Chromatin
Chromatin Immunoprecipitation
Chromatin Assembly and Disassembly
Promoter Regions, Genetic
Histones
Transcription, Genetic
Transcription Factors
Protein Binding
Immunoprecipitation
Gene Expression Regulation
DNA-Binding Proteins
Response Elements
Binding Sites
Nucleosomes
Base Sequence
Precipitin Tests
Transcriptional Activation
Repressor Proteins
Nuclear Proteins
Molecular Sequence Data
Electrophoretic Mobility Shift Assay
Gene Silencing
Histone Deacetylases
Chromosomal Proteins, Non-Histone
Sp1 Transcription Factor
DNA
Cell Nucleus
Epigenesis, Genetic
RNA, Messenger
RNA, Small Interfering
Methylation
Cells, Cultured
Trans-Activators
Histone Acetyltransferases
HeLa Cells
RNA Polymerase II
DNA Methylation
Reverse Transcriptase Polymerase Chain Reaction
Blotting, Western
Micrococcal Nuclease
Transfection
RNA Interference
Gene Expression Regulation, Neoplastic
Mutation
Genes, Reporter
Oligonucleotide Array Sequence Analysis
Saccharomyces cerevisiae Proteins
Heterochromatin
p300-CBP Transcription Factors
Signal Transduction
Gene Knockdown Techniques
Luciferases
Transcription Initiation Site
Histone-Lysine N-Methyltransferase
Saccharomyces cerevisiae
Enhancer Elements, Genetic
Histone Deacetylase 1
Phosphorylation
CCAAT-Binding Factor
Histone Deacetylase Inhibitors
Cell Cycle Proteins
Gene Expression Regulation, Developmental
Up-Regulation
Cell Differentiation
Protein Structure, Tertiary
Down-Regulation
DNA Primers
Deoxyribonuclease I
Homeodomain Proteins
Amino Acid Sequence
Gene Expression Profiling
E1A-Associated p300 Protein
Regulatory Elements, Transcriptional
Gene Expression Regulation, Enzymologic
Gene Expression Regulation, Fungal
E-Box Elements
Models, Genetic
Models, Biological
Kruppel-Like Transcription Factors
NIH 3T3 Cells
Chromatin Assembly Factor-1
Centromere
Sex Chromatin
Euchromatin
CpG Islands
Sp3 Transcription Factor
Acetyltransferases
Protein Processing, Post-Translational
CREB-Binding Protein
Plasmids
5' Flanking Region
Cell Cycle
Genome
Gene Expression
Estrogen Receptor alpha
HEK293 Cells
Immunoblotting
Proto-Oncogene Proteins c-myc
Mice, Knockout
Two-Hybrid System Techniques
Chromosomes
Drosophila Proteins
Basic Helix-Loop-Helix Transcription Factors
Insulator Elements
Nucleotide Motifs
Fibroblasts
Polymerase Chain Reaction
DNA Helicases
Transcription Factor RelA
CCAAT-Enhancer-Binding Protein-beta
Recombinant Fusion Proteins
Protein Methyltransferases
NF-kappa B
Upstream Stimulatory Factors
Transcription Factor AP-1
DNA Damage
Polycomb-Group Proteins
Genome, Human
Regulatory Sequences, Nucleic Acid
K562 Cells
E2F1 Transcription Factor
Cyclic AMP Response Element-Binding Protein
Hep G2 Cells
Sequence Analysis, DNA
Multiprotein Complexes
Histone Deacetylase 2
Transcription Factor AP-2
Liver
Apoptosis
Embryonic Stem Cells
Carrier Proteins
Protein Transport
Tumor Suppressor Protein p53
Tumor Cells, Cultured
Electrophoresis, Polyacrylamide Gel
Azacitidine
Hepatocyte Nuclear Factor 3-alpha
Polycomb Repressive Complex 2
Basic-Leucine Zipper Transcription Factors
Gene Deletion
Methyl-CpG-Binding Protein 2
Tumor Suppressor Proteins
High Mobility Group Proteins
Erythroid Cells
RNA
Mitosis
High-Throughput Nucleotide Sequencing
GATA1 Transcription Factor
Mi-2 Nucleosome Remodeling and Deacetylase Complex
Neoplasm Proteins
Conserved Sequence
Proto-Oncogene Proteins
Proto-Oncogene Protein c-ets-1
Mice, Transgenic
Chickens
Polycomb Repressive Complex 1
Drosophila
Membrane Proteins
Fluorescent Antibody Technique
Jumonji Domain-Containing Histone Demethylases
Proto-Oncogene Proteins c-jun
Drosophila melanogaster
Co-Repressor Proteins
Microscopy, Fluorescence
S Phase
Receptors, Cytoplasmic and Nuclear
Adenosine Triphosphatases
Early Growth Response Protein 1
Protein Isoforms
Embryo, Mammalian
Immunosorbent Techniques
Consensus Sequence
Hepatocyte Nuclear Factor 4
Enzyme Inhibitors
Cloning, Molecular
Telomere
Silencer Elements, Transcriptional
YY1 Transcription Factor
Core Binding Factor Alpha 1 Subunit
Cercopithecus aethiops
DNA Footprinting
Active Transport, Cell Nucleus
Histone Code
Genetic Loci
DNA Repair
Gene Expression Regulation, Viral
COS Cells
Specific targeting and constitutive association of histone deacetylase complexes during transcriptional repression. (1/5197)
Specific recruitment of corepressor complexes containing histone deacetylases (HDAC) by transcription factors is believed to play an essential role in transcriptional repression. Recent studies indicate that repression by unliganded nuclear hormone receptors and by the Mad family of repressors requires distinct HDAC-containing corepressor complexes. In this work, we show that unliganded TR specifically recruits only the closely related N-CoR and SMRT-HDAC3 complexes, whereas the Mad1 recruits only the Sin3-HDAC1/2 complex. Significantly, both the Sin3 and Mi-2/NURD complexes also exhibit constitutive association with chromatin and contribute to chromatin deacetylation in a nontargeted fashion. These results suggest that HDAC complexes can contribute to gene repression by two distinct mechanisms as follows: (1) specific targeting by repressors and (2) constitutive association with chromatin. (+info)Partially phosphorylated Pho4 activates transcription of a subset of phosphate-responsive genes. (2/5197)
