E. coli BW25141 (rrnB3 DElacZ4787 DEphoBR580 hsdR514 DE(araBAD)567 DE(rhaBAD)568 galU95 DEendA9::FRT DEuidA3::pir(wt) recA1 rph-1) was used for maintenance of the template plasmid pKD13 (GenBank™ Accession number AY048744). pKD46 (GenBank™ Accession number AY048746; Datsenko and Wanner, 2000 (link)) was made by PCR amplification of the Red recombinase genes from phage λ and cloning into pKD16, a derivative of INT-ts (Haldimann and Wanner, 2001 (link)) carrying araC and araBp from pBAD18 (Guzman et al, 1995 (link)).
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Ara-C
Ara-C
Ara-C, also known as cytarabine, is a medication used in the treatment of various types of cancer, particularly acute myeloid leukemia and acute lymphocytic leukemia.
It works by interfering with the synthesis of DNA, preventing cancer cells from dividing and growing.
Ara-C is typically administered intravenously or subcutaneously and is often used in combination with other chemotherapeutic agents.
Researchers studying Ara-C may use PubCompare.ai's AI-driven protocol comparison platform to easily locate and compare protocols from literature, pre-prints, and patents, helping to identify the best solutions for their needs and streamline the research process to drive breakthrough discoveries in cancer treatment.
It works by interfering with the synthesis of DNA, preventing cancer cells from dividing and growing.
Ara-C is typically administered intravenously or subcutaneously and is often used in combination with other chemotherapeutic agents.
Researchers studying Ara-C may use PubCompare.ai's AI-driven protocol comparison platform to easily locate and compare protocols from literature, pre-prints, and patents, helping to identify the best solutions for their needs and streamline the research process to drive breakthrough discoveries in cancer treatment.
Most cited protocols related to «Ara-C»
E. coli BW25141 (rrnB3 DElacZ4787 DEphoBR580 hsdR514 DE(araBAD)567 DE(rhaBAD)568 galU95 DEendA9::FRT DEuidA3::pir(wt) recA1 rph-1) was used for maintenance of the template plasmid pKD13 (GenBank™ Accession number AY048744). pKD46 (GenBank™ Accession number AY048746; Datsenko and Wanner, 2000 (link)) was made by PCR amplification of the Red recombinase genes from phage λ and cloning into pKD16, a derivative of INT-ts (Haldimann and Wanner, 2001 (link)) carrying araC and araBp from pBAD18 (Guzman et al, 1995 (link)).
Ara-C
Bacteriophages
Escherichia coli
Gene Amplification
Plasmids
Recombinase
The plasmid pBL was constructed by insertion of a 70-bp chemically synthesized multiple cloning site into the 2.5-kb PCR-generated plasmid backbone of pBluescript II KS(+) (Stratagene) and deletion of the LacZα ORF by conventional cloning. The plasmid pBL-DL was constructed by insertion of a 1-kb PCR fragment from pGEM®-luc (Promega) into the NotI/SalI sites of pBL by SLiCE. The suicide plasmid pGT1 was constructed by SLiCE-mediated insertion of a 830-bp PCR-amplified fragment spanning the 3′ region of the E. coli DH10B cynX gene and an araC-pBAD-redα/EM7-redβ/Tn5-gam expression cassette isolated from plasmid pBAD24 (8 (link)) and lambda phage DNA (NEB) into the SmaI site of plasmid pEL04 (9 (link)). pGT1 also contains a temperature-sensitive replicon and a chloramphenicol selection marker.
Ara-C
Bacteriophage lambda
Chloramphenicol
Deletion Mutation
Escherichia coli
Genes
HMN (Hereditary Motor Neuropathy) Proximal Type I
KS 5-2
Plasmids
Promega
prostaglandin M
Replicon
Vertebral Column
All plasmids listed in Table S1 were created using circular polymerase extension cloning (CPEC)24 (link). The primers listed in Table S2 were used to create linear dsDNA products that were subsequently DpnI digested for at least 15 minutes and then gel-purified. The DNA was eluted in 6 ul of dH2O and mixed with corresponding linear product. These products were then used as template for a reaction with Q5 polymerase for 15 cycles. The product was then used to directly transform chemically competent E. coli DH5α or NEB Turbo cells. The following plasmids and maps have been deposited to Addgene (Cambridge, MA); pCas9cr4 (Plasmid #62655), pKDsg-ack (Plasmid #62654), and pKDsg-p15 (Plasmid #62656).
