the severity of the disease, and the response to treatment. Overall, the survival rate for T-ALL is relatively low, but with intensive treatment, many patients can achieve long-term remission.
Some common types of nervous system neoplasms include:
1. Brain tumors: These are abnormal growths that develop in the brain, including gliomas (such as glioblastoma), meningiomas, and acoustic neuromas.
2. Spinal cord tumors: These are abnormal growths that develop in the spinal cord, including astrocytomas, oligodendrogliomas, and metastatic tumors.
3. Nerve sheath tumors: These are abnormal growths that develop in the covering of nerves, such as neurofibromas and schwannomas.
4. Pineal gland tumors: These are abnormal growths that develop in the pineal gland, a small endocrine gland located in the brain.
Symptoms of nervous system neoplasms can vary depending on their location and size, but may include headaches, seizures, weakness or numbness in the arms or legs, and changes in vision, speech, or balance. Diagnosis is typically made through a combination of imaging studies (such as MRI or CT scans) and tissue biopsy. Treatment options vary depending on the type and location of the tumor, but may include surgery, radiation therapy, and chemotherapy.
In summary, nervous system neoplasms are abnormal growths that can develop in the brain, spinal cord, and nerves, and can have a significant impact on the body. Diagnosis and treatment require a comprehensive approach, involving a team of medical professionals with expertise in neurology, neurosurgery, radiation oncology, and other related specialties.
Also known as Burkitt's Lymphoma.
There are several different types of leukemia, including:
1. Acute Lymphoblastic Leukemia (ALL): This is the most common type of leukemia in children, but it can also occur in adults. It is characterized by an overproduction of immature white blood cells called lymphoblasts.
2. Acute Myeloid Leukemia (AML): This type of leukemia affects the bone marrow's ability to produce red blood cells, platelets, and other white blood cells. It can occur at any age but is most common in adults.
3. Chronic Lymphocytic Leukemia (CLL): This type of leukemia affects older adults and is characterized by the slow growth of abnormal white blood cells called lymphocytes.
4. Chronic Myeloid Leukemia (CML): This type of leukemia is caused by a genetic mutation in a gene called BCR-ABL. It can occur at any age but is most common in adults.
5. Hairy Cell Leukemia: This is a rare type of leukemia that affects older adults and is characterized by the presence of abnormal white blood cells called hairy cells.
6. Myelodysplastic Syndrome (MDS): This is a group of disorders that occur when the bone marrow is unable to produce healthy blood cells. It can lead to leukemia if left untreated.
Treatment for leukemia depends on the type and severity of the disease, but may include chemotherapy, radiation therapy, targeted therapy, or stem cell transplantation.
The most common types of hemoglobinopathies include:
1. Sickle cell disease: This is caused by a point mutation in the HBB gene that codes for the beta-globin subunit of hemoglobin. It results in the production of sickle-shaped red blood cells, which can cause anemia, infections, and other complications.
2. Thalassemia: This is a group of genetic disorders that affect the production of hemoglobin and can result in anemia, fatigue, and other complications.
3. Hemophilia A: This is caused by a defect in the F8 gene that codes for coagulation factor VIII, which is essential for blood clotting. It can cause bleeding episodes, especially in males.
4. Glucose-6-phosphate dehydrogenase (G6PD) deficiency: This is caused by a point mutation in the G6PD gene that codes for an enzyme involved in red blood cell production. It can cause hemolytic anemia, especially in individuals who consume certain foods or medications.
5. Hereditary spherocytosis: This is caused by point mutations in the ANK1 or SPTA1 genes that code for proteins involved in red blood cell membrane structure. It can cause hemolytic anemia and other complications.
Hemoglobinopathies can be diagnosed through genetic testing, such as DNA sequencing or molecular genetic analysis. Treatment options vary depending on the specific disorder but may include blood transfusions, medications, and in some cases, bone marrow transplantation.
* Peripheral T-cell lymphoma (PTCL): This is a rare type of T-cell lymphoma that can develop in the skin, lymph nodes, or other organs.
