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Gene Activation
Gene Activation
Gene activation is the process by which a gene is switched on or turned up, leading to the increased production of the corresponding protein or other gene product.
This can involve a variety of mechanisms, such as the binding of transcriptional activators, the removal of repressors, or the modification of chromatin structure.
Effective gene activation is crucial for many biological processes, from normal development to cellular responses to environmental stimuli.
Researchers can leverage AI-driven tools like PubCopare.ai to optimize gene activation protocols, identify the most effective approaches, and enhance the reproducibility of their experiments.
By comparing gene activation methods across published literature, preprints, and patents, PubCompare.ai helps scientists discover the most powerful techniques and prodcuts to advance their resarch.
This can involve a variety of mechanisms, such as the binding of transcriptional activators, the removal of repressors, or the modification of chromatin structure.
Effective gene activation is crucial for many biological processes, from normal development to cellular responses to environmental stimuli.
Researchers can leverage AI-driven tools like PubCopare.ai to optimize gene activation protocols, identify the most effective approaches, and enhance the reproducibility of their experiments.
By comparing gene activation methods across published literature, preprints, and patents, PubCompare.ai helps scientists discover the most powerful techniques and prodcuts to advance their resarch.
Most cited protocols related to «Gene Activation»
Adenocarcinoma of Lung
Cosmic composite resin
Gene, Cancer
Gene Activation
Genes
Genes, Dominant
Genetic Diversity
Hemizygote
Homozygote
K-ras Genes
Malignant Neoplasms
Missense Mutation
Mutation
Oncogenes
Patients
TP53 protein, human
Tumor Suppressor Genes
Cells
Culture Media
Fetal Bovine Serum
GAPDH protein, human
Gene Activation
Gene Expression
Glucose
lipofectamine 2000
Lysine
Penicillins
Plasmids
Poly A
Pyruvate
Reverse Transcription
Sodium
Streptomycin
Transcription, Genetic
Transfection
To explore the effects of CLKs on HIV-1 protein expression/RNA, HeLa cells stably transduced with an inducible Tet-On HIV-1 system were used [41 (link),42 (link)]. Activation of HIV-1 gene expression was achieved by either addition of doxycyline (Dox) at a concentration of 2 μg/ml or transfection with the constitutively active Tet activator, tTA. Modification of the published HIV Tet-ON system consisted of deleting the RT and IN genes by Mls1 digestion and using the resulting construct to generate the HeLa rtTA HIVΔmls cell line by retroviral transduction and cloning (Figure S1). To explore the effect of CLK overexpression on HIV-1 gene expression, cells were transfected with empty expression plasmid (CMVmyc 3xterm) or vectors expressing GFP-CLK1, GFP-CLK2, GFP-CLK3, GFP-CLK4 (provided by J. Bell, University of Ottawa) or GFP-CLK2 KR (provided by S. Stamm, University of Kentucky) along with CMVtTA to induce provirus expression in cells taking up DNA. Transfections were performed using polyethylene imine (PEI, Polysciences Inc.). Cells and media were harvested 48 h post-transfection to assess effects on HIV-1 gene expression.
In the case of drug treatment, cells were seeded onto 6-well plates at approximately 0.5 × 106 cells per well (~50-75% confluence) in IMDM with 10% FBS and antibiotics (1 × Pen-Strep, 100 μg/mL, 1 × Amphotericin B, 0.5 μg/mL) (Wisent Corporation). Drugs were obtained from Sigma-Aldrich (Chlorhexidine, cat. #C6143)) or provided by Masatoshi Hagiwara (TG003/TG009, Tokyo Medical & Dental University) and solubilized to 10 mM with DMSO. After 4-5 hours of drug treatment, HIV expression was induced by addition of doxycycline (2 μg/ml final concentration). After approximately 24 hours, cell supernatants were harvested for p24 ELISA, while cells were harvested for RNA or protein analyses. Cell viability was monitored by either trypan blue exclusion (Gibco) or XTT assay (Sigma-Aldrich) [54 (link)].
In the case of drug treatment, cells were seeded onto 6-well plates at approximately 0.5 × 106 cells per well (~50-75% confluence) in IMDM with 10% FBS and antibiotics (1 × Pen-Strep, 100 μg/mL, 1 × Amphotericin B, 0.5 μg/mL) (Wisent Corporation). Drugs were obtained from Sigma-Aldrich (Chlorhexidine, cat. #C6143)) or provided by Masatoshi Hagiwara (TG003/TG009, Tokyo Medical & Dental University) and solubilized to 10 mM with DMSO. After 4-5 hours of drug treatment, HIV expression was induced by addition of doxycycline (2 μg/ml final concentration). After approximately 24 hours, cell supernatants were harvested for p24 ELISA, while cells were harvested for RNA or protein analyses. Cell viability was monitored by either trypan blue exclusion (Gibco) or XTT assay (Sigma-Aldrich) [54 (link)].