The 20 bp targeting sequences of the sgRNA were re-targeted by CPEC cloning of two linear PCR fragments. The re-targeting primers listed inTable S2 were approximately 40-mers that had overlapping protospacer sequences. The primer pair protospacerF and gamR were used to yield a 3 kb product. The protospacer R primer was paired with pKDseq1F to yield a product of about 4 kb. This design yielded PCR product with about 280 bp of overlapping homology between the gam and araC (Fig. 2 ), as well as 20 bp of overlap in the protospacer. PCR products were gel purified, mixed together in equal volumes and CPEC cloned with Q5 polymerase. The mixture was used to transform chemically competent DH5α or NEB Turbo cells (New England Biolabs), recovered for 1 hour in super optimal broth with catabolite repression (SOC), and then plated on LB with 50 mg L−1 spectinomycin (spec) and incubated at 30 °C. A step-by-step protocol for primer design and retargeting is available as part of the no-SCAR protocol at Addgene.
The 20 bp targeting sequences of the sgRNA were re-targeted by CPEC cloning of two linear PCR fragments. The re-targeting primers listed in
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Ara-C
Catabolite Repression
Cells
Cicatrix
cyclopentenyl cytosine
DNA, Double-Stranded
Escherichia coli
GPER protein, human
Microtubule-Associated Proteins
Oligonucleotide Primers
Plasmids
Spectinomycin
The dual-feedback oscillator circuit was constructed by placing araC, lacI and yemGFP under the control of the hybrid Plac/ara-1 promoter14 (link) in three separate transcriptional cassettes. An ssrA degradation tag28 (link) was added to each gene to decrease protein lifetime and increase temporal resolution. These transcriptional cassettes were placed on two modular plasmids14 (link) and cotransformed into an ΔaraC ΔlacI E. coli strain. The negative feedback oscillator circuit was constructed by placing ssrA-tagged lacI and yemGFP under the control of the PLlacO-1 promoter14 (link) in two separate transcriptional cassettes, which were incorporated onto two modular plasmids and cotransformed into a ΔlacI strain. Cells were either grown in LB medium or minimal A medium with 2 g/L glucose. Oscillations were induced using arabinose (0.1–3%) and IPTG (0–30 mM). Single-cell microscopic data were collected by loading induced cells into PDMS-based microfluidic platforms that constrained the cells to a monolayer while supplying them with nutrients29 , then supplying a constant source of medium and inducers and imaging GFP fluorescence every 2–3 min for at least 4–6 h. These data were further analyzed using ImageJ and custom-written MATLAB scripts to extract single-cell fluorescence trajectories. Flow cytometry was performed either by taking samples from a continuously grown and serially diluted culture or by growing multiple cultures in parallel for varying durations. In either case, samples were read directly from their growth medium and low-scatter noise was removed by thresholding. Flow cytometry oscillatory periods were defined as the time elapsed between the first and second fluorescence peaks. Details of the models discussed are presented in Supplementary Information . Stochastic simulations were performed using Gillespie’s algorithm27 , and deterministic simulations were performed using custom MATLAB scripts.
