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Proto-Oncogene Proteins B-raf
Proto-Oncogene Proteins B-raf
Proto-Oncogene Proteins B-raf: A family of serine/threonine-protein kinases that play a critical role in the regulation of the mitogen-activated protein kinase (MAPK) signaling pathway.
These proteins are frequently mutated in various types of cancer, leading to constitutive activation of the MAPK pathway and uncontrolled cell growth.
Leveraging PubCompare.ai, researchers can optimize their B-raf proto-oncogene research protocols for reproducibility and accuarcy, identifying the best procedures and products from literature, preprints, and patents to advance their studies.
These proteins are frequently mutated in various types of cancer, leading to constitutive activation of the MAPK pathway and uncontrolled cell growth.
Leveraging PubCompare.ai, researchers can optimize their B-raf proto-oncogene research protocols for reproducibility and accuarcy, identifying the best procedures and products from literature, preprints, and patents to advance their studies.
Most cited protocols related to «Proto-Oncogene Proteins B-raf»
A dilution series of BRAF V600E mutant DNA (HTB-38D) from a HT-29 cell line (ATCC) was prepared in a high, constant background (5 000 copies/μL) of wildtype DNA (NA19205, Coriell). For ddPCR, when the concentration of intact human genomic DNA is >66 ng/20 μL reaction, the accompanying increase in viscosity can cause the average droplet volume to change, which in turn could affect the accuracy of DNA quantitation. Therefore, for samples of this nature, restriction enzyme digestion is recommended to fragment the DNA and reduce solution viscosity. In our experience, once fragmented, the human genomic DNA concentration can exceed 1 μg/20 μL reaction without affecting the average droplet volume. Therefore, prior to ddPCR, each sample of the dilution series was digested with 40 U of HaeIII (NEB) in 100 μL containing 1× NEB buffer 4 and BSA. The BRAF V600E/wildtype duplex TaqMan assay used common primers (forward) 5′-CTACTGTTTTCCTTTACTTACTACACCTCAGA-3′, (reverse) 5′-ATCCAGACAACTGTTCAAACTGATG-3′, and specific probes (BRAF V600E) 6FAM-TAGCTACAGAGAAATC-MGBNFQ and (wildtype) VIC-CTAGCTACAGTGAAATC-MGBNFQ. Eight ddPCR wells were used for each sample of the dilution series. Thermal cycling conditions were 95 °C × 10 min (1 cycle), 94 °C × 30 s and 62.7 °C × 60 s (55 cycles), and 12 °C hold.
Biological Assay
Buffers
Digestion
DNA, A-Form
DNA Restriction Enzymes
Genome, Human
HT29 Cells
Oligonucleotide Primers
Proto-Oncogene Proteins B-raf
Technique, Dilution
Viscosity
MCF 10A, Hs 578T, MDA-MB-231, MCF7, SK-BR-3, and BT-20 were plated at densities ranging from 156 to 5000 cells per well in 384-well plates using the Multidrop Combi Reagent Dispenser (Thermo Scientific) and grown for 24 hours. Cells were treated with a dilution series of the indicated drugs using a D300 Digital Dispenser (Hewlett-Packard). Cells were stained and fixed for analysis at the time of drug treatment and after 72 hours of incubation with drug. For these experiments, we used the following drugs:
Erlotinib, EGFR inhibitor
Etoposide, Topiosomerase inhibitor
Lapatinib, EGFR/ErbB2 inhibitor
Linsitinib, IGF1R inhibitor
Methotrexate, dihydrofolate reductase inhibitor
Omipalisib/GSK2126458, panPI3K/mTOR inhibitor
Paclitaxel, target microtubules
Palbociclib, CDK4/6 inhibitor
PLX4720, B-RAF inhibitor
TAE684, ALK inhibitor
Tanespimycin/17-AAG, HSP90 inhibitor
Cells
EGFR protein, human
Erlotinib
Fingers
FRAP1 protein, human
GSK 2126458
herstatin protein, human
HSP90 Heat-Shock Proteins
IGF1R protein, human
MCF-7 Cells
Pharmaceutical Preparations
Proto-Oncogene Proteins B-raf
tanespimycin
Technique, Dilution
Tetrahydrofolate Dehydrogenase
Cells
Etoposide
Fingers
FRAP1 protein, human
GSK 2126458
HSP90 Heat-Shock Proteins
IGF1R protein, human
Pharmaceutical Preparations
Proto-Oncogene Proteins B-raf
tanespimycin
Technique, Dilution
MCF10 A-H2B-mCherry and BT-20-H2B-mCherry at 1250 and 2500 cells per well respectively in 384-well plates using the Multidrop Combi Reagent Dispenser (Thermo Scientific) and grown for 24 hours. Cells were treated with a dilution series of the indicated drugs using a D300 Digital Dispenser (Hewlett-Packard) and imaged after drug addition in an Operetta (Perkin Elmer) for high content imaging system equipped with a live-cell chamber over a period of 96 hours. For these experiments, we used the following drugs:
Etoposide, Topiosomerase inhibitor