* Cutaneous T-cell lymphoma (CTCL): This is a type of PTCL that affects the skin and can cause lesions, rashes, and other skin changes.
* Anaplastic large cell lymphoma (ALCL): This is a rare subtype of PTCL that can develop in the lymph nodes, spleen, or bone marrow.
* Adult T-cell leukemia/lymphoma (ATLL): This is a rare and aggressive subtype of PTCL that is caused by the human T-lymphotropic virus type 1 (HTLV-1).
Symptoms of T-cell lymphoma can include:
* Swollen lymph nodes
* Fever
* Fatigue
* Weight loss
* Night sweats
* Skin lesions or rashes
Treatment options for T-cell lymphoma depend on the subtype and stage of the cancer, but may include:
* Chemotherapy
* Radiation therapy
* Immunotherapy
* Targeted therapy
Prognosis for T-cell lymphoma varies depending on the subtype and stage of the cancer, but in general, the prognosis for PTCL is poorer than for other types of non-Hodgkin lymphoma. However, with prompt and appropriate treatment, many people with T-cell lymphoma can achieve long-term remission or even be cured.
There are different types of Breast Neoplasms such as:
1. Fibroadenomas: These are benign tumors that are made up of glandular and fibrous tissues. They are usually small and round, with a smooth surface, and can be moved easily under the skin.
2. Cysts: These are fluid-filled sacs that can develop in both breast tissue and milk ducts. They are usually benign and can disappear on their own or be drained surgically.
3. Ductal Carcinoma In Situ (DCIS): This is a precancerous condition where abnormal cells grow inside the milk ducts. If left untreated, it can progress to invasive breast cancer.
4. Invasive Ductal Carcinoma (IDC): This is the most common type of breast cancer and starts in the milk ducts but grows out of them and invades surrounding tissue.
5. Invasive Lobular Carcinoma (ILC): It originates in the milk-producing glands (lobules) and grows out of them, invading nearby tissue.
Breast Neoplasms can cause various symptoms such as a lump or thickening in the breast or underarm area, skin changes like redness or dimpling, change in size or shape of one or both breasts, discharge from the nipple, and changes in the texture or color of the skin.
Treatment options for Breast Neoplasms may include surgery such as lumpectomy, mastectomy, or breast-conserving surgery, radiation therapy which uses high-energy beams to kill cancer cells, chemotherapy using drugs to kill cancer cells, targeted therapy which uses drugs or other substances to identify and attack cancer cells while minimizing harm to normal cells, hormone therapy, immunotherapy, and clinical trials.
It is important to note that not all Breast Neoplasms are cancerous; some are benign (non-cancerous) tumors that do not spread or grow.
Bcl-2-like protein 1
Bcl-2-associated X protein
Bcl-2-associated death promoter
Bcl-2
Marginal zone B-cell lymphoma
Bcl-2 family
Sexually dimorphic nucleus
Phycocyanin
Bcl-xL
C-Raf
Protein kinase B
Venetoclax
Presenilin-1
MTCH2
Jerry Adams
Bcl-x interacting domain
BCL2L12
FASTK
BCL2-related protein A1
BCL-6 corepressor
Obatoclax
Apoptosis
Mitochondrial ribosomal protein L41
Hypothermia therapy for neonatal encephalopathy
BNIP3
Apoptosome
RRAS
HRK (gene)
Bcl-2-interacting killer
AI-10-49
Caspase-activated DNase
PIR (gene)
BMF (gene)
Galectin-9
GLI2
Erinna Lee
Waldenström macroglobulinemia
MIR195
BCL2L13
Prostate cancer
AP-1 transcription factor
Index of biochemistry articles
Methylsulfonylmethane
Belimumab
Nuclear receptor 4A1
STAT6
Steven J. Burakoff
Calcineurin
Histone H2A.Z
PPP1CA
Neprilysin
Anticancer gene
Unfolded protein response
CLPTM1L
Cyclin-dependent kinase 1
Chronic lymphocytic leukemia
Gapmer
S100 protein
Minimal residual disease
MicroRNA 148a
Vaccinia virus lacking the Bcl-2-like protein N1 induces a stronger natural killer cell response to infection
Anti-Apoptotic and Pro-Apoptotic Bcl-2 Family Proteins in Peri-Implant Diseases. | Clin Oral Implants Res;34(6): 582-590, 2023...