5'-palmitoyl cytarabine
Ara-C
Arabinose
Cells
Culture Media
Escherichia coli
Flow Cytometry
Fluorescence
Genes
Glucose
Hybrids
Isopropyl Thiogalactoside
Microscopy
Plasmids
Proteins
Strains
tmRNA
Transcription, Genetic
Protocol full text hidden due to copyright restrictions
Open the protocol to access the free full text link
5-hydroxyethoxy-N-acetyltryptamine
Amino Acids, Essential
Ara-C
Cells
Dietary Supplements
Doxycycline
Eagle
Fetal Bovine Serum
Induced Pluripotent Stem Cells
Laminin
Lysine
matrigel
Mus
Neuroglia
Neurotrophic Factor, Brain-Derived
Neurotrophin 3
Poly A
Stem Cells, Hematopoietic
Y 27632
Most recents protocols related to «Ara-C»
Twenty-eight non-M3 AML patients who were monitored at the Hematology Department of the Chinese People’s Liberation Army General Hospital between August 2014 and June 2016 were enrolled in this study and underwent DNA methylation sequencing, as described previously [13 (link)]. Three of these patients had the t(8;21) translocation. A methylation sequencing dataset comprising 33 bone marrow samples was generated, including 23 non-paired de novo samples, 2 paired t(8;21) de novo/complete remission (CR) samples, and 3 paired non-t(8;21) de novo/CR samples. All de novo AML samples were collected before treatment, while CR samples were obtained after the first round of treatment with the DCAG regimen, which involved decitabine (20 mg/m2 on days 1–5), Ara-C (10 mg/m2 every 12 h on days 1–5), aclarubicin (20 mg on days 1, 3, and 5), and granulocyte colony-stimulating factor (300 μg/d from d0 to neutrophil recovery). All patients were diagnosed and assessed according to the AML guidelines of the National Comprehensive Cancer Network (version 1.2017; http://www.nccn.org/ ). As described previously [13 (link)], specimen collection was conducted only after written informed consent was obtained from each participant. Patient characteristics are summarized in Tables 1 and 2 .
Characteristics of the de novo patient study cohort (n = 28)
| Characteristic | Value |
|---|---|
| Age at diagnosis, years | 49.07 ± 17.94 |
| Sex, no. (%) | |
| Male | 11 (39) |
| Female | 17 (61) |
| Bone marrow blast, no. (%) | 67.55 ± 23.74 |
| AML FAB subtype, no. (%) | |
| M1 | 1 (3.57) |
| M2 | 5 (17.86) |
| M4 | 10 (35.71) |
| M5 | 11 (39.29) |
| M6 | 1 (3.57) |
| 2017 NCCN cytogenetic risk classification, no. (%) | |
| Good | 5 (17.86) |
| Intermediate | 20 (71.43) |
| Poor | 3 (10.71) |
| 2017 NCCN molecular risk classification, no. (%) | |
| Good | 12 (42.86) |
| Intermediate | 7 (25.00) |
| Poor | 9 (32.14) |
| Mutation, no. (%) | |
| t(8;21) | 3 (10.71) |
| inv(16) | 2 (7.14) |
| NPM1 | 4 (14.29) |
| FLT3 | 6 (21.43) |
| DNMT3A | 3 (10.71) |
| IDH1 or IDH2 | 4 (14.29) |
| KRAS or NRAS | 4 (14.29) |
| TP53 | 2 (7.14) |
| biCEBPA | 7 (25.00) |
Characteristics of the de novo/CR paired samples (n = 5)
| Age (years) | Sex | Bone marrow blast at diagnosis % | Cytogenetics at diagnosis | Risk classification | Induction regimen | |
|---|---|---|---|---|---|---|
| Pair 1 | 59 | Female | 45.2 | Normal karyotype | Intermediate | DCAG |
| Pair 2 | 34 | Female | 67.2 | 46, XX, inv(16) | Good | DCAG |
| Pair 3 | 60 | Female | 56.4 | 46, XX, t(11;20) | Intermediate | DCAG |
| Pair 4 | 73 | Female | 81 | 46, XX, t(8;21) | Good | DCAG |
| Pair 5 | 50 | Female | 83.2 | 45, XX, − X, t(8;21) | Good | DCAG |
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Aclarubicin
Ara-C
Bone Marrow
Chinese
Decitabine
Diagnosis
DNA Methylation
Granulocyte Colony-Stimulating Factor
K-ras Genes
Malignant Neoplasms
Marrow
Methylation
Mutation
Neutrophil
Patients
Specimen Collection
Translocation, Chromosomal
Treatment Protocols
Kasumi-1, SKNO-1, U937, and K562 cell lines were purchased from the American Type Culture Collection (Manassas, VA, USA) and maintained in Gibco RPMI-1640 (Thermo Fisher Scientific, Waltham, MA, USA) supplemented with streptomycin (100 µg/mL, Gibco), penicillin (50 U/mL, Gibco), and 10% fetal bovine serum (FBS; Gibco). As previously described [13 (link)], SKNO-1-siAE cell line was generated by transfection with a lentiviral vector encoding siAGF1 oligonucleotides against the AML1-ETO mRNA fusion site to silence the expression of the AML1-ETO protein in SKNO-1 cells [17 (link)]. Cells were cultured in plastic tissue culture plates in a humidified 5% CO2 atmosphere at 37 °C. SKNO-1-siAE cell were cultured for a month before sequencing. Lyophilized DAC (Topscience, Shanghai, China) and Ara-C (Topscience) were dissolved in dimethyl sulfoxide (Thermo Fisher Scientific) and stored at − 80 °C.