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Aftercare
Amphotericin B
Antibiotics
Biological Assay
Cell Lines
Cells
Cell Survival
Chlorhexidine
Cloning Vectors
Dental Health Services
Digestion
Doxycycline
Enzyme-Linked Immunosorbent Assay
Gene Activation
Gene Expression
Genes
HeLa Cells
HIV-1
Pharmaceutical Preparations
Plasmids
poly(ethylene imine)
Proteins
Proviruses
Retroviridae
Streptococcal Infections
Sulfoxide, Dimethyl
TG 003
Transfection
Trypan Blue
HeLa, HEK293T and NIH3T3 cells were cultured in DMEM with 10% inactivated FBS, 1% Penn/Strep, 1% Glutamine, 1% non-essential amino acids. Transfection was done using Fugene HD (Promega) using a 2:6 ratio (a total DNA amount of 2 μg and 6 μl of Fugene HD reagent) in 6-well plates. For TetO::tdTomato experiment, 2 μg of the chimeric vector was used. For endogenous gene activation experiments, the U6 promoter-sgRNA-terminator sequence was amplified from the PBneo-sgRNA plasmids, purified by PCR purification kit (QIAGEN), and transfected as linear DNA (1 μg Total sgRNA expressing DNA) with 1 μg of pmax-dCas9VP160 plasmid. When there are multiple sgRNAs for multiple genes, the amount per sgRNA was evenly divided among genes first, then among the sgRNAs targeting each gene.
Amino Acids, Essential
Chimera
Cloning Vectors
DNA, A-Form
FuGene
Gene Activation
Genes
Glutamine
HeLa Cells
NIH 3T3 Cells
Plasmids
Promega
Streptococcal Infections
tdTomato
Terminator Regions, Genetic
Transfection
We compared five gene-set activation metrics. Given a gene g, let Xtg be the expression value (log10 fold change, relative to background) for gene g in tissue t. Let S be the set of genes in a pathway. For tissue t, if <XtS > and <Xt > are the mean of Xtg over the genes in S and all the genes on the microarray, respectively, and σt is the standard deviation of Xtg over all the genes on the microarray, then the Z-score activation metric used to measure the relative expression level of pathway S in tissue t is:
where |S| is the number of genes in S. The value of Z is expressed in units of standard deviation and is a measure of violation of the null hypothesis that the genes in S are independently sampled from a distribution similar to that of all the genes on the microarray. If the null hypothesis is valid, then Z will have approximately a standard normal distribution, and so a large positive value of Zt suggests collective upregulation of the genes in S (which we consider to represent 'activation' of S) in tissue t; a large negative value suggests collective downregulation. The normalization by makes comparison of different-sized gene sets possible and reflects the fact that, for larger gene sets, even a slight collective shift in fold change can be significant.
Because the Z-statistic essentially measures a shift in location (mean expression) for the genes in S, we compared its sensitivity to several other possible signed measures of location shift, which were created by modifying, where necessary, standard statistics with a sign to indicate the direction of expression change. The Wilcoxon Z statistic is a well-known statistic that is calculated according to a similar formula, but using the ranks of the Xtg among all genes in tissue t, rather than the actual fold changes. To calculate a signed KS statistic, we computed each of the two one-sided KS statistics, comparing the distribution of the expression values in S with the distribution of the genes on the microarray as a whole, and took the larger of the two statistics, with the appropriate sign. To calculate a hypergeometric p value, we used a threshold of two-fold differential expression (other threshold values showed qualitatively similar results, data not shown) to define an induced or repressed gene, and then calculated the probability that the relative enrichment of differentially expressed genes observed in a gene set in a particular tissue could have been observed by chance, using the hypergeometric distribution. To provide a sign for the hypergeometric p value, the calculation was done separately for the induced and repressed genes in each set, and the smaller of the two p value was used, as well as its 'sign' (negative if repressed genes were more enriched in the gene set than induced genes, positive otherwise). The relative insensitivity of the HG metric was little changed by varying the differential expression threshold. Finally, for the PCA statistic, we calculated PC1, the first principal component of the expression values of the genes in S across all tissues, and used the projection (scalar product) of the expression values in a tissue with PC1 as a measure of activation of the gene set in that tissue.