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The proper assembly of sperm flagellar proteins is fundamental for sperm - Discovery and optimization of potent BCL-2 Inhibitors
Langerhans Cell Histiocytosis: Background, Pathophysiology, Etiology
Moreover, in addition, it inhibited the manifestation of anti\apoptotic BCL\2 family members proteins such as for example BCL\2...
Venetoclax: A First-in-Class Oral BCL-2 Inhibitor for the Management of Lymphoid Malignancies - PubMed
Protective effect of avicularin on rheumatoid arthritis and its associated mechanisms
Identification of novel molecular regulators of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced...
FITC anti-Bcl-2 Antibody anti-Bcl-2 - BCL/10C4
Publication Detail
Structural Biophysics | NHLBI, NIH
Figure 1 - Immune Cell Apoptosis Prevention as Potential Therapy for Severe Infections - Volume 13, Number 2-February 2007 -...
regulation of protein localization Antibodies | Invitrogen
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NIH Guide: ENGINEERED ISOGENIC CELL LINES WITH RELEVANT CANCER TARGETS
Fluoride Action Network | Fluoride induces apoptosis and autophagy through the IL-17 signaling pathway in mice hepatocytes.
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Sulodexide pretreatment attenuates renal ischemia-reperfusion injury in rats | Oncotarget
CCND1
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Frontiers | Identification of AIDS-Associated Kaposi Sarcoma: A Functional Genomics Approach
Anti-apoptotic protein5
- Bcl-xl, an anti-apoptotic protein of this family, is known to form heterodimers with multiple pro-apoptotic proteins, such as Bad, Bim, Bak, and Bid. (omicsdi.org)
- A fifth protein-peptide complex composed of another anti-apoptotic protein, Bcl-w, in complex with the peptide from Bim was also studied. (omicsdi.org)
- Functional and structural studies of the vaccinia virus virulence factor N1 reveal a Bcl-2-like anti-apoptotic protein. (ox.ac.uk)
- This study illustrates the importance of the evolutionary conservation of structure, rather than sequence, in protein function and reveals a novel anti-apoptotic protein from orthopoxviruses. (ox.ac.uk)
- A recent study demonstrated the lack of beta-amyloid (Aβ) plaque formation and accumulation of the amyloid precursor protein (APP) in a triple transgenic mouse model of Alzheimer's disease (3xTg-AD) following overexpression of the anti-apoptotic protein, Bcl-2 (Rohn et al. (uthscsa.edu)
Member of the BCL-2 family2
- Here, we show that the molecular pathway leading to TFEC-mediated cell death is associated with an early cytosolic to mitochondrial translocation of BAX, a pro-apoptotic member of the BCL-2 family. (nih.gov)
- Bcl-2 (B-cell leukemia 2) is an apoptotic protein and a member of the Bcl-2 family containing BH1-4 domains. (biolegend.com)
Peptides1
- To elucidate the molecular basis of this recognition process, we used molecular dynamics simulations coupled with the Molecular Mechanics/Poisson-Boltzmann Surface Area approach to identify the amino acids that make significant energetic contributions to the binding free energy of four complexes formed between Bcl-xl and pro-apoptotic Bcl-2 homology 3 peptides. (omicsdi.org)
Apoptosis Regulato1
- These findings indicate a novel pathway for redox regulation of apoptosis regulatory proteins, which could be important in the understanding of chemotherapy-induced toxicities and development of preventive treatment strategies which are currently lacking. (cdc.gov)
GENES3
- Membrane proteins encoded by the BCL-2 GENES and serving as potent inhibitors of cell death by APOPTOSIS. (nih.gov)
- In addition, the expression levels of genes and proteins were determined reverse transcription quantitative polymerase chain reaction and western blot analysis. (spandidos-publications.com)