Linsitinib, IGF1R inhibitor
Omipalisib/GSK2126458, panPI3K/mTOR inhibitor
PLX4720, B-RAF inhibitor
Tanespimycin/17-AAG, HSP90 inhibitor
Cells
Etoposide
Fingers
FRAP1 protein, human
GSK 2126458
HSP90 Heat-Shock Proteins
IGF1R protein, human
Pharmaceutical Preparations
Proto-Oncogene Proteins B-raf
tanespimycin
Technique, Dilution
Two experiments were applied for each target:
Autodock parameters were defined in a similar way as in Glide, with grid boxes dimensions of 20 × 20 × 20 Å3. AutoDock uses a semi-empirical free energy force field to predict binding energies or ligands to macromolecular targets and Lamarckian genetic algorithm (GA) to search for docking solutions [69 (link)]. The force field is based on a comprehensive thermodynamic model that allows incorporation of intramolecular energies into the predicted free energy of binding [70 (link)]. Each ligand was located in the grid box for each docking run and torsional degrees of freedom were defined. The GA was applied with an initial population of 100 randomly placed individuals, a maximum number of 1 × 106 energy evaluations, a maximum number of 3 × 104 generations, a mutation rate of 0.02, a crossover rate of 0.80, and an elitism value of 2.
Each self-docking or cross-docking experiment between a target protein (MAO-B, thrombin or B-RAF) and a ligand was repeated three times, accounting for replicated instances. The effectiveness of the docking experiment (self-docking or cross-docking) in reproducing the crystallographic binding orientation of a ligand was determined by comparing the docked pose with the orientation of the ligand in its native crystallographic structure . In the case of MAO-B, the cofactor FAD was present in the binding site during docking experiments. The RMSD was employed as the term for performing such comparison, where ligand atoms were matched one to one and symmetrical atoms were considered equivalent. For comparing cross-docking poses, receptor structures were superimposed using Cα of binding site amino acids, by considering that amino acids that surround 10 Å the ligand in its native crystallographic structure form the binding site.
Self-docking of each ligand inside its own protein structural conformation.
Cross-docking of three selected ligands inside the remaining nine protein structures.
Autodock parameters were defined in a similar way as in Glide, with grid boxes dimensions of 20 × 20 × 20 Å3. AutoDock uses a semi-empirical free energy force field to predict binding energies or ligands to macromolecular targets and Lamarckian genetic algorithm (GA) to search for docking solutions [69 (link)]. The force field is based on a comprehensive thermodynamic model that allows incorporation of intramolecular energies into the predicted free energy of binding [70 (link)]. Each ligand was located in the grid box for each docking run and torsional degrees of freedom were defined. The GA was applied with an initial population of 100 randomly placed individuals, a maximum number of 1 × 106 energy evaluations, a maximum number of 3 × 104 generations, a mutation rate of 0.02, a crossover rate of 0.80, and an elitism value of 2.
Each self-docking or cross-docking experiment between a target protein (MAO-B, thrombin or B-RAF) and a ligand was repeated three times, accounting for replicated instances. The effectiveness of the docking experiment (self-docking or cross-docking) in reproducing the crystallographic binding orientation of a ligand was determined by comparing the docked pose with the orientation of the ligand in its native crystallographic structure . In the case of MAO-B, the cofactor FAD was present in the binding site during docking experiments. The RMSD was employed as the term for performing such comparison, where ligand atoms were matched one to one and symmetrical atoms were considered equivalent. For comparing cross-docking poses, receptor structures were superimposed using C
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Amino Acids
Binding Sites
Crystallography
Ligands
Monoamine Oxidase B
Proteins
Protein Targeting, Cellular
Proto-Oncogene Proteins B-raf
Reproduction
Thrombin
Most recents protocols related to «Proto-Oncogene Proteins B-raf»
Cobimetinib (provided by Hoffmann-La Roche) is an oral selective inhibitor of the MEK pathway. Vemurafenib (provided by Hoffmann-La Roche) is a low-molecular-weight inhibitor of BRAF serine–threonine kinase. Atezolizumab (provided by Hoffmann-La Roche) is an anti-PD-L1 antibody.