where |S| is the number of genes in S. The value of Z is expressed in units of standard deviation and is a measure of violation of the null hypothesis that the genes in S are independently sampled from a distribution similar to that of all the genes on the microarray. If the null hypothesis is valid, then Z will have approximately a standard normal distribution, and so a large positive value of Zt suggests collective upregulation of the genes in S (which we consider to represent 'activation' of S) in tissue t; a large negative value suggests collective downregulation. The normalization by makes comparison of different-sized gene sets possible and reflects the fact that, for larger gene sets, even a slight collective shift in fold change can be significant.
Because the Z-statistic essentially measures a shift in location (mean expression) for the genes in S, we compared its sensitivity to several other possible signed measures of location shift, which were created by modifying, where necessary, standard statistics with a sign to indicate the direction of expression change. The Wilcoxon Z statistic is a well-known statistic that is calculated according to a similar formula, but using the ranks of the Xtg among all genes in tissue t, rather than the actual fold changes. To calculate a signed KS statistic, we computed each of the two one-sided KS statistics, comparing the distribution of the expression values in S with the distribution of the genes on the microarray as a whole, and took the larger of the two statistics, with the appropriate sign. To calculate a hypergeometric p value, we used a threshold of two-fold differential expression (other threshold values showed qualitatively similar results, data not shown) to define an induced or repressed gene, and then calculated the probability that the relative enrichment of differentially expressed genes observed in a gene set in a particular tissue could have been observed by chance, using the hypergeometric distribution. To provide a sign for the hypergeometric p value, the calculation was done separately for the induced and repressed genes in each set, and the smaller of the two p value was used, as well as its 'sign' (negative if repressed genes were more enriched in the gene set than induced genes, positive otherwise). The relative insensitivity of the HG metric was little changed by varying the differential expression threshold. Finally, for the PCA statistic, we calculated PC1, the first principal component of the expression values of the genes in S across all tissues, and used the projection (scalar product) of the expression values in a tissue with PC1 as a measure of activation of the gene set in that tissue.
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Down-Regulation
Gene Activation
Gene Components
Genes
Hypersensitivity
Microarray Analysis
Tissues
Up-Regulation (Physiology)
Most recents protocols related to «Gene Activation»
Example 7
The anti-GD2 CAR was co-expressed with the RQR8 sort-suicide gene. (
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Deletion Mutation
Figs
Gene Activation
Gene Expression
Genes
Rituximab
T-Lymphocyte
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Animals
Animals, Laboratory
Biological Assay
Gene Activation
Lanugo
Males
Mus
Muscle Tissue
Myogenesis
Myogenin
OGG1 protein, human
Inducible LEUTX cell lines used for NET-CAGE and ChIP-Seq were generated on hiPSC line HEL24.3. Inducible dCas9-activator cell line for endogenous gene activation was generated on hESC line H9 (WA09, WiCell).
HEL24.3. and H9 cells were treated with 10 μM ROCK inhibitor Y27632 (Selleckhem) for 4 h before electroporations. Cells were incubated with StemPro Accutase (Thermo Fisher Scientific) until the edges of the colonies started to curl up. The Accutase was aspirated and the cells were gently detached in cold 5% FBS (Thermo Fisher Scientific) 1×PBS (Corning) and counted. One million cells were centrifuged at 200xg for 5 min and the pellet was transferred into 120 μl of R-buffer containing 1 μg of either one of the LEUTX vectors (pB-tetON-LEUTX-ires-GFP-PGK-Puro/ pB-tetON-LEUTX-HA-V5-ires-GFP-PGK-Puro) or DDdCas9 plasmid cocktail below and 0.5 μg of transposase plasmid. 100 μl of the cell-plasmid suspension was electroporated with two pulses of 1100V, 20 ms pulse width, using Neon Transfection system (Thermo Fischer Scientific). Activator cell line was generated by electroporating H9 cells with two plasmids containing DDdCas9VP192 (1 μg of SB-tight-DDdCas9VP192- GFP-Zeo-WPRE) and rtTA (1 μg of SB-CAG-rtTA-IN-IRES-Neo) sequences, which were integrated into the genome by sleeping beauty transposase (0.5 μg of CAG-SB-100X-bghpA). Guide plasmids (1.5 μg / reaction) were electroporated into H9 DDdCas9VP192 activator cells and integrated with piggyBac transposase (0.5 μg of pCMV-HAhy-Pbase).