- To screen genes associated with poor prognosis of clear cell renal cell carcinoma (CcRCC) from the public databases HPA (Human Protein Atlas), UALCAN, and GEPIA (Gene Expression Profiling Interactive Analysis) and to investigate the expression of FKBP10 in CcRCC and the effect on prognosis of the patients and the biological behavior of CcRCC cells. (hindawi.com)
Apoptotic protein2
- Purpose: Bcl-2 is an apoptotic protein that is highly expressed in advanced melanoma. (elsevier.com)
- Humanin selectively prevents the activation of pro-apoptotic protein BID by sequestering it into fibers. (nih.gov)
Overexpression2
Inhibitors of apoptosis2
- Vaccinia virus (VACV) encodes many immunomodulatory proteins, including inhibitors of apoptosis and modulators of innate immune signalling. (ox.ac.uk)
- 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)
Modulator of apoptosis1
- A p53 upregulated modulator of apoptosis that binds Bcl-2. (nih.gov)
Mitochondrial8
- The proteins are found on mitochondrial, microsomal, and NUCLEAR MEMBRANE sites within many cell types. (nih.gov)
- Taken together, our findings provide a "Membrane-mediated Permissive" model, in which the BH3-only proteins only indirectly activate BAX/BAK by neutralizing the anti-apoptotic BCL-2 proteins, and thus allowing BAX/BAK to undergo unimpeded, spontaneous activation in the mitochondrial outer membrane milieu, leading to apoptosis initiation. (omicsdi.org)
- Flow cytometric detection of the mitochondrial BCL-2 protein in normal and neoplastic human lymphoid cells. (ox.ac.uk)
- The bcl-2 proto-oncogene, rearranged and deregulated in B-cell lymphomas bearing the t(14;18) translocation, encodes an inner mitochondrial membrane protein that blocks apoptotic cell death. (ox.ac.uk)
- Mitochondrial superoxide mediates doxorubicin-induced keratinocyte apoptosis through oxidative modification of ERK and Bcl-2 ubiquitination. (cdc.gov)
- The BCL-2 family of proteins is pivotal in regulating cell death through the control of the integrity of the outer mitochondrial membrane. (lifechemicals.com)
- Bcl-2 is distributed in the outer mitochondrial membrane, the nuclear envelope, and the endoplasmic reticulum. (biolegend.com)
- This protein blocks apoptotic death by controlling mitochondrial membrane permeability. (biolegend.com)
Cleavage3
- However, unlike the caspase cleavage products of cellular Bcl-2, Bcl-x(L), and Bid, which are potent inducers of apoptosis, the cleavage product of gammaHV68 Bcl-2 lacked proapoptotic activity. (nih.gov)
- Communication between the pathways exists through cleavage of Bcl-2 interacting domain (Bid) by active caspase-8 to form truncated Bid (tBid). (cdc.gov)
- Cleavage of Bcl-2 can convert to pro-apoptotic (by cleavage of BH4 domain). (biolegend.com)
Antibodies2
- American blotting Total proteins was extracted from cells lysates using RIPA lysis launching and buffer buffer as prior described.17 Protein were separated with SDS\Web page and incubated with particular antibodies. (neighborhoodhousecharterschool.org)
- 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)
Amino Acids2
- The results identified amino acids of both the anti-apoptotic proteins as well as the Bcl-2 homology 3 (BH3) domains of the pro-apoptotic proteins that make strong, recurrent interactions in the protein complexes. (omicsdi.org)
- Quantifying in live cells the contributions of individual amino acids revealed that residue L185 previously thought involved in binding Bim to membranes, instead contributes to binding to anti-apoptotic proteins. (omicsdi.org)
Viral Proteins1
- Dr. Tjandra is studying how viral proteins aggregate into specific shapes (e.g. eicosahedral or conical) and how that organization relates to viral function. (nih.gov)
Virulence factor1
- The vaccinia virus (VACV) N1 protein is an intracellular virulence factor that has a Bcl-2-like structure and inhibits both apoptosis and signalling from the interleukin 1 receptor, leading to nuclear factor kappa B activation. (nih.gov)
Interactions6
- Protein-peptide interactions are often associated with large-scale conformational changes that are difficult to study either by classical molecular modeling or by experiment. (nature.com)