The study will include three possible treatments: (1) Vemurafenib 960 mg twice daily per os from day 1 to 42; (2) Vemurafenib 720 mg twice daily per os from day 1 to 42; (3) Cobimetinib 60 mg once daily per os from day 1 to 21 and from day 29 to 42; Cobimetinib should not be taken on days 22–28; and (4) Atezolizumab 840 mg intravenous for two cycles (days 22 and 43).
Patients will be randomized to three different arms: A) BRAF-mutated patients will receive (1) + (3) for 6 weeks; B) BRAF-mutated patients will receive (2) + (3) + (4) for 6 weeks; C) BRAF WT patients will receive (3) + (4) for 6 weeks.
All patients will also receive Atezolizumab 1200 mg intravenous every 3 weeks for 17 cycles after surgery and after a second screening period (up to 6 weeks).
The study will include three possible treatments: (1) Vemurafenib 960 mg twice daily per os from day 1 to 42; (2) Vemurafenib 720 mg twice daily per os from day 1 to 42; (3) Cobimetinib 60 mg once daily per os from day 1 to 21 and from day 29 to 42; Cobimetinib should not be taken on days 22–28; and (4) Atezolizumab 840 mg intravenous for two cycles (days 22 and 43).
Patients will be randomized to three different arms: A) BRAF-mutated patients will receive (1) + (3) for 6 weeks; B) BRAF-mutated patients will receive (2) + (3) + (4) for 6 weeks; C) BRAF WT patients will receive (3) + (4) for 6 weeks.
All patients will also receive Atezolizumab 1200 mg intravenous every 3 weeks for 17 cycles after surgery and after a second screening period (up to 6 weeks).
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Antibodies, Anti-Idiotypic
Arm, Upper
atezolizumab
CD274 protein, human
cobimetinib
Operative Surgical Procedures
Patients
Protein-Serine-Threonine Kinases
Proto-Oncogene Proteins B-raf
Vemurafenib
Dead Cell Apoptosis Kit with Alexa Fluor 488 Annexin V and PI for Flow Cytometry (Thermo Fisher Scientific, V13241) was applied to determine cell death after BRAF transduction and CM treatment described as above. Cells were washed with cold PBS and resuspended with annexin V binding buffer, 5 µl Alexa Fluor 488 annexin V and 1 µl 100 μg/mL PI working solution were added to 100 µl of cell suspension. Cells were then incubated in the dark at room temperature for 15 min and another 400 µl of binding buffer was added. Data were collected on flow cytometer and were analyzed with FlowJo.
alexa fluor 488
Annexin A5
Apoptosis
Buffers
Cell Death
Cells
Cold Temperature
Flow Cytometry
Proto-Oncogene Proteins B-raf
An open-label, multicenter, single-arm, non-randomized phase 1b clinical trial was conducted in Australia and China, where 16 sites enrolled patients with NSCLC.
The study enrolled nine cohorts of patients with various advanced solid tumors, including five cohorts of patients with NSCLC (figure 1 ; online supplemental table 1 ). All patients in the NSCLC cohorts were required to be aged ≥18 years, with histologically or cytologically confirmed disease, at least one measurable lesion (as defined by Response Evaluation Criteria in Solid Tumors [RECIST] V.1.1), with the selected target lesion(s) not previously treated with local therapy, or with progression following local therapy, with an Eastern Cooperative Oncology Group performance status ≤1, and no documented epidermal growth factor receptor mutation (wild-type status was required for non-squamous cohorts), anaplastic lymphoma kinase/proto-oncogene tyrosine-protein kinase ROS1 rearrangement, or B-Raf proto-oncogene, serine/threonine kinase mutations.
Additional cohort-specific inclusion criteria are summarized infigure 1 and in online supplemental file , which include full inclusion and exclusion criteria.