A cell's ability to generate different responses to different levels of stimulus is an important component of an adaptive environmental response. Transcriptional responses are frequently controlled by transcription factors regulated by phosphorylation. We demonstrate that differential phosphorylation of the budding yeast transcription factor Pho4 contributes to differential gene expression. When yeast cells are grown in high-phosphate growth medium, Pho4 is phosphorylated on four critical residues by the cyclin-CDK complex Pho80-Pho85 and is inactivated. When yeast cells are starved for phosphate, Pho4 is dephosphorylated and fully active. In intermediate-phosphate conditions, a form of Pho4 preferentially phosphorylated on one of the four sites accumulates and activates transcription of a subset of phosphate-responsive genes. This Pho4 phosphoform binds differentially to phosphate-responsive promoters and helps to trigger differential gene expression. Our results demonstrate that three transcriptional outputs can be generated by a pathway whose regulation is controlled by one kinase, Pho80-Pho85, and one transcription factor, Pho4. Differential phosphorylation of Pho4 by Pho80-Pho85 produces phosphorylated forms of Pho4 that differ in their ability to activate transcription, contributing to multiple outputs. (+info)Distinct mechanisms determine transposon inheritance and methylation via small interfering RNA and histone modification. (3/5197)
Heritable, but reversible, changes in transposable element activity were first observed in maize by Barbara McClintock in the 1950s. More recently, transposon silencing has been associated with DNA methylation, histone H3 lysine-9 methylation (H3mK9), and RNA interference (RNAi). Using a genetic approach, we have investigated the role of these modifications in the epigenetic regulation and inheritance of six Arabidopsis transposons. Silencing of most of the transposons is relieved in DNA methyltransferase (met1), chromatin remodeling ATPase (ddm1), and histone modification (sil1) mutants. In contrast, only a small subset of the transposons require the H3mK9 methyltransferase KRYPTONITE, the RNAi gene ARGONAUTE1, and the CXG methyltransferase CHROMOMETHYLASE3. In crosses to wild-type plants, epigenetic inheritance of active transposons varied from mutant to mutant, indicating these genes differ in their ability to silence transposons. According to their pattern of transposon regulation, the mutants can be divided into two groups, which suggests that there are distinct, but interacting, complexes or pathways involved in transposon silencing. Furthermore, different transposons tend to be susceptible to different forms of epigenetic regulation. (+info)Role of Saccharomyces single-stranded DNA-binding protein RPA in the strand invasion step of double-strand break repair. (4/5197)
The single-stranded DNA (ssDNA)-binding protein replication protein A (RPA) is essential for both DNA replication and recombination. Chromatin immunoprecipitation techniques were used to visualize the kinetics and extent of RPA binding following induction of a double-strand break (DSB) and during its repair by homologous recombination in yeast. RPA assembles at the HO endonuclease-cut MAT locus simultaneously with the appearance of the DSB, and binding spreads away from the DSB as 5' to 3' exonuclease activity creates more ssDNA. RPA binding precedes binding of the Rad51 recombination protein. The extent of RPA binding is greater when Rad51 is absent, supporting the idea that Rad51 displaces RPA from ssDNA. RPA plays an important role during RAD51-mediated strand invasion of the MAT ssDNA into the donor sequence HML. The replication-proficient but recombination-defective rfa1-t11 (K45E) mutation in the large subunit of RPA is normal in facilitating Rad51 filament formation on ssDNA, but is unable to achieve synapsis between MAT and HML. Thus, RPA appears to play a role in strand invasion as well as in facilitating Rad51 binding to ssDNA, possibly by stabilizing the displaced ssDNA. (+info)ATF6 modulates SREBP2-mediated lipogenesis. (5/5197)
Activating transcription factor 6 (ATF6) and sterol regulatory element-binding proteins (SREBPs) are activated by proteolytic cleavage. The ensuing nuclear translocation of their N-termini (i.e., ATF6(N) and SREBP(N)) activates the respective target genes involved in unfolded protein response and lipogenesis. Here, we report that glucose deprivation activated ATF6 but suppressed the SREBP2-regulated transcription. Overexpression of ATF6(N) had similar inhibitory effects on SREBP2-targeted genes. The blockade of ATF6 cleavage by BiP/grp78 reversed this inhibitory effect. GST pull-down and immunoprecipitation assays revealed that ATF6(N) bound to SREBP2(N). Deletion analysis of the various functional domains of ATF6 indicated that the interaction was through its leucine-zipper domain. Chromatin immunoprecipitation assays revealed that ATF6(N) formed a complex with the SRE-bound SREBP2(N). The attenuated transcriptional activity of SREBP2 was due, in part, to the recruitment of HDAC1 to the ATF6-SREBP2 complex. As a functional consequence, the lipogenic effect of SREBP2(N) in liver cells was suppressed by ATF6(N). Our results provide a novel mechanism by which ATF6 antagonizes SREBP2 to regulate the homeostasis of lipid and glucose. (+info)Formation, maintenance and consequences of the imprint at the mating-type locus in fission yeast. (6/5197)