- Molecular basis for Bcl-2 homology 3 domain recognition in the Bcl-2 protein family: identification of conserved hot spot interactions. (omicsdi.org)
- Molecular basis for the interplay of apoptosis and proliferation mediated by Bcl-xL:Bim interactions in pancreatic cancer cells. (omicsdi.org)
- The importance of the complex network of direct interactions between proteins - known as the interactome - to both biological systems and the development of diseases is widely recognized. (lifechemicals.com)
- Life Chemicals has designed PPI Screening Libraries by a receptor-based approach that gathered a number of the most attractive PPI targets for therapeutic intervention via disrupting specific functional interactions between proteins. (lifechemicals.com)
- The goal is to understand how protein-protein interactions involving CP can manage a relatively fast actin polymerization response to cellular stimuli. (nih.gov)
Membrane3
- Here, through reconstitution of cells lacking all eight pro-apoptotic BH3-only proteins, we demonstrate that all BH3-only proteins primarily target the anti-apoptotic BCL-2 proteins BCL-xL/MCL-1, whose simultaneous suppression enables membrane-mediated spontaneous activation of BAX/BAK. (omicsdi.org)
- 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)
- During viral replication, these proteins assemble and interact with the host membrane to bud off forming infectious particles. (nih.gov)
Intracellular2
- VACV protein N1 is an intracellular homodimer that contributes to virus virulence and was reported to inhibit nuclear factor (NF)-kappaB signalling. (ox.ac.uk)
- C57BL/6 splenocytes intracellular stained with BCL/10C4 FITC. (biolegend.com)
Regulator1
- Apoptosis regulator proteins, Bcl-2 family, BH1-4 domains. (biolegend.com)
Gene4
- On lymphoblastoid cell lines, the bcl-2 staining intensity was variable and not necessarily correlated to molecular rearrangements of the bcl-2 gene. (ox.ac.uk)
- Of four centroblastic-centrocytic cases with rearrangements of the bcl-2 gene, only two presented elevated amounts of bcl-2 protein, indicating that the levels of bcl-2 are not diagnostic of the translocation. (ox.ac.uk)
- The gene encoding p53 protein is mutated or deleted in half of the human cancers, which inactivates tumor suppressor activity. (lifechemicals.com)
- TP53-induced gene 3 protein. (nih.gov)
Homologs3
- Gamma herpesviruses also encode homologs of the Bcl-2 family. (nih.gov)
- All tested herpesvirus Bcl-2 homologs possess antiapoptotic activity, including the more distantly related homologs encoded by murine gammaherpesvirus 68 (gammaHV68) and bovine herpesvirus 4 (BHV4), as described here. (nih.gov)
- To determine if viral Bcl-2 proteins can be converted into death factors, similar to their cellular counterparts, five herpesvirus Bcl-2 homologs from five different viruses were tested for their susceptibility to caspases. (nih.gov)
Proliferation4
- The role of apoptosis, proliferation, and the Bcl-2-related proteins in the myelodysplastic syndromes and acute myeloid leukemia secondary to MDS. (bvsalud.org)
- Bone marrow CD34(+) cell apoptosis ( annexin V ), proliferation (Ki-67), and Bcl-2-related protein expression was evaluated by flow cytometry in 102 patients with myelodysplastic syndrome (MDS) and acute myeloid leukemia secondary to MDS (MDS-AML) and in 30 normal donors (NBM). (bvsalud.org)
- Additionally, apoptotic-enhancing fusion proteins of the current invention could be used to inhibit cell growth, e.g., uncontrolled cellular proliferation. (nih.gov)
- Moreover, knockdown of FKBP10 significantly inhibited the proliferation of CcRCC cells, notably declined the protein expression of c-Myc, cyclin D1, and Bcl-2, and promoted cell adhesion. (hindawi.com)
Cells24
- To help resolve this question, we have permanently and stably down-regulated Bcl-2 protein and mRNA expression in 518A2 cells by two different technologies and evaluated the resulting clones both in vitro and in vivo. (elsevier.com)