The study enrolled nine cohorts of patients with various advanced solid tumors, including five cohorts of patients with NSCLC (
Additional cohort-specific inclusion criteria are summarized in
Anaplastic Lymphoma Kinase
Disease Progression
Epidermal Growth Factor Receptor
Mutation
Neoplasms
Non-Small Cell Lung Carcinoma
Patients
Protein-Serine-Threonine Kinases
Protein Tyrosine Kinase
Proto-Oncogene Proteins B-raf
Proto-Oncogenes
ROS1 protein, human
Therapeutics
Patient-derived organoid generation was attempted from baseline biopsies of all patients. A total of 10 colorectal tumor organoid lines were successfully generated from tumor baseline biopsies of 10 patients enrolled in the BRAF/MEK/PD-1 inhibition trial (patients 1, 2, 4, 10, 11, 14, 16, 18, 21 and 24). Tumor biopsies were transported in ice-cold RPMI with 10% human serum and transferred into a petri dish on ice before processing. Tumor biopsies were minced and subjected to enzymatic dissociation in 4.75 ml minimum essential medium for suspension cultures (Gibco) supplemented with 250 µl Liberase for 45 min at 37 °C using a heater-shaker. Following the dissociation, tumor biopsies were centrifuged at 300g for 5 min, seeded into Matrigel in a prewarmed 24-well plate and cultured with 500 µl of basal growth media. For passaging, organoids were mechanically pipetted out of Matrigel using Corning Cell Recovery Solution (Corning), followed by a 1-h incubation at 4 °C. Organoid fragments were then centrifuged and subjected to enzymatic dissociation in Tryple E (Gibco) for 5 min at 37 °C. A 20-gauge needle was used to further disrupt the organoids mechanically. DMEM/F12 media supplemented with 10% FBS was added to the conical tube to stop the enzymatic reaction. Dissociated organoids were collected by centrifugation and seeded in Matrigel as above; 10 µM Rko-Kinase inhibitor was added to the basal growth media for organoid passaging. For drug treatment, dissociated organoids were resuspended in basal growth media supplemented with 2% Matrigel and plated in a 24-well plate coated with 250 µl Matrigel. The next day, organoids were treated with dabrafenib (100 nM) + trametinib (10 nM), dabrafenib (100 nM) + ERAS007 (100 nM), or dabrafenib (100 nM) + panitumumab (3 µg ml−1; McKesson) for 72 h. The drugs were refreshed every 24 h. After the treatment, organoids were collected and subjected to RNA extraction. For cell viability experiments, dissociated organoids supplemented with 2% Matrigel were plated in a 96-well plate coated with 70 µl Matrigel; 48 h later, organoids were treated with various doses of dabrafenib + trametinib or dabrafenib + ERAS007 for 72 h and subjected to cell viability measurement using CellTiter-Glo 3D (Promega).
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Biopsy
Cells
Cell Survival
Centrifugation
Colorectal Neoplasms
Common Cold
Culture Media
dabrafenib
Enzymes
Homo sapiens
Hyperostosis, Diffuse Idiopathic Skeletal
Liberase
MAP2K1 protein, human
matrigel
Needles
Neoplasms
Organoids
Panitumumab
Patients
Pharmaceutical Preparations
Phosphotransferases
Promega
Proto-Oncogene Proteins B-raf
Psychological Inhibition
Serum
trametinib
Data collected included sex, age, surgical method, thyroid peroxidase antibody (TPOAb), thyroglobulin antibody (TGAb), thyroid hormone receptor antibody (TRAb), microcalcification foci, positive lymph node number, BRAF gene mutation(V600E), TERT promoter mutation(C228, C250), RET/PTC chromosomal rearrangement(RET/PTC1, RET/PTC3), HRAS gene mutation(Q61), KRAS gene mutation(G12, G13), and NRAS gene mutation(Q61). All data from preoperative examinations and postoperative pathological reports, such as cervical ultrasonic and CT, laboratory examination, and gene test results, were evaluated.