The electroporated cells were plated on Geltrex-coated dishes in Essential 8 medium with 10 μM ROCK inhibitor Y27632. The following day, the medium was exchanged with fresh Essential 8 medium without ROCK inhibitor. The cells were selected with Neomycin (G418, Life Technologies) at 50 μg/ml and Zeocin (Sigma) at 1 μg/ml (after DDdCas9VP192-GFP-Zeo-WPRE plasmid transfection) or Puromycin (Sigma) at 0.5 μg/ml (after LEUTX vectors and guide plasmids). The TetOn-LEUTX hPSC clones were picked manually on Geltrex-coated 24-well plates, expanded and selected again with Puromycin. Appearance of the GFP reporter protein was tested using Doxicycline at concentration 0.5 μg/ml and detected using an EVOS FL Cell imaging system (Thermo Fisher Scientific).
For the experiments presented in this paper, the LEUTX TetOn cells were treated with 1 μg/ml of Doxycycline for 6-7 h (NET-CAGE, q-PCR validation) or 24 h (ChIP-Seq, qPCR validation), DD-dCas9 activator cell line was treated with 1 μg/ml of Doxycycline and 1 μM Trimethoprim for 24 h, 48 h or 72 h, prior to harvesting cells for STRT-Seq.
HEL24.3. and H9 cells were treated with 10 μM ROCK inhibitor Y27632 (Selleckhem) for 4 h before electroporations. Cells were incubated with StemPro Accutase (Thermo Fisher Scientific) until the edges of the colonies started to curl up. The Accutase was aspirated and the cells were gently detached in cold 5% FBS (Thermo Fisher Scientific) 1×PBS (Corning) and counted. One million cells were centrifuged at 200xg for 5 min and the pellet was transferred into 120 μl of R-buffer containing 1 μg of either one of the LEUTX vectors (pB-tetON-LEUTX-ires-GFP-PGK-Puro/ pB-tetON-LEUTX-HA-V5-ires-GFP-PGK-Puro) or DDdCas9 plasmid cocktail below and 0.5 μg of transposase plasmid. 100 μl of the cell-plasmid suspension was electroporated with two pulses of 1100V, 20 ms pulse width, using Neon Transfection system (Thermo Fischer Scientific). Activator cell line was generated by electroporating H9 cells with two plasmids containing DDdCas9VP192 (1 μg of SB-tight-DDdCas9VP192- GFP-Zeo-WPRE) and rtTA (1 μg of SB-CAG-rtTA-IN-IRES-Neo) sequences, which were integrated into the genome by sleeping beauty transposase (0.5 μg of CAG-SB-100X-bghpA). Guide plasmids (1.5 μg / reaction) were electroporated into H9 DDdCas9VP192 activator cells and integrated with piggyBac transposase (0.5 μg of pCMV-HAhy-Pbase).
The electroporated cells were plated on Geltrex-coated dishes in Essential 8 medium with 10 μM ROCK inhibitor Y27632. The following day, the medium was exchanged with fresh Essential 8 medium without ROCK inhibitor. The cells were selected with Neomycin (G418, Life Technologies) at 50 μg/ml and Zeocin (Sigma) at 1 μg/ml (after DDdCas9VP192-GFP-Zeo-WPRE plasmid transfection) or Puromycin (Sigma) at 0.5 μg/ml (after LEUTX vectors and guide plasmids). The TetOn-LEUTX hPSC clones were picked manually on Geltrex-coated 24-well plates, expanded and selected again with Puromycin. Appearance of the GFP reporter protein was tested using Doxicycline at concentration 0.5 μg/ml and detected using an EVOS FL Cell imaging system (Thermo Fisher Scientific).
For the experiments presented in this paper, the LEUTX TetOn cells were treated with 1 μg/ml of Doxycycline for 6-7 h (NET-CAGE, q-PCR validation) or 24 h (ChIP-Seq, qPCR validation), DD-dCas9 activator cell line was treated with 1 μg/ml of Doxycycline and 1 μM Trimethoprim for 24 h, 48 h or 72 h, prior to harvesting cells for STRT-Seq.