Mating-type switching in the fission yeast Schizosaccharomyces pombe is initiated by a strand-specific imprint located at the mating-type (mat1) locus. We show that the imprint corresponds to a single-strand DNA break (SSB), which is site- but not sequence-specific. We identified three novel cis-acting elements, involved in the formation and stability of the SSB. One of these elements is essential for a replication fork pause next to mat1 and interacts in vivo with the Swi1 protein. Another element is essential for maintaining the SSB during cell cycle progression. These results suggest that the DNA break appears during the S-phase and is actively protected against repair. Consequently, during the following round of replication, a polar double-strand break is formed. We show that when the replication fork encounters the SSB, the leading-strand DNA polymerase is able to synthesize DNA to the edge of the SSB, creating a blunt-ended recombination intermediate. (+info)MDR1 promoter hypermethylation in MCF-7 human breast cancer cells: changes in chromatin structure induced by treatment with 5-Aza-cytidine. (7/5197)
Resistance to the cytotoxic actions of antineoplastic drugs, whether intrinsic or acquired, remains a barrier to the establishment of curative chemotherapy regimens for advanced breast cancer. Over-expression of P-glycoprotein (P-gp), encoded by the MDR1 gene and known to mediate resistance to many antineoplastic drugs, may contribute to poor breast cancer treatment outcome. Nonetheless, the precise molecular mechanisms responsible for high or low level P-gp expression in breast cancer cells have not been established. We assessed the role of DNA hypermethylation near the MDR1 transcriptional regulatory region in MDR1 expression in MCF-7 breast cancer cells, which fail to express MDR1 mRNA, and MCF-7/ADR cells, known to express high MDR1 mRNA levels. When compared to MCF-7/ADR cells, MCF-7 cells manifested markedly diminished MDR1 transcription rates by nuclear run-off assay, but equivalent MDR1 promoter trans-activation activity in transient transfection experiments, indicating that cis factors were most likely responsible for the differences in MDR1 transcription between MCF-7/ADR cells and MCF-7 cells. Bisulfite genomic sequencing analyses revealed substantially less extensive MDR1 promoter methylation in MCF-7/ADR cells than in MCF-7 cells, suggesting that CpG dinucleotide methylation might contribute to the observed MDR1 transcription differences. Chromatin immunoprecipitation analyses indicated an inactive MDR1 chromatin conformation in MCF-7 cells, with a paucity of acetylated histones and the presence of 5-mC-binding proteins MeCP2 and MBD2, and an active MDR1 chromatin conformation in MCF-7/ADR cells, with an abundance of acetylated histones and the presence of the transcriptional trans-activator YB-1. Stable MCF-7 sublines which had been treated with the DNA methyltransferase inhibitor 5-azacytidine, exhibited a reduction in MDR1 promoter methylation and a complex MDR1 chromatin configuration, characterized by the simultaneous presence of transcriptional activators and repressors. In this state, MDR1 expression was markedly sensitive to treatment with the histone deacetylase inhibitor trichostatin A. (+info)Spatial organization and dynamics of the association of Rec102 and Rec104 with meiotic chromosomes. (8/5197)
Meiotic double-strand breaks (DSBs) are formed by Spo11 in conjunction with at least nine other proteins whose roles are not well understood. We find that two of these proteins, Rec102 and Rec104, interact physically, are mutually dependent for proper subcellular localization, and share a requirement for Spo11 and Ski8 for their recruitment to meiotic chromosomes, suggesting that they work together as a functional unit. Rec102 associated extensively with chromatin loops during leptotene and zygotene and showed preferential binding in the vicinity at least of most DSB sites, consistent with a direct role in DSB formation. However, Rec102 was associated with both DSB-hot and DSB-cold regions, ruling out a simple model in which sites of DSB formation are dictated by where Rec102/104 complexes load. Both proteins persisted on chromatin until pachytene before abruptly disappearing, indicating that they remain on chromosomes well after DSB formation. These studies reveal unexpected behaviors for Rec102 and Rec104, and point to distinct roles and subcomplexes among the DSB proteins. (+info)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.