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Ara-C
Atmosphere
CBFA2T1 protein, human
Cell Lines
Cells
Cloning Vectors
Oligonucleotides
Penicillins
RNA, Messenger
RUNX1 protein, human
Streptomycin
Sulfoxide, Dimethyl
Tissues
Transfection
Cell viability was assessed using the MTS assay (G1111; Promega) following treatment with different concentrations of DAC for 7 days; the optical density was measured at 490 nm. Cell viability was calculated using the following formula: cell viability (%) = (Abstreated blank/Abscontrol blank) × 100%.
After successfully transfecting cells with shNC or shLIN7A lentivirus, the cells were treated with 10 nM DAC for 3 days; the medium was then replaced with fresh medium. On day 4, 2 × 105 cells/well were seeded into 6-well plates and either left untreated or treated with 100 nM Ara-C for an additional 3 days. Thereafter, on day 7, the cells were harvested and stained with annexin V-FITC (BD Biosciences, Franklin Lakes, NJ, USA) for 15 min at room temperature in the dark. Propidium iodide was added to the samples before analysis to distinguish live cells from dead ones, and the apoptosis rate was determined using a CytExpert flow cytometer (Beckman Coulter Life Sciences, Indianapolis, IN, USA). Apoptosis experiments were performed in triplicate using the following treatment groups: DAC alone, Ara-C alone, and DAC followed by Ara-C.
After successfully transfecting cells with shNC or shLIN7A lentivirus, the cells were treated with 10 nM DAC for 3 days; the medium was then replaced with fresh medium. On day 4, 2 × 105 cells/well were seeded into 6-well plates and either left untreated or treated with 100 nM Ara-C for an additional 3 days. Thereafter, on day 7, the cells were harvested and stained with annexin V-FITC (BD Biosciences, Franklin Lakes, NJ, USA) for 15 min at room temperature in the dark. Propidium iodide was added to the samples before analysis to distinguish live cells from dead ones, and the apoptosis rate was determined using a CytExpert flow cytometer (Beckman Coulter Life Sciences, Indianapolis, IN, USA). Apoptosis experiments were performed in triplicate using the following treatment groups: DAC alone, Ara-C alone, and DAC followed by Ara-C.
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Apoptosis
Ara-C
Biological Assay
Cells
Cell Survival
FITC-annexin A5
Lentivirus
Promega
Propidium Iodide
Vision
Patients ≥ 60 years of age with non-promyelocytic AML were centrally randomized up-front in a 9:1 assignment to study specific arms of the German AML cooperative Group (AMLCG) or the East German Study Group Hematology and Oncology (OSHO) compared to a CSA (suppl. Figure S1 ). The AMLCG study arm randomized TAD (ara-C 100 mg/m2/d continuous infusion (CI) d1-2 followed by 30-min IV infusion BID d 3–8, daunorubicin 60 mg/m2/d IV d 3–5 and 6-thioguanine 100 mg/m2/d p.o. BID d 3–9) followed by HAM (ara-C 1 g/m2/d IV BID d 1–3 and mitoxantrone 10 mg/m2/d IV d 3–5) versus two courses of HAM ± G-CSF, with the second induction course only applied in case of blast persistence. One course of TAD was given as consolidation followed by maintenance chemotherapy over three years [21 (link)]. The OSHO AML04 study included ara-C 1 g/m2/d BID IV d 1 + 3 + 5 + 7 and mitoxantrone 10 mg/m2/d IV d 1 – 3 for one or two induction courses and ara-C 500 mg/m2 BID 1 h IV d 1 + 3 + 5 in combination with mitoxantrone 10 mg/m2/d IV d 1 + 2 as consolidation twice. Pegfilgrastim 6 mg s.c. was given on day 10 of induction and on day 8 of consolidation. Allogeneic related or unrelated HSCT following non-myeloablative conditioning was considered after CR. The CSA consisted of one or two induction cycles of ara-C 100 mg/m2/d CI d 1–7 and daunorubicin 60 mg/m2/d IV d 3, 4, 5 (3 + 7 regimen) followed by two courses of ara-C 1 g/m2/d BID IV d 1 + 3 + 5 as consolidation [20 (link)]. Detailed information on therapies of the study groups and CSA are given in suppl. Figure 1. Cytogenetic and molecular risk was determined as previously described [22 (link)].