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accutase
antibiotic G 418
Buffers
Cell Lines
Cells
Chromatin Immunoprecipitation Sequencing
Clone Cells
Cloning Vectors
Cold Temperature
Doxycycline
Electroporation
Endocytic Vesicles
Gene Activation
Genome
Human Embryonic Stem Cells
Human Induced Pluripotent Stem Cells
Hyperostosis, Diffuse Idiopathic Skeletal
Internal Ribosome Entry Sites
Neomycin
Neon
Plasmids
Proteins
Pulse Rate
Pulses
Puromycin
Transfection
Transposase
Trimethoprim
Y 27632
Zeocin
Adult cardiac fibroblasts were isolated from ~2–3 months old WT mice and placed in 35 mm glass-bottom dishes. After 2 h, attached cells were washed with 1× PBS 3 times, changed to fresh CF culturing medium (DMEM containing 10% FBS and 1% penicillin/streptomycin), and cultured at 37 °C for 12 h (or overnight). Then, cells were treated with serum starvation for 12 h and stimulated with TGFβ (10 nM) for 24 h. Immediately, cells were fixed with 4% paraformaldehyde (PFA) for immunofluorescence staining, or lysed in TRIzol reagent for RNA isolation to detect the gene expression levels of myofibroblast activation markers by RT-qPCR. Cardiac fibroblast cells were isolated from WT mouse hearts and cultured for 24 or 48 h.
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Adult
Cells
Culture Media
Fibroblasts
Gene Activation
Gene Expression
Heart
Hyperostosis, Diffuse Idiopathic Skeletal
Immunofluorescence
isolation
Mus
Myofibroblasts
paraform
Penicillins
Serum
Streptomycin
Transforming Growth Factor beta
trizol
scRNA-seq was performed as previously described (8 (link), 9 (link)). Cells were loaded on the Chromium platform using the 3′ v2 profiling chemistry (10X Genomics). For StimDrop experiments, gene expression libraries were enriched for immune transcripts with the Target Hybridization Kit and the Human Immunology Gene Panel (10X Genomics). Gene expression and hashtag libraries were sequenced to a depth of ~10,000 and ~2000 reads per cell, respectively, on NextSeq 550 (Illumina). The data were aligned to the GRCh38 reference genome using cellranger v3.1 (10X Genomics). Single-cell data analysis was performed using scanpy (58 (link)) with the same preprocessing and filtering parameters described in a previous publication (9 (link)). Hashtag assignment and doublet removal were performed using demuxEM (59 (link)) and compared with genotype-based classifications from souporcell (60 (link)), both using default parameters.
cNMF analysis was performed as detailed in a previous publication (25 ). Briefly, highly variable genes from the primary StimDrop gene expression data were first selected to filter the gene expression matrix. NMF was then performed with k = 5 to 25 (10 iterations for each k). The number of modules (k) for downstream analysis was selected on the basis of biological interpretability of the modules and stability of the cNMF solution. To ensure that no modules from technical artifacts were analyzed, only gene programs with mean usage > 5 across cells were included for further analysis. To obtain a score for the inflammatory activation gene module in the corresponding bulk RNA-seq experiment, the average expression of top 20 genes from the modules was calculated and subtracted by the average expression of a randomly sampled set of 150 reference genes (61 (link)).
cNMF analysis was performed as detailed in a previous publication (25 ). Briefly, highly variable genes from the primary StimDrop gene expression data were first selected to filter the gene expression matrix. NMF was then performed with k = 5 to 25 (10 iterations for each k). The number of modules (k) for downstream analysis was selected on the basis of biological interpretability of the modules and stability of the cNMF solution. To ensure that no modules from technical artifacts were analyzed, only gene programs with mean usage > 5 across cells were included for further analysis. To obtain a score for the inflammatory activation gene module in the corresponding bulk RNA-seq experiment, the average expression of top 20 genes from the modules was calculated and subtracted by the average expression of a randomly sampled set of 150 reference genes (61 (link)).
Biopharmaceuticals
Cells
Chromium
Crossbreeding
Dietary Fiber
Gene Activation
Gene Expression
Gene Library
Genes
Genome
Genotype
Inflammation
RNA-Seq
Single-Cell Analysis
Single-Cell RNA-Seq
Top products related to «Gene Activation»
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Lipofectamine 2000 is a cationic lipid-based transfection reagent designed for efficient and reliable delivery of nucleic acids, such as plasmid DNA and small interfering RNA (siRNA), into a wide range of eukaryotic cell types. It facilitates the formation of complexes between the nucleic acid and the lipid components, which can then be introduced into cells to enable gene expression or gene silencing studies.
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The Dual-Luciferase Reporter Assay System is a laboratory tool designed to measure and compare the activity of two different luciferase reporter genes simultaneously. The system provides a quantitative method for analyzing gene expression and regulation in transfected or transduced cells.