Malignant prostatic neoplasms are cancerous tumors that can be aggressive and spread to other parts of the body (metastasize). The most common type of malignant prostatic neoplasm is adenocarcinoma of the prostate, which accounts for approximately 95% of all prostate cancers. Other types of malignant prostatic neoplasms include sarcomas and small cell carcinomas.
Prostatic neoplasms can be diagnosed through a variety of tests such as digital rectal examination (DRE), prostate-specific antigen (PSA) test, imaging studies (ultrasound, CT scan or MRI), and biopsy. Treatment options for prostatic neoplasms depend on the type, stage, and grade of the tumor, as well as the patient's age and overall health. Treatment options can include active surveillance, surgery (robotic-assisted laparoscopic prostatectomy or open prostatectomy), radiation therapy (external beam radiation therapy or brachytherapy), and hormone therapy.
In summary, Prostatic Neoplasms are tumors that occur in the prostate gland, which can be benign or malignant. The most common types of malignant prostatic neoplasms are adenocarcinoma of the prostate, and other types include sarcomas and small cell carcinomas. Diagnosis is done through a variety of tests, and treatment options depend on the type, stage, and grade of the tumor, as well as the patient's age and overall health.
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.
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
There are several types of genomic instability, including:
1. Chromosomal instability (CIN): This refers to changes in the number or structure of chromosomes, such as aneuploidy (having an abnormal number of chromosomes) or translocations (the movement of genetic material between chromosomes).
2. Point mutations: These are changes in a single base pair in the DNA sequence.
3. Insertions and deletions: These are changes in the number of base pairs in the DNA sequence, resulting in the insertion or deletion of one or more base pairs.
4. Genomic rearrangements: These are changes in the structure of the genome, such as chromosomal breaks and reunions, or the movement of genetic material between chromosomes.
Genomic instability can arise from a variety of sources, including environmental factors, errors during DNA replication and repair, and genetic mutations. It is often associated with cancer, as cancer cells have high levels of genomic instability, which can lead to the development of resistance to chemotherapy and radiation therapy.
Research into genomic instability has led to a greater understanding of the mechanisms underlying cancer and other diseases, and has also spurred the development of new therapeutic strategies, such as targeted therapies and immunotherapies.
In summary, genomic instability is a key feature of cancer cells and is associated with various diseases, including cancer, neurodegenerative disorders, and aging. It can arise from a variety of sources and is the subject of ongoing research in the field of molecular biology.
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.
1. Tumor size and location: Larger tumors that have spread to nearby tissues or organs are generally considered more invasive than smaller tumors that are confined to the original site.
2. Cellular growth patterns: The way in which cancer cells grow and divide can also contribute to the overall invasiveness of a neoplasm. For example, cells that grow in a disorganized or chaotic manner may be more likely to invade surrounding tissues.
3. Mitotic index: The mitotic index is a measure of how quickly the cancer cells are dividing. A higher mitotic index is generally associated with more aggressive and invasive cancers.
4. Necrosis: Necrosis, or the death of cells, can be an indication of the level of invasiveness of a neoplasm. The presence of significant necrosis in a tumor is often a sign that the cancer has invaded surrounding tissues and organs.
5. Lymphovascular invasion: Cancer cells that have invaded lymphatic vessels or blood vessels are considered more invasive than those that have not.
6. Perineural invasion: Cancer cells that have invaded nerve fibers are also considered more invasive.
7. Histological grade: The histological grade of a neoplasm is a measure of how abnormal the cancer cells look under a microscope. Higher-grade cancers are generally considered more aggressive and invasive than lower-grade cancers.
8. Immunohistochemical markers: Certain immunohistochemical markers, such as Ki-67, can be used to evaluate the proliferative activity of cancer cells. Higher levels of these markers are generally associated with more aggressive and invasive cancers.
Overall, the degree of neoplasm invasiveness is an important factor in determining the likelihood of the cancer spreading to other parts of the body (metastasizing) and in determining the appropriate treatment strategy for the patient.
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.
Neuroblastoma is caused by a genetic mutation that affects the development and growth of nerve cells. The cancerous cells are often sensitive to chemotherapy, but they can be difficult to remove surgically because they are deeply embedded in the nervous system.
