bovine serum fbs  (ATCC)


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    Name:
    Fetal Bovine Serum FBS
    Description:
    Triple filtered through 0 1 μm filters Each lot of fetal bovine serum is tested for sterility and for the ability to support the growth of several different cell lines using both sequential growth curves and plating efficiencies Fetal bovine serum is manufactured from fetal bovine blood collected in USDA inspected abattoirs located in the United States
    Catalog Number:
    30-2021
    Price:
    None
    Applications:
    Triple filtered through 0.1 μm filters. Each lot of fetal bovine serum is tested for sterility and for the ability to support the growth of several different cell lines using both sequential growth curves and plating efficiencies. Fetal bovine serum is manufactured from fetal bovine blood collected in USDA-inspected abattoirs located in the United States.
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    Structured Review

    ATCC bovine serum fbs
    Flow-charts showing the preparation of RIN-5F cells and their survival rate evaluation. A. Preparation of RIN-5F cells before starting 1–5-day preservation experiments at +4°C. B. Procedures to estimate the number of living cells using the hemocytometer. C. Procedures to measure the amount of insulin secreted from the living cells. Medium-A consists of <t>RPMI-1640</t> medium containing 10% of fetal bovine serum <t>(FBS).</t> Medium-B consists of the medium containing 1% of FBS. Trypsin-A consists of 0.25% bovine trypsin plus 1 mM of EDTA dissolved in phosphate buffered saline (PBS).
    Triple filtered through 0 1 μm filters Each lot of fetal bovine serum is tested for sterility and for the ability to support the growth of several different cell lines using both sequential growth curves and plating efficiencies Fetal bovine serum is manufactured from fetal bovine blood collected in USDA inspected abattoirs located in the United States
    https://www.bioz.com/result/bovine serum fbs/product/ATCC
    Average 97 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    bovine serum fbs - by Bioz Stars, 2021-04
    97/100 stars

    Images

    1) Product Images from "Antifreeze Protein Prolongs the Life-Time of Insulinoma Cells during Hypothermic Preservation"

    Article Title: Antifreeze Protein Prolongs the Life-Time of Insulinoma Cells during Hypothermic Preservation

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0073643

    Flow-charts showing the preparation of RIN-5F cells and their survival rate evaluation. A. Preparation of RIN-5F cells before starting 1–5-day preservation experiments at +4°C. B. Procedures to estimate the number of living cells using the hemocytometer. C. Procedures to measure the amount of insulin secreted from the living cells. Medium-A consists of RPMI-1640 medium containing 10% of fetal bovine serum (FBS). Medium-B consists of the medium containing 1% of FBS. Trypsin-A consists of 0.25% bovine trypsin plus 1 mM of EDTA dissolved in phosphate buffered saline (PBS).
    Figure Legend Snippet: Flow-charts showing the preparation of RIN-5F cells and their survival rate evaluation. A. Preparation of RIN-5F cells before starting 1–5-day preservation experiments at +4°C. B. Procedures to estimate the number of living cells using the hemocytometer. C. Procedures to measure the amount of insulin secreted from the living cells. Medium-A consists of RPMI-1640 medium containing 10% of fetal bovine serum (FBS). Medium-B consists of the medium containing 1% of FBS. Trypsin-A consists of 0.25% bovine trypsin plus 1 mM of EDTA dissolved in phosphate buffered saline (PBS).

    Techniques Used: Flow Cytometry, Preserving

    Related Articles

    Multiple Displacement Amplification:

    Article Title: MEK inhibition activates STAT signaling to increase breast cancer immunogenicity via MHC-I expression
    Article Snippet: In order to further clarify the relationship between MEKi treatment and PD-L1/MHC-I expression, we need to first determine whether this relationship is conserved in additional breast cancer models, and second, further examine the mechanism by which MEKi treatment induces immune-associated protein expression. .. Cell lines and treatmentHuman breast cancer cell lines MDA-MB-231 (DMEM + 10% fetal bovine serum; FBS), HCC1143 (RPMI + 10% FBS), and HCC1954 (RPMI + 10% FBS) were obtained from American Type Culture Collection (ATCC). .. Murine mammary cancer cell lines 4T1 (DMEM-F12 + 10% FBS) and EMT6 (DMEM-F12 + 10% FBS) were also obtained from ATCC.

    Modification:

    Article Title: A peptide factor secreted by Staphylococcus pseudintermedius exhibits properties of both bacteriocins and virulence factors
    Article Snippet: The residual activity was determined with the radial diffusion assay using Bacillus subtilis as an indicator strain. .. Cytotoxicity and haemolytic assays Human skin fibroblasts (HSF, ATCC CRL-2522), adipose-derived stem cells (ASCs, ATCC PCS-500-011), and HeLa human epithelioid cervix carcinoma cells (ATCC CCL-2) were maintained in Dulbecco’s modified Eagle’s medium (DMEM, Sigma) containing 1 g/l glucose, 10% (v/v) foetal bovine serum (FBS), 1 U/ml penicillin, 1 μg/ml streptomycin, and 2.5 μg/ml amphotericin B. Murine P388/D1 monocyte/macrophage cells (ATCC CCL-46) and murine RAW264.7 macrophage-like cells (ATCC TIB-71) were cultured in DMEM containing 4.5 g/l glucose, 5% (v/v) FBS, and antibiotics, as indicated above. .. Keratinocytes from human skin were grown in KBM Gold Medium (Lonza).