- Experimental Design: 518A2 melanoma cells were transfected with plasmids engineered to produce either a single-stranded antisense oligonucleotide targeted to the initiation codon region of the Bcl-2 mRNA or a short hairpin RNA also targeted to the Bcl-2 mRNA. (elsevier.com)
- However, when xenografted into severe combined immunodeficient mice, cells with silenced Bcl-2, using either technology, either failed to grow at all or grew to tumors of low volume and then completely regressed. (elsevier.com)
- In contrast, control cells with "normal" levels of Bcl-2 protein expression expanded to be large, necrotic tumors. (elsevier.com)
- Conclusions: The presence of Bcl-2 protein profoundly affects the ability of 518A2 melanoma cells to grow as human tumor xenografts in severe combined immunodeficient mice. (elsevier.com)
- The in vivo role of Bcl-2 in melanoma cells thus differs significantly from its in vitro role, and these experiments further suggest that Bcl-2 may be an important therapeutic target even in tumors that do not contain the t14:18 translocation. (elsevier.com)
- For example, fusing various cell-binding domains to Bcl-X L and Bad allows targeting to specific subsets of cells in vivo, permitting treatment and/or prevention of cell-death related consequences of various diseases and injuries. (nih.gov)
- Remarkably, death ligand-induced apoptosis in cells lacking BH3-only proteins and MCL-1 is fully restored by BID mutants capable of neutralizing BCL-xL, but not direct activation of BAX/BAK. (omicsdi.org)
- A major mechanism through which cancer cells avoid apoptosis is by promoting the association of anti-apoptotic members of the pro-survival Bcl-2 protein family (like Bcl-2 and Bcl-xL) with BH(3) domain-only proteins (like Bim and Bid). (omicsdi.org)
- We have developed a sensitive immunofluorescence assay for the single- and multicolor flow cytometric analysis of bcl-2 protein in relation to other markers and cell cycle, based on a fixation-permeation step of cells with paraformaldehyde and Triton X100 and the use of a bcl-2 specific monoclonal antibody (MoAb). (ox.ac.uk)
- As an application of this method, we have examined the expression of bcl-2 in normal and neoplastic lymphoid cells. (ox.ac.uk)
- following in vitro mitogen activation, the bcl-2 reactivity decreased slightly in the former but markedly in latter cells. (ox.ac.uk)
- 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)
- Small molecules that disrupt this interaction by binding to the anti-apoptotic BCL-2 family proteins have been designed to induce apoptosis of cancer cells [2]. (lifechemicals.com)
- 37. Von Hippel-Lindau tumor suppressor protein transforms human neuroblastoma cells into functional neuron-like cells. (nih.gov)
- 38. Regulation of Bcl-2 oncoprotein levels with differentiation of human neuroblastoma cells. (nih.gov)
- BCL-2 is a protein that promotes cell survival by preventing cells from undergoing a natural self-destruct process called apoptosis. (aacr.org)
- Elevated levels of BCL-2 have been seen in several types of leukemia cells, including AML cells and chronic lymphocytic leukemia (CLL) cells. (aacr.org)
- By blocking BCL-2, venetoclax triggers the leukemia cells to die by apoptosis. (aacr.org)
- In addition, these data suggested that avicularin prevented the activation of the mitogen‑activated protein kinase kinase (MEK)/nuclear factor kappa light‑chain‑enhancer of activated B‑cells (NF‑κB) pathway activated by TNF‑α. (spandidos-publications.com)
- Cystinosis is a rare inheritable disorder in which cystine, a small protein, accumulates in all cells throughout the body. (hrb.ie)
- It works by blocking the action of a certain protein in the body that helps cancer cells survive. (medlineplus.gov)
- Western blot was utilized to examine the protein expression level of c-Myc, cyclin D1, and Bcl-2 in the cells. (hindawi.com)