There are several different types of neuroblastoma, including:
1. Infantile neuroblastoma: This type of neuroblastoma occurs in children under the age of one and is often more aggressive than other types of the cancer.
2. Juvenile neuroblastoma: This type of neuroblastoma occurs in children between the ages of one and five and tends to be less aggressive than infantile neuroblastoma.
3. Adult neuroblastoma: This type of neuroblastoma occurs in adults and is rare.
4. Metastatic neuroblastoma: This type of neuroblastoma has spread to other parts of the body, such as the bones or liver.
Symptoms of neuroblastoma can vary depending on the location and size of the tumor, but they may include:
* Abdominal pain
* Fever
* Loss of appetite
* Weight loss
* Fatigue
* Bone pain
* Swelling in the abdomen or neck
* Constipation
* Increased heart rate
Diagnosis of neuroblastoma typically involves a combination of imaging tests, such as CT scans and MRI scans, and biopsies to confirm the presence of cancerous cells. Treatment for neuroblastoma usually involves a combination of chemotherapy, surgery, and radiation therapy. The prognosis for neuroblastoma varies depending on the type of cancer, the age of the child, and the stage of the disease. In general, the younger the child and the more aggressive the treatment, the better the prognosis.
Neoplasm refers to an abnormal growth of cells that can be benign (non-cancerous) or malignant (cancerous). Neoplasms can occur in any part of the body and can affect various organs and tissues. The term "neoplasm" is often used interchangeably with "tumor," but while all tumors are neoplasms, not all neoplasms are tumors.
Types of Neoplasms
There are many different types of neoplasms, including:
1. Carcinomas: These are malignant tumors that arise in the epithelial cells lining organs and glands. Examples include breast cancer, lung cancer, and colon cancer.
2. Sarcomas: These are malignant tumors that arise in connective tissue, such as bone, cartilage, and fat. Examples include osteosarcoma (bone cancer) and soft tissue sarcoma.
3. Lymphomas: These are cancers of the immune system, specifically affecting the lymph nodes and other lymphoid tissues. Examples include Hodgkin lymphoma and non-Hodgkin lymphoma.
4. Leukemias: These are cancers of the blood and bone marrow that affect the white blood cells. Examples include acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL).
5. Melanomas: These are malignant tumors that arise in the pigment-producing cells called melanocytes. Examples include skin melanoma and eye melanoma.
Causes and Risk Factors of Neoplasms
The exact causes of neoplasms are not fully understood, but there are several known risk factors that can increase the likelihood of developing a neoplasm. These include:
1. Genetic predisposition: Some people may be born with genetic mutations that increase their risk of developing certain types of neoplasms.
2. Environmental factors: Exposure to certain environmental toxins, such as radiation and certain chemicals, can increase the risk of developing a neoplasm.
3. Infection: Some neoplasms are caused by viruses or bacteria. For example, human papillomavirus (HPV) is a common cause of cervical cancer.
4. Lifestyle factors: Factors such as smoking, excessive alcohol consumption, and a poor diet can increase the risk of developing certain types of neoplasms.
5. Family history: A person's risk of developing a neoplasm may be higher if they have a family history of the condition.
Signs and Symptoms of Neoplasms
The signs and symptoms of neoplasms can vary depending on the type of cancer and where it is located in the body. Some common signs and symptoms include:
1. Unusual lumps or swelling
2. Pain
3. Fatigue
4. Weight loss
5. Change in bowel or bladder habits
6. Unexplained bleeding
7. Coughing up blood
8. Hoarseness or a persistent cough
9. Changes in appetite or digestion
10. Skin changes, such as a new mole or a change in the size or color of an existing mole.
Diagnosis and Treatment of Neoplasms
The diagnosis of a neoplasm usually involves a combination of physical examination, imaging tests (such as X-rays, CT scans, or MRI scans), and biopsy. A biopsy involves removing a small sample of tissue from the suspected tumor and examining it under a microscope for cancer cells.
The treatment of neoplasms depends on the type, size, location, and stage of the cancer, as well as the patient's overall health. Some common treatments include:
1. Surgery: Removing the tumor and surrounding tissue can be an effective way to treat many types of cancer.
2. Chemotherapy: Using drugs to kill cancer cells can be effective for some types of cancer, especially if the cancer has spread to other parts of the body.
3. Radiation therapy: Using high-energy radiation to kill cancer cells can be effective for some types of cancer, especially if the cancer is located in a specific area of the body.
4. Immunotherapy: Boosting the body's immune system to fight cancer can be an effective treatment for some types of cancer.
5. Targeted therapy: Using drugs or other substances to target specific molecules on cancer cells can be an effective treatment for some types of cancer.