Inclusion criteria contained all consecutive AML (de novo, secondary, and therapy related, except APL) diagnosed in the study period. Exclusion criteria included inability of the patient to understand the study and give informed consent, non AML-related renal insufficiency, liver insufficiency, cardiac insufficiency NYHA III + IV, concurrent acute myocardial infarction, and uncontrolled infection such as pneumonia with hypoxia or septic shock.
The study was approved by the Institutional Review Board (IRB) of the University of Leipzig, registered at clinicaltrials.gov (NCT01497002 and NCT00266136) and the approval notified to IRBs of the participating centers. Patients had given written informed consent prior to study enrollment and randomization.
Inclusion criteria contained all consecutive AML (de novo, secondary, and therapy related, except APL) diagnosed in the study period. Exclusion criteria included inability of the patient to understand the study and give informed consent, non AML-related renal insufficiency, liver insufficiency, cardiac insufficiency NYHA III + IV, concurrent acute myocardial infarction, and uncontrolled infection such as pneumonia with hypoxia or septic shock.
The study was approved by the Institutional Review Board (IRB) of the University of Leipzig, registered at clinicaltrials.gov (NCT01497002 and NCT00266136) and the approval notified to IRBs of the participating centers. Patients had given written informed consent prior to study enrollment and randomization.
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Ara-C
ARA 100
Daunorubicin
Ethics Committees, Research
Granulocyte Colony-Stimulating Factor
Group Therapy
Heart Failure
Hepatic Insufficiency
Hypoxia
Infection
Intravenous Infusion
Kidney Failure
Mitoxantrone
Myocardial Infarction
Neoplasms
Patients
pegfilgrastim
Pneumonia
Promyelocytes
Septic Shock
Therapeutics
Thioguanine
Treatment Protocols
Cytotoxic agents were purchased from Sigma-Aldrich. Ara-C was reconstituted in DMSO and daunorubicin or 5′-Aza in distilled H2O, and aliquots were prepared and stored at –80°C. Stocks were diluted in CM immediately prior to use in cytotoxicity assays.
To compare cell proliferation between parental and CRISPR/Cas9-mutated HEL clones, exponentially growing cells were seeded at low density (2 × 104 cells/mL) in CM and counted using a hemocytometer at regular intervals up to 192 hours postseeding. Cell growth at each time point was calculated relative to initial seeding density. Two-way ANOVA was used to test for significant differences in relative cell growth based on TET2 mutation status.
For drug sensitivity experiments, cells were incubated in CM supplemented with appropriate concentrations of cytotoxic agent (5′-Aza, daunorubicin, or Ara-C) or relevant VC for 96 hours, after which viable cells were identified by trypan blue dye exclusion and counted using a hemocytometer. Survival fractions were determined at each drug concentration relative to VC-treated controls. Two-way ANOVA was used to test for significant differences in drug sensitivity based on TET2 mutation status. Inhibition of proliferation in drug-treated cultures was compared with VC-treated cultures and used to calculate the IC50 and IC90 values in GraphPad Prism (6.0.2, GraphPad Software).
For determination of CE, exponentially growing cells were seeded in soft agar (CM supplemented with 0.2% agarose) supplemented with cytotoxic agent (5′-Aza, daunorubicin, or Ara-C) or VC. Macroscopically visible colonies were counted on day 30, and CE was calculated relative to number of cells initially seeded. Student’s t tests (2-tailed) were used to identify significant differences in CE based on TET2 mutation status.