- We further demonstrated that 1g inhibited cell growth, suppressed migration and invasion, and induced apoptosis of CNE-2Z cells by down-regulating HIF-1α, MMP-2, MMP-9, Bcl-2, Akt and up-regulating Bax protein levels. (bvsalud.org)
Induces1
- Superoxide induces dephosphorylation of Bcl-2 through MAP kinase ERK1/2 inactivation, which promotes ubiquitination of Bcl-2. (cdc.gov)
Antibody1
- The BCL\2 antibody was bought from Dako (Agilent Technology, Santa Clara, CA, USA). (neighborhoodhousecharterschool.org)
Kinase6
- However the manifestation and assembly of rat FS parts during spermiogenesis have not been precisely examined aside from A-kinase anchoring proteins 4 (AKAP4) [15] and tissue-specific testicular thioredoxin-2 (SPTRX-2) [11]. (monossabios.com)
- This protein is modified by ASK1/JNK1, PKC, ERKs, and stress-activated kinase phosphorylation and can be ubiquitinated. (biolegend.com)
- also called Cdc2) cyclin-dependent protein kinase. (nih.gov)
- a protein kinase that inhibits Cdk1. (nih.gov)
- ataxia telangiectasia mutated) a protein kinase that signals the presence of certain types of DNA damage. (nih.gov)
- Ibrutinib is an inhibitor of Bruton's tyrosine kinase (BTK) in the B-cell receptor signaling cascade, and venetoclax inhibits B-cell lymphoma protein 2 (Bcl-2) interaction with select BH3 domain proteins, thereby promoting apoptosis. (medscape.com)
Residues1
- These include the BH3 sequence shared with other pro-apoptotic proteins and an unexpected sequence located near the Bim carboxyl-terminus (residues 181-192). (omicsdi.org)
Inactivation1
- Further, BID and BIM do not distinguish BAX from BAK or accelerate BAX/BAK activation following inactivation of BCL-xL/MCL-1. (omicsdi.org)
Therapeutic2
Tumor2
Venetoclax1
- Venetoclax is in a class of medications called B-cell lymphoma-2 (BCL-2) inhibitors. (medlineplus.gov)
Cell11
- The present invention relates to the field of apoptosis, in particular, it relates to apoptosis-modifying fusion proteins with at least two domains, one of which targets the fusion proteins to a target cell, and another of which modifies an apoptotic response of the target cell. (nih.gov)
- The proteins of the Bcl-2 family are important regulators of apoptosis, or programmed cell death. (omicsdi.org)
- In both cases the bcl-2 expression was not restricted to a specific phase of the cell cycle, as evidenced by two-color analysis. (ox.ac.uk)
- Among fresh B-cell non-Hodgkin's lymphomas (B-NHL), most sporadic Burkitt's cases were bcl-2 negative. (ox.ac.uk)
- One is the Bcl-2 protein Bax, which is a critical component in programmed cell death. (nih.gov)
- Bcl-2 has been reported to regulate cell cycle progression via ROS. (biolegend.com)
- This work also suggests that calcium-binding proteins are useful markers for studies on inner ear hair cell differentiation and regeneration. (jneurosci.org)
- also called CCNB1) cyclin B, a cell cycle inducible protein, prominent in mitosis, which activates cdks. (nih.gov)
- a protein that binds to the Cdt1 component of the pre-replication complex and inactivates it, preventing assembly of the pre-replication complex at inappropriate times during the cell cycle. (nih.gov)
- also called CCNA1) cyclin A, a cell cycle inducible protein, prominent in S-phase, which activates cdks. (nih.gov)
- CCND1 is a member of the highly conserved cyclin family, whose members are characterized by a dramatic periodicity in protein abundance throughout the cell cycle. (nih.gov)
MRNA2
- Several strategies have been employed to target the expression of this protein, including G3139, an 18-mer phosphorothioate oligodeoxyribonucleotide targeted to the initiation region of the Bcl-2 mRNA. (elsevier.com)
- Concurrently, avicularin inhibited the mRNA and protein expression levels of iNOS and COX‑2 increased by TNF‑α. (spandidos-publications.com)
Family members6
- Although disease progression is accompanied by a fall in pro-apoptotic versus anti-apoptotic Bcl-2-related protein ratios, heterogeneity in patterns of protein expression indicates that factors additional to Bcl-2 family members play a role in the deregulated apoptosis in MDS. (bvsalud.org)