Prevention of Neoplasms
While it is not always possible to prevent neoplasms, there are several steps that can reduce the risk of developing cancer. These include:
1. Avoiding exposure to known carcinogens (such as tobacco smoke and radiation)
2. Maintaining a healthy diet and lifestyle
3. Getting regular exercise
4. Not smoking or using tobacco products
5. Limiting alcohol consumption
6. Getting vaccinated against certain viruses that are associated with cancer (such as human papillomavirus, or HPV)
7. Participating in screening programs for early detection of cancer (such as mammograms for breast cancer and colonoscopies for colon cancer)
8. Avoiding excessive exposure to sunlight and using protective measures such as sunscreen and hats to prevent skin cancer.
It's important to note that not all cancers can be prevented, and some may be caused by factors that are not yet understood or cannot be controlled. However, by taking these steps, individuals can reduce their risk of developing cancer and improve their overall health and well-being.
Chromatin immunoprecipitation
Regulome
Mammalian promoter database
Biotinylation
Tiling array
Cellular differentiation
SUZ12
BECN1
Chromosome conformation capture
ATAC-seq
Staphylococcus aureus
ChIP-exo
CCDC188
Eileen Furlong
Pseudo-response regulator
ChIP sequencing
E2F3
CBX5 (gene)
E2F2
FAM227B
ChIP-on-chip
Michael P. Snyder
GAS2L1
HIST2H4A
CSDA (gene)
Transcription factor
HIST1H2BJ
RECQL
HIST1H2AG
MFAP1
Epigenomics
Mediator (coactivator)
H4K8ac
MECOM
C18orf63
Multiple displacement amplification
AI-10-49
DNA adenine methyltransferase identification
Sono-Seq
Survivin
Forkhead box protein O1
Facioscapulohumeral muscular dystrophy
MOWChIP-seq
MEME suite
H2BK5ac
H3K36ac
SMIM19
GSTM3
G0 phase
MNase-seq
H4K91ac
Sirtuin 7
β-arrestin1/YAP/mutant p53 complexes orchestrate the endothelin A receptor signaling in high-grade serous ovarian cancer |...
Isotype: MIgG2c, RIgG2b, Recommended Applications: Chromatin-Immunoprecipitation, Immunoprecipitation
culture cells meaning - ChiP antibodies for Chromatin immunoprecipitation
Frontiers | IL-23R is Epigenetically Regulated and Modulated by Chemotherapy in Non-Small Cell Lung Cancer
What is Chromatin Immunoprecipitation (ChIP) and how does it
work? - JustAAA
DNMT3A and TET1 cooperate to regulate promoter epigenetic landscapes in mouse embryonic stem cells | Genome Biology | Full Text
The E3 ubiquitin ligase TRIM23 regulates adipocyte differentiation via stabilization of the adipogenic activator PPARγ | eLife
Runx1t1 (Runt-related transcription factor 1; translocated to, 1) epigenetically regulates the proliferation and nitric oxide...
Cross-talk between Colon Cells and Macrophages Increases ST6GALNAC1 and MUC1-sTn Expression in Ulcerative Colitis and Colitis...
Impact of Glycemic Variability on Chromatin Remodeling, Oxidative Stress, and Endothelial Dysfunction in Patients With Type 2...
NINDS Interpretation of the NIH GDS Policy | National Institute of Neurological Disorders and Stroke
W-ChIPMotifs -- ChIP-based protein Motif discovery web server | HSLS
Hamartin/TSC1 (D43E2) Rabbit mAb | Cell Signaling Technology
JMJD3 promotes survival of diffuse large B-cell lymphoma subtypes via distinct mechanisms | Oncotarget
Human hg18 TAPT1 UCSC Genome Browser v448
scPCOR-seq enables co-profiling of chromatin occupancy and RNAs in single cells - PubMed
Building Blocks, Biological Pathways and Networks - Laboratory Methods
i|ASXL1|/i| mutations accelerate bone marrow fibrosis via EGR1-TNFA axis-mediated neoplastic fibrocyte generation in...
Publication Detail
Robin Webster's Problem Solver Profile on IdeaConnection
Studies - Leping Li, Ph.D.