To determine the effect of ABCB1 inhibition on 5′-Aza sensitivity, cells were incubated in CM supplemented with increasing doses of 5′-Aza and an ABCB1 inhibitor (verapamil or tariquidar) or VC. After 96 hours of incubation, viable cells were identified using CellTiter-Glo Luminescent Cell Viability Assay (Promega), and the surviving fraction was determined at each drug concentration relative to VC-treated controls. The resulting dose-response matrix was used to calculate drug synergy using SynergyFinder 2.0. Student’s t test (2-tailed) was used to identify significant differences in synergy scores based on TET2 mutation status.
All assays were performed in triplicate at a minimum and means ± SD were calculated.
To compare cell proliferation between parental and CRISPR/Cas9-mutated HEL clones, exponentially growing cells were seeded at low density (2 × 104 cells/mL) in CM and counted using a hemocytometer at regular intervals up to 192 hours postseeding. Cell growth at each time point was calculated relative to initial seeding density. Two-way ANOVA was used to test for significant differences in relative cell growth based on TET2 mutation status.
For drug sensitivity experiments, cells were incubated in CM supplemented with appropriate concentrations of cytotoxic agent (5′-Aza, daunorubicin, or Ara-C) or relevant VC for 96 hours, after which viable cells were identified by trypan blue dye exclusion and counted using a hemocytometer. Survival fractions were determined at each drug concentration relative to VC-treated controls. Two-way ANOVA was used to test for significant differences in drug sensitivity based on TET2 mutation status. Inhibition of proliferation in drug-treated cultures was compared with VC-treated cultures and used to calculate the IC50 and IC90 values in GraphPad Prism (6.0.2, GraphPad Software).
For determination of CE, exponentially growing cells were seeded in soft agar (CM supplemented with 0.2% agarose) supplemented with cytotoxic agent (5′-Aza, daunorubicin, or Ara-C) or VC. Macroscopically visible colonies were counted on day 30, and CE was calculated relative to number of cells initially seeded. Student’s t tests (2-tailed) were used to identify significant differences in CE based on TET2 mutation status.
To determine the effect of ABCB1 inhibition on 5′-Aza sensitivity, cells were incubated in CM supplemented with increasing doses of 5′-Aza and an ABCB1 inhibitor (verapamil or tariquidar) or VC. After 96 hours of incubation, viable cells were identified using CellTiter-Glo Luminescent Cell Viability Assay (Promega), and the surviving fraction was determined at each drug concentration relative to VC-treated controls. The resulting dose-response matrix was used to calculate drug synergy using SynergyFinder 2.0. Student’s t test (2-tailed) was used to identify significant differences in synergy scores based on TET2 mutation status.
All assays were performed in triplicate at a minimum and means ± SD were calculated.
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ABCB1 protein, human
Agar
Ara-C
Azacitidine
Biological Assay
Cell Proliferation
Cells
Cell Survival
Clone Cells
Clustered Regularly Interspaced Short Palindromic Repeats
Cytotoxin
Daunorubicin
Hypersensitivity
Luminescent Measurements
Mutation
neuro-oncological ventral antigen 2, human
Parent
Pharmaceutical Preparations
prisma
Promega
Psychological Inhibition
Sepharose
Student
Sulfoxide, Dimethyl
tariquidar
Trypan Blue
Verapamil
Top products related to «Ara-C»
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Ara-C is a lab equipment product manufactured by Merck Group. It is a pyrimidine nucleoside analog used in research and laboratory settings. The core function of Ara-C is to serve as a tool for scientific investigation and analysis, without any specific interpretation or extrapolation on its intended use.
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GlutaMAX is a chemically defined, L-glutamine substitute for cell culture media. It is a stable source of L-glutamine that does not degrade over time like L-glutamine. GlutaMAX helps maintain consistent cell growth and performance in cell culture applications.
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Neurobasal medium is a cell culture medium designed for the maintenance and growth of primary neuronal cells. It provides a defined, serum-free environment that supports the survival and differentiation of neurons. The medium is optimized to maintain the phenotypic characteristics of neurons and minimizes the growth of non-neuronal cells.
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B27 supplement is a serum-free and animal component-free cell culture supplement developed by Thermo Fisher Scientific. It is designed to promote the growth and survival of diverse cell types, including neurons, embryonic stem cells, and other sensitive cell lines. The core function of B27 supplement is to provide a defined, optimized combination of vitamins, antioxidants, and other essential components to support cell culture applications.