All preoperative examinations were confirmed by a radiologist and chief surgeon, who confirmed the number, size, and calcification of carcinoma and evaluated the lymph node state. Metastatic lymph nodes were suspected when lymph nodes showed increased size (>0.5 cm), demarcation of the cortex and medulla was unclear or the structure of the medulla disappeared, gravel-like calcification or cystic degeneration, rounded bulging shape, and abnormal blood flow or vascularity. Hashimoto’s thyroiditis (HT) was diagnosed when the thyroid gland was diffusely enlarged with hypoechogenicity, and the gland parenchyma was inhomogeneous with grid-like or compartment-like changes or appeared abnormal TPOAb, TGAb, TRAb results (8 (link), 9 (link)). A gene mutation detection kit (Shanghai Anjia Biological Technology Co., Ltd.) was used to detect BRAF, TERT, HRAS, KRAS, NRAS mutations and RET/PTC rearrangements according to the manufacturer’s instructions. The scope of CLND was superior to the hyoid bone, lateral to the carotid sheath, inferior to the sternum notch or the innominate artery, medial to the trachea and dorsal to the prevertebral fascia.
All preoperative examinations were confirmed by a radiologist and chief surgeon, who confirmed the number, size, and calcification of carcinoma and evaluated the lymph node state. Metastatic lymph nodes were suspected when lymph nodes showed increased size (>0.5 cm), demarcation of the cortex and medulla was unclear or the structure of the medulla disappeared, gravel-like calcification or cystic degeneration, rounded bulging shape, and abnormal blood flow or vascularity. Hashimoto’s thyroiditis (HT) was diagnosed when the thyroid gland was diffusely enlarged with hypoechogenicity, and the gland parenchyma was inhomogeneous with grid-like or compartment-like changes or appeared abnormal TPOAb, TGAb, TRAb results (8 (link), 9 (link)). A gene mutation detection kit (Shanghai Anjia Biological Technology Co., Ltd.) was used to detect BRAF, TERT, HRAS, KRAS, NRAS mutations and RET/PTC rearrangements according to the manufacturer’s instructions. The scope of CLND was superior to the hyoid bone, lateral to the carotid sheath, inferior to the sternum notch or the innominate artery, medial to the trachea and dorsal to the prevertebral fascia.
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anti-thyroglobulin antibody
Biopharmaceuticals
Blood Circulation
Blood Vessel
Calcinosis
Carcinoma
Carotid Arteries
Chromosomes
Cortex, Cerebral
Cyst
Fascia
Gene Rearrangement
Genetic Testing
Hashimoto Disease
Hyoid Bone
Immunoglobulins
K-ras Genes
Medulla Oblongata
Microcalcification
Mutation
Neck
Nodes, Lymph
NRAS protein, human
Operative Surgical Procedures
Physical Examination
Proto-Oncogene Proteins B-raf
PTCH1 protein, human
Radiologist
Renal Adysplasia
Sternum
Surgeons
TERT protein, human
Thyroid Gland
Thyroid Hormone Receptor
thyroid microsomal antibodies
Trachea
Trunks, Brachiocephalic
Ultrasonics
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Fetal Bovine Serum (FBS) is a cell culture supplement derived from the blood of bovine fetuses. FBS provides a source of proteins, growth factors, and other components that support the growth and maintenance of various cell types in in vitro cell culture applications.
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B-Raf is a lab equipment product that is a serine/threonine-protein kinase involved in regulating the MAP kinase/ERK signaling pathway. It plays a role in cell division, differentiation, and secretion.
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DMEM (Dulbecco's Modified Eagle's Medium) is a cell culture medium formulated to support the growth and maintenance of a variety of cell types, including mammalian cells. It provides essential nutrients, amino acids, vitamins, and other components necessary for cell proliferation and survival in an in vitro environment.
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PLX4032 is a laboratory compound used for research purposes. It functions as a selective inhibitor for the BRAF kinase enzyme. This compound is intended for use in scientific research and analysis, and its specific applications should be determined by the user.
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β-actin is a cytoskeletal protein that is ubiquitously expressed in eukaryotic cells. It is an important component of the microfilament system and is involved in various cellular processes such as cell motility, structure, and integrity.
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C-Raf is a protein kinase that plays a key role in the Ras-Raf-MEK-ERK signaling pathway. It is a serine/threonine-protein kinase that acts as a central regulator of the MAPK/ERK signaling cascade.
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Vemurafenib is a laboratory reagent used in research applications. It functions as a kinase inhibitor, specifically targeting the BRAF V600E mutation. This product is intended for research use only and its specific applications may vary depending on the research objectives.
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FBS, or Fetal Bovine Serum, is a commonly used cell culture supplement. It is derived from the blood of bovine fetuses and provides essential growth factors, hormones, and other nutrients to support the growth and proliferation of a wide range of cell types in vitro.