NIMH » Macrophage Infection by HIV: Implications for Pathogenesis and Cure: Day One
Genes | Free Full-Text | Contribution of Topological Domains and Loop Formation to 3D Chromatin Organization
cChIP-seq: a robust small-scale method for investigation of histone modifications | BMC Genomics | Full Text
Molecular Neuroscience: A Laboratory Manual
Gene Expression: Transcription, Splicing and Translation | Biology | JoVE
Publications | Tanay Group
ChIP-Seq3
- Purification of nanogram-range immunoprecipitated DNA in ChIP-seq utility Chromatin immunoprecipitation-sequencing (ChIP-seq) is a broadly used epigenetic strategy for investigating genome-wide protein-DNA interactions in cells and tissues. (chipready.com)
- Chromatin immunoprecipitation (ChIP) coupled with microarray (ChIP-chip) or sequencing (ChIP- seq) is a widely used technique for understanding the genome-wide binding pattern of regulatory proteins. (sbir.gov)
- He and his colleagues therefore developed novel sequencing-based methods to study the epigenome, such as ChIP-Seq, which combines chromatin immunoprecipitation (ChIP) with the Next Generation Sequencing technique, and micrococcal nuclease sequencing (MNase-Seq). (nih.gov)
Assay5
- It is a powerful assay technique that can be used to probe DNA-protein interaction within a cell's neutral chromatin environment. (justaaa.com)
- We offer ATAC-seq (Assay for Transposase Accessible Chromatin with high-throughput sequencing) to assess genome-wide chromatin accessibility, transcription factor binding, and nucleosome positioning and CUT&RUN (Cleavage Under Targets and Release Using Nuclease) for genome-wide profiling of DNA-bound proteins. (mdanderson.org)
- We investigated via chromatin immunoprecipitation (ChIP) assay whether or not non-androgen stimuli (β-estradiol and EGF) could lead to AR binding to the known androgen receptor elements (AREs) of several genes: prostate specific antigen (PSA), FK506 binding protein 5 (FKBP5), insulin-like growth factor 1 (IGF-1), cyclin-dependent kinase inhibitor 1A (CDKN1A), and transmembrane protease, serine 2 (TMPRSS2). (thermofisher.com)
- Using HepG2 and SMMC-7721 cells that aberrantly overexpressed COMMD7 , we found that NF-κB directly binds with COMMD7 promoter and serves as an activator for COMMD7 transcription by luciferase reporter assay, chromatin immunoprecipitation (ChIP), and electrophoretic mobility shift assay (EMSA). (oncotarget.com)
- 5. A rapid micro chromatin immunoprecipitation assay (microChIP). (nih.gov)
Binding protein1
- In conclusion, we identified PfBDP7 as a chromatin binding protein that is a constitutive part of the P. falciparum BDP1/BDP2 core complex and established PfBDP1 and PfBDP7 as novel players in the silencing of heterochromatin regulated virulence gene families of the malaria parasite P. falciparum . (frontiersin.org)
Antibodies2
- All ChIPAb+ antibodies are individually validated for chromatin precipitation, every lot, every time. (anobase.org)
- After shearing the DNA into small fragments, specific DNA-protein complexes are isolated by immunoprecipitation with protein-specific ANTIBODIES . (nih.gov)
Input chromatin2
- PCR reactions should be performed in duplicate and should include a tube with no DNA to control for contamination, and a serial dilution of a 2% total input chromatin DNA (undiluted, 1:5, 1:25, 1:125), which is used to create a standard curve and determine amplification efficiency. (cellsignal.com)
- Data is presented as percent input of each IP sample relative to input chromatin for each amplicon and ChIP sample as indicated. (anobase.org)
Real-tim1
- 10. Chromatin Immunoprecipitation and Quantitative Real-Time PCR to Assess Binding of a Protein of Interest to Identified Predicted Binding Sites Within a Promoter. (nih.gov)
Primers3
- SimpleChIP ® Human MX1 Promoter Primers were tested on DNA isolated from cross-linked cells using the SimpleChIP ® Enzymatic Chromatin IP Kit (Magnetic Beads) #9003. (cellsignal.com)
- These primers can be used to amplify DNA that has been isolated using chromatin immunoprecipitation (ChIP). (cellsignal.com)
- Successful immunoprecipitation of HDAC1 associated DNA fragments was verified by qPCR using ChIP Primers, p21 flanking an Sp1 binding site in the human p21 promoter (Figure 1). (anobase.org)
Assays2
Histone3
- 9. Linker histone epitopes are hidden by in situ higher-order chromatin structure. (nih.gov)
- 20. Chromatin immunoprecipitation (ChIP) for analysis of histone modifications and chromatin-associated proteins. (nih.gov)
- His laboratory is studying how the interplay between transcription factors and various chromatin modifying enzymes, including both histone modifying enzymes and ATP-dependent chromatin remodeling complexes, regulates the dynamic epigenomic landscapes in various hematopoietic lineages. (nih.gov)
Polymerase1
- This led to the hypothesis that HDACs operate dynamically to reset chromatin after RNA polymerase II directs transcriptional elongation at active genes, whereas HDACs and HATs function together to maintain inactive genes at a poised state that can be induced rapidly in response to environmental cues. (nih.gov)
Sequencing2
- This study examined plasma cell -free DNA chromatin immunoprecipitation sequencing (cfChIP-seq) as a noninvasive proxy to define molecular gene sets and sources of tissue injury in heart transplant patients . (bvsalud.org)
- Chromatin immunoprecipitation and sequencing showed an increase in H3K27me3 'marks' and a dramatic shift in their location. (nih.gov)