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Poly-L-lysine is a synthetic polymer composed of the amino acid L-lysine. It is commonly used as a coating agent for various laboratory applications, such as cell culture and microscopy. Poly-L-lysine enhances the attachment and growth of cells on surfaces by providing a positively charged substrate.
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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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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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L-glutamine is an amino acid that is commonly used as a dietary supplement and in cell culture media. It serves as a source of nitrogen and supports cellular growth and metabolism.
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Poly-D-lysine is a synthetic polymer commonly used as a coating for cell culture surfaces. It enhances cell attachment and promotes cell growth by providing a positively charged substrate that facilitates cell adhesion.
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MEM is a cell culture medium designed for the growth and maintenance of a variety of cell types in vitro. It provides a balanced salt solution, amino acids, vitamins, and other essential nutrients required for cell proliferation and survival.
More about "Ara-C"
Ara-C, also known as cytarabine, is a potent chemotherapeutic agent widely used in the treatment of various types of cancer, particularly acute myeloid leukemia (AML) and acute lymphocytic leukemia (ALL).
This medication works by interfering with the synthesis of DNA, effectively preventing cancer cells from dividing and growing.
Ara-C is typically administered intravenously or subcutaneously and is often used in combination with other chemotherapeutic agents to enhance its effectiveness.
For researchers studying Ara-C, PubCompare.ai's AI-driven protocol comparison platform can be a valuable tool.
This platform allows researchers to easily locate and compare protocols from literature, pre-prints, and patents, helping them identify the best solutions for their needs and streamlining the research process.
By harnessing the power of AI, researchers can drive breakthrough discoveries in cancer treatment.
In addition to Ara-C, researchers may also explore the use of other compounds and media for their studies.
GlutaMAX, a stable form of L-glutamine, is commonly used in cell culture to support cell growth and metabolism.
Neurobasal medium, supplemented with B27, is often used for the culture of neuronal cells.
Poly-L-lysine and Poly-D-lysine are commonly used as cell culture coatings to promote cell adhesion and differentiation.
Fetal bovine serum (FBS) and penicillin/streptomycin are also widely used in cell culture to provide essential nutrients and prevent bacterial contamination, respectively.
L-glutamine is another important component in cell culture, serving as a source of energy and nitrogen for cells.
By leveraging the insights and tools provided by PubCompare.ai, researchers can streamline their Ara-C investigations and drive progress in the field of cancer treatment.
The combination of Ara-C's potent anti-cancer properties and the efficiency of AI-driven protocol comparison can help unlock new frontiers in cancer research and therapeutics.
This medication works by interfering with the synthesis of DNA, effectively preventing cancer cells from dividing and growing.
Ara-C is typically administered intravenously or subcutaneously and is often used in combination with other chemotherapeutic agents to enhance its effectiveness.
For researchers studying Ara-C, PubCompare.ai's AI-driven protocol comparison platform can be a valuable tool.
This platform allows researchers to easily locate and compare protocols from literature, pre-prints, and patents, helping them identify the best solutions for their needs and streamlining the research process.
By harnessing the power of AI, researchers can drive breakthrough discoveries in cancer treatment.
In addition to Ara-C, researchers may also explore the use of other compounds and media for their studies.
GlutaMAX, a stable form of L-glutamine, is commonly used in cell culture to support cell growth and metabolism.
Neurobasal medium, supplemented with B27, is often used for the culture of neuronal cells.
Poly-L-lysine and Poly-D-lysine are commonly used as cell culture coatings to promote cell adhesion and differentiation.
Fetal bovine serum (FBS) and penicillin/streptomycin are also widely used in cell culture to provide essential nutrients and prevent bacterial contamination, respectively.
L-glutamine is another important component in cell culture, serving as a source of energy and nitrogen for cells.
By leveraging the insights and tools provided by PubCompare.ai, researchers can streamline their Ara-C investigations and drive progress in the field of cancer treatment.
The combination of Ara-C's potent anti-cancer properties and the efficiency of AI-driven protocol comparison can help unlock new frontiers in cancer research and therapeutics.