More about "Proto-Oncogene Proteins B-raf"
Proto-oncogene proteins B-raf, also known as BRAF, are a family of serine/threonine-protein kinases that play a critical role in the regulation of the mitogen-activated protein kinase (MAPK) signaling pathway.
These proteins are frequently mutated in various types of cancer, leading to constitutive activation of the MAPK pathway and uncontrolled cell growth.
Researchers can utilize tools like PubCompare.ai to optimize their B-raf proto-oncogene research protocols for reproducibility and accuracy.
By leveraging AI-driven comparisons, researchers can identify the best procedures and products from literature, preprints, and patents to advance their studies on B-raf proto-oncogenes.
Some key subtopics and related terms include: - MAPK pathway: The mitogen-activated protein kinase (MAPK) signaling pathway is a critical cellular signaling cascade that regulates cell growth, differentiation, and survival. - Serine/threonine-protein kinases: These enzymes phosphorylate serine and threonine residues, playing a key role in signal transduction and cellular regulation. - Oncogenes: Proto-oncogenes are normal genes that, when mutated, become oncogenes and can lead to the development of cancer. - Cell growth and proliferation: Constitutive activation of the MAPK pathway due to B-raf mutations can result in uncontrolled cell growth and division, a hallmark of cancer. - BRAF mutations: Specific mutations in the BRAF gene, such as the V600E mutation, are frequently observed in various cancers, including melanoma, colorectal cancer, and thyroid cancer. - DMEM: Dulbecco's Modified Eagle Medium, a commonly used cell culture medium for the growth and maintenance of mammalian cells. - FBS: Fetal bovine serum, a supplement added to cell culture media to provide essential growth factors and nutrients for cell proliferation. - QIAamp DNA Mini Kit: A DNA extraction kit used for the purification of genomic DNA from various biological samples. - PLX4032 (Vemurafenib): A targeted therapy drug that inhibits the BRAF V600E mutation, used in the treatment of certain types of cancer. - β-actin: A ubiquitously expressed cytoskeletal protein used as a reference gene or loading control in molecular biology experiments. - PVDF membranes: Polyvinylidene fluoride membranes used in Western blotting techniques for the detection and quantification of proteins. - C-Raf: Another member of the Raf kinase family, which also plays a role in the MAPK signaling pathway.
These proteins are frequently mutated in various types of cancer, leading to constitutive activation of the MAPK pathway and uncontrolled cell growth.
Researchers can utilize tools like PubCompare.ai to optimize their B-raf proto-oncogene research protocols for reproducibility and accuracy.
By leveraging AI-driven comparisons, researchers can identify the best procedures and products from literature, preprints, and patents to advance their studies on B-raf proto-oncogenes.
Some key subtopics and related terms include: - MAPK pathway: The mitogen-activated protein kinase (MAPK) signaling pathway is a critical cellular signaling cascade that regulates cell growth, differentiation, and survival. - Serine/threonine-protein kinases: These enzymes phosphorylate serine and threonine residues, playing a key role in signal transduction and cellular regulation. - Oncogenes: Proto-oncogenes are normal genes that, when mutated, become oncogenes and can lead to the development of cancer. - Cell growth and proliferation: Constitutive activation of the MAPK pathway due to B-raf mutations can result in uncontrolled cell growth and division, a hallmark of cancer. - BRAF mutations: Specific mutations in the BRAF gene, such as the V600E mutation, are frequently observed in various cancers, including melanoma, colorectal cancer, and thyroid cancer. - DMEM: Dulbecco's Modified Eagle Medium, a commonly used cell culture medium for the growth and maintenance of mammalian cells. - FBS: Fetal bovine serum, a supplement added to cell culture media to provide essential growth factors and nutrients for cell proliferation. - QIAamp DNA Mini Kit: A DNA extraction kit used for the purification of genomic DNA from various biological samples. - PLX4032 (Vemurafenib): A targeted therapy drug that inhibits the BRAF V600E mutation, used in the treatment of certain types of cancer. - β-actin: A ubiquitously expressed cytoskeletal protein used as a reference gene or loading control in molecular biology experiments. - PVDF membranes: Polyvinylidene fluoride membranes used in Western blotting techniques for the detection and quantification of proteins. - C-Raf: Another member of the Raf kinase family, which also plays a role in the MAPK signaling pathway.