Cells6
- Temporary cross-linking of protein and associated chromatin is done in live cells or tissues with the help of formaldehyde or UV. (justaaa.com)
- LincRNAs were identified first in mammalian cells, and they are key regulators of diverse biological processes such as transcription and chromatin epigenetics [ 3 , 4 ]. (biomedcentral.com)
- 17. Chromatin Immunoprecipitation in Human and Yeast Cells. (nih.gov)
- 18. Chromatin immunoprecipitation in adult zebrafish red cells. (nih.gov)
- U2OS cells (3 X 10E6 cell equivalents per IP) was subjected to chromatin immunoprecipitation using using 2 µg of either Normal Rabbit IgG, or 2 µg of Anti-HDAC1 and the Magna ChIP ® A Kit (Cat. (anobase.org)
- This FOA requests proposals that will develop an affinity reagent resource for human transcription factors of the broadest possible utility, including possible detection of the target protein in a sample, immuno-chemical labeling of a tissue sample or cells, or immunoprecipitation of the target protein. (nih.gov)
Regulatory1
- To identify primary GR target genes, in which GR is a component of the transcriptional regulatory complex, we developed a strategy that uses chromatin immunoprecipitation to scan putative regulatory regions of target genes for sites occupied by specifically bound GR. We screened 11 glucocorticoid-regulated genes, and we identified GR-binding regions for eight of them (five induced and three repressed). (nih.gov)
Gene4
- The position of chromatin in regulating common gene expression has been extensively studied. (chipready.com)
- 2. Two-step cross-linking method for identification of NF-kappaB gene network by chromatin immunoprecipitation. (nih.gov)
- 14. Distinct alterations in chromatin organization of the two IGF-I promoters precede growth hormone-induced activation of IGF-I gene transcription. (nih.gov)
- Setd1a and NURF mediate chromatin dynamics and gene regulation during erythroid lineage commitment and differentiation. (nih.gov)
Pathways1
- Cell-free chromatin immunoprecipitation to detect molecular pathways in heart transplantation. (bvsalud.org)
Epigenome1
- Chromatin immunoprecipitation provides understanding of such mechanisms that clock and non-clock transcription factors along with co-regulators and chromatin modifications dictate circadian epigenome through cyclic alterations of chromatin structures and molecular functions in a concerted fashion. (elsevier.com)
Modifications1
- Nucleosomes, the fundamental constructions used to bundle genetic info into chromatin, are topic to a various array of chemical modifications. (chipready.com)
Epigenetic1
- Further Chromatin immunoprecipitation (ChIP) analysis confirmed that the KLF2 and active epigenetic marks (H3K27Ac and H3K4me3) were upregulated in the promoter region ATG7 during OB differentiation. (nih.gov)
Proteins1
- It involves formaldehyde fixation of CHROMATIN to crosslink the DNA-BINDING PROTEINS to the DNA . (nih.gov)
Detect1
- Chromosome construction seize expertise can detect the three-dimensional building of chromatin. (chipready.com)
Biological1
- Recommended use: ~2 μg of antibody per chromatin immunoprecipitation (dependent upon biological context). (anobase.org)
Protocols1
- The qPCR protocol and primer sequences are provided, allowing researchers to validate ChIP protocols when using our antibody in their chromatin context. (anobase.org)
Interactions1
- 1. Two-step cross-linking for analysis of protein-chromatin interactions. (nih.gov)
Structure2
- This controversy might have been influenced by the confounding effect of subtelomeric regions and interstitial telomeric sequences (ITSs) on telomeric chromatin structure analyses. (nih.gov)
- We have developed a reliable procedure to study the chromatin structure of human telomeres independently of subtelomeres and ITSs. (nih.gov)
Human1
- 6. Acetylation of nucleosomal histones by p300 facilitates transcription from tax-responsive human T-cell leukemia virus type 1 chromatin template. (nih.gov)
Data1
- Find de novo protein motifs from chromatin immunoprecipitation data. (pitt.edu)
Sample2
- Instruments are available for sample shearing, automated chromatin immunoprecipitation, automated library construction, library quality assessment and purification, and real-time qPCR. (nih.gov)
- This FOA requests applications that will develop an affinity reagent resource of the broadest possible utility, including detection of the target protein in a sample, immuno-histochemical labeling of a tissue sample, or immunoprecipitation or other affinity capture of the target protein. (nih.gov)
Analysis3
- The Epigenomics Profiling Core is pleased to announce that it now offers cfMeDIP (circulating cell-free methylated DNA immunoprecipitation) as part of its DNA methylation analysis repertoire. (mdanderson.org)
- 8. Analysis of in vivo transcription factor recruitment by chromatin immunoprecipitation of mouse embryonic kidney. (nih.gov)
- 16. Analysis of p300 occupancy at the early stage of stem cell differentiation by chromatin immunoprecipitation. (nih.gov)
Method1
- Chromatin Immunoprecipitation (ChIP) is a method of determining the interaction between a protein of interest and a specific sequence of DNA. (justaaa.com)
Sites1
- 7. Assessing sites of NF-κB DNA binding using chromatin immunoprecipitation. (nih.gov)
Cell1
- The change of H3K27me3 chromatin-binding pattern is directly related to cell cycle reentry and cell death of ATM-deficient neurons. (nih.gov)