- These proteins regulate this fundamental biological process via the formation of heterodimers involving both pro- and anti-apoptotic family members. (omicsdi.org)
- The structure also reveals that N1 has a constitutively open surface groove similar to the grooves of other anti-apoptotic Bcl-2 proteins, which bind the BH3 motifs of pro-apoptotic Bcl-2 family members. (ox.ac.uk)
- Instead, BH3-only proteins appear to control apoptosis by neutralizing pro-survival Bcl2 family members. (the-scientist.com)
- The Bcl-2 protein forms homo- or hetero-dimers with other Bcl-2 family members. (biolegend.com)
- BCL2 associated x protein, highly homologous Bcl-2 family members lacking the BH4 domain. (nih.gov)
Inhibitory1
- FLIP, Fas-associated death domain-like interleukin-1β converting enzyme-like inhibitory protein. (cdc.gov)
Cyclin1
- CDK - a family of cyclin-dependent protein kinases. (nih.gov)
Complexes2
- Using automated Fluorescence Lifetime Imaging Microscopy - Fluorescence Resonance Energy Transfer (FLIM-FRET) we show that the two binding interfaces enable Bim to double-bolt lock Bcl-XL and Bcl-2 in complexes resistant to displacement by BH3-mimetic drugs currently in use or being evaluated for cancer therapy. (omicsdi.org)
- 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)
Caspase1
- Only the viral Bcl-2 protein encoded by gammaHV68 was susceptible to caspase digestion. (nih.gov)
Peptide5
- Recently, we have developed the CABS-dock method for flexible protein-peptide docking that enables large-scale rearrangements of the protein chain. (nature.com)
- The presented case study demonstrates that CABS-dock methodology opens up new opportunities for protein-peptide docking with large-scale changes of the protein receptor structure. (nature.com)
- The protein-peptide binding process frequently involves significant conformational rearrangements of protein receptor and peptide chains. (nature.com)
- Typically, these PPI inhibitors disrupt the interaction between a globular protein and a single peptide chain on the partner protein by binding into pockets on the surface of the globular protein. (lifechemicals.com)
- PPIs can be classified into groups based on common structural elements in both the globular protein and the peptide chain. (lifechemicals.com)
Regulation1
- Results: In vitro, down-regulation of Bcl-2 expression by either method produced no change either in the rate of growth or in sensitivity to standard cytotoxic chemotherapeutic agents. (elsevier.com)
Interaction2
- Different Roles of Beclin1 in the Interaction Between Glia and Neurons after Exposure to Morphine and the HIV- Trans-Activator of Transcription (Tat) Protein. (nih.gov)
- Several docking constraints (positional, H-bond, metal chelation) and amino acid rotatable groups involved in protein-ligand interaction are allowed where reasonable. (lifechemicals.com)
Members2
- Our results provide insight into the molecular basis for the promiscuous nature of this molecular recognition process by members of the Bcl-2 protein family. (omicsdi.org)
- Remarkably, although N1 shows no sequence similarity to cellular proteins, its three-dimensional structure closely resembles Bcl-x(L) and other members of the Bcl-2 protein family. (ox.ac.uk)
Transcription1
- 24. Transcription factor activating protein 2 beta (TFAP2B) mediates noradrenergic neuronal differentiation in neuroblastoma. (nih.gov)
Compounds1
- Examples of virtual hit compounds (binding site: 6GL8) from the BCL-2 compound set. (lifechemicals.com)
Engage1
- It has been widely accepted that mitochondria-dependent apoptosis initiates when select BH3-only proteins (BID, BIM, etc.) directly engage and allosterically activate effector proteins BAX/BAK. (omicsdi.org)
Clone1
- Clone BCL/10C4 has been shown to be useful for Western blotting, immunoprecipitation, and immunofluorescence of the mouse and rat Bcl-2 protein. (biolegend.com)