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The Luciferase Assay System is a laboratory tool designed to measure the activity of the luciferase enzyme. Luciferase is an enzyme that catalyzes a bioluminescent reaction, producing light. The Luciferase Assay System provides the necessary reagents to quantify the level of luciferase activity in samples, enabling researchers to study biological processes and gene expression.
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Lipofectamine 3000 is a transfection reagent used for the efficient delivery of nucleic acids, such as plasmid DNA, siRNA, and mRNA, into a variety of mammalian cell types. It facilitates the entry of these molecules into the cells, enabling their expression or silencing.
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The PGBKT7 is a plasmid vector used for gene expression in yeast cells. It contains a yeast selectable marker and a multiple cloning site for the insertion of DNA sequences.
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The AH109 is a high-performance laboratory centrifuge designed for a variety of applications. It features a compact and durable construction, accommodating a range of rotors and sample volumes. The AH109 provides reliable and consistent performance for laboratory workflows.
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Penicillin/streptomycin is a commonly used antibiotic solution for cell culture applications. It contains a combination of penicillin and streptomycin, which are broad-spectrum antibiotics that inhibit the growth of both Gram-positive and Gram-negative bacteria.
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PsPAX2 is a packaging plasmid used for the production of lentiviral particles. It contains the necessary genes for lentiviral packaging, but does not contain the viral genome. PsPAX2 is commonly used in lentiviral production workflows.
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The PMD2.G is a lab equipment product. It is a plasmid that can be used for various research applications.
LentiSAMv2 is a lentiviral CRISPR activation system designed for effective and robust gene activation in mammalian cells. It consists of a lentivirally packaged single guide RNA expression cassette and a lentiviral dCas9-VP64 effector component.
More about "Gene Activation"
Gene activation is a crucial process in biology, where a gene is switched on or upregulated, leading to increased production of the corresponding protein or other gene product.
This can involve various mechanisms, such as the binding of transcriptional activators, the removal of repressors, or the modification of chromatin structure.
Effective gene activation is vital for many biological processes, from normal development to cellular responses to environmental stimuli.
Researchers can leverage AI-driven tools like PubCompare.ai to optimize gene activation protocols, identify the most effective approaches, and enhance the reproducibility of their experiments.
By comparing gene activation methods across published literature, preprints, and patents, PubCompare.ai helps scientists discover the most powerful techniques and products to advance their research.
Some key tools and techniques used in gene activation research include Lipofectamine 2000, a widely used transfection reagent, the Dual-Luciferase Reporter Assay System and Luciferase Assay System, which are common methods for measuring gene activation, and Lipofectamine 3000, an improved version of the Lipofectamine transfection reagent.
Additionally, researchers may utilize plasmids like pGBKT7 and yeast strains such as AH109 for gene activation studies.
Other important factors in gene activation experiments include the use of antibiotics like Penicillin/Streptomycin, as well as lentiviral packaging plasmids like psPAX2 and pMD2.G, and the LentiSAMv2 system for gene activation via CRISPR-Cas9 technology.
By understanding the various mechanisms, tools, and techniques involved in gene activation, researchers can optimize their experimental protocols, enhance the reproducibility of their findings, and make significant advancements in their field of study.
This can involve various mechanisms, such as the binding of transcriptional activators, the removal of repressors, or the modification of chromatin structure.
Effective gene activation is vital for many biological processes, from normal development to cellular responses to environmental stimuli.
Researchers can leverage AI-driven tools like PubCompare.ai to optimize gene activation protocols, identify the most effective approaches, and enhance the reproducibility of their experiments.
By comparing gene activation methods across published literature, preprints, and patents, PubCompare.ai helps scientists discover the most powerful techniques and products to advance their research.
Some key tools and techniques used in gene activation research include Lipofectamine 2000, a widely used transfection reagent, the Dual-Luciferase Reporter Assay System and Luciferase Assay System, which are common methods for measuring gene activation, and Lipofectamine 3000, an improved version of the Lipofectamine transfection reagent.
Additionally, researchers may utilize plasmids like pGBKT7 and yeast strains such as AH109 for gene activation studies.
Other important factors in gene activation experiments include the use of antibiotics like Penicillin/Streptomycin, as well as lentiviral packaging plasmids like psPAX2 and pMD2.G, and the LentiSAMv2 system for gene activation via CRISPR-Cas9 technology.
By understanding the various mechanisms, tools, and techniques involved in gene activation, researchers can optimize their experimental protocols, enhance the reproducibility of their findings, and make significant advancements in their field of study.