    Cell Culture:

    Article Title: A peptide factor secreted by Staphylococcus pseudintermedius exhibits properties of both bacteriocins and virulence factors
    Article Snippet: The residual activity was determined with the radial diffusion assay using Bacillus subtilis as an indicator strain. .. Cytotoxicity and haemolytic assays Human skin fibroblasts (HSF, ATCC CRL-2522), adipose-derived stem cells (ASCs, ATCC PCS-500-011), and HeLa human epithelioid cervix carcinoma cells (ATCC CCL-2) were maintained in Dulbecco’s modified Eagle’s medium (DMEM, Sigma) containing 1 g/l glucose, 10% (v/v) foetal bovine serum (FBS), 1 U/ml penicillin, 1 μg/ml streptomycin, and 2.5 μg/ml amphotericin B. Murine P388/D1 monocyte/macrophage cells (ATCC CCL-46) and murine RAW264.7 macrophage-like cells (ATCC TIB-71) were cultured in DMEM containing 4.5 g/l glucose, 5% (v/v) FBS, and antibiotics, as indicated above. .. Keratinocytes from human skin were grown in KBM Gold Medium (Lonza).

    Article Title: Adipose-derived mesenchymal stem cells promote the malignant phenotype of cervical cancer
    Article Snippet: Our results showed that ADSCs promote cell movement, angiogenesis, migration, and the epithelial–mesenchymal transition (EMT) and increase the malignant properties of CC cells through the positive regulation of NF-kappa B signaling, a pathway involved in initiation, progression and resistance to treatment in various types of cancer. .. Cell culture HeLa, SiHa, CaSki, HaCaT and ADSC were obtained from ATCC (Manassas, VA, USA) and cultured in DMEM medium supplied with 5% fetal bovine serum (FBS) (ATCC, 30-2020) at 37 °C/5% CO2 . .. To grow and expand ADSCs we used a commercially available medium (Mesenchymal Stem Cell Basal Medium, ATCC PCS 500030) containing essential and non-essential amino acids, vitamins, other organic compounds, trace minerals, and inorganic salts.

    Article Title: The role of LPA and YAP signaling in long-term migration of human ovarian cancer cells
    Article Snippet: OVCA433 cells were cultured in RPMI 1640 with glutamine, 10% FBS (ATCC, Manassas, VA), and 100 μg/mL penicillin/streptomycin (P/S). .. CAOV3, OVCAR5 and Monty-1 cells were cultured in DMEM with glutamine, 10% FBS (ATCC, Manassas, VA), and 100 μg/mL P/S. .. For serum starvation, cells were incubated in growth medium without FBS or antibiotics.

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  • 94
    ATCC hcc1143
    MAPK signaling and STAT activation are inversely correlated in human TNBC cell lines and basal-like patient samples. A: immunoblot analysis of <t>HCC1143,</t> HCC1954, and MDA-MB-231 cells grown in either base media or PMEC media treated with or without trametinib (50 nM; MEKi) for 48 h prior to lysis; B: immunoblot analysis of HCC1143 cells grown in RPMI media supplemented with EGF (20 ng/mL), hydrocortisone (0.5 μg/mL), or insulin (10 μg/mL) along with being treated with or without trametinib (50 nM; MEKi) for 48 h prior to lysis; C: transcriptional analysis of STAT1 and Ras/MAPK scores for 211 Basal-like breast cancers. MAPK: mitogen activated protein kinase; TNBC: triple negative breast cancer; MEKi: MEK inhibition
    Hcc1143, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 94 stars, based on 1 article reviews
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    fbs  (ATCC)
    86
    ATCC fbs
    LPA-induced FOXM1 in other EOC cell lines and FOXM1C was the dominant form in CAOV3 cells A. LPA (10 μM and 6 hr) induced FOXM1 up-regulation in CAOV3 and OVCAR5 cells. CAOV3 and OVCAR5 cells expressed the FOXM1B with apparent MW of 80 KDa (Sigma, Cat. Log # AV39518). B. <t>OVCA433</t> cells did not express FOXM1C, while CAOV3 cells expressed the FOXM1C with apparent MW of 100 KDa (Cell Signaling, Cat. Log # D12D5). C. CAOV3-FOXM1-KD cell line was established using shRNA against FOXM1 (detailed in Methods). The parental or control-shRNA transfected CAOV3 cells responded to LPA (10 μM, 6 hr) for FOXM1 up-regulation, which was blocked by KD-FOXM1. D. The dominant splicing form of FOXM1 in CAOV3 was FOXM1C. E. Comparison of the relative mRNA expression levels FOXM1 isoform in three EOC cell lines. F. KD-YAP and PTX inhibited LPA-induced FOXM1 up-regulation in CAOV3 cells. G. KD-FOXM1 inhibited LPA-induced cell migration and invasion. H. KD-FOXM1 inhibited <t>FBS</t> (2%)-induced cell proliferation. * P
    Fbs, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    bxpc 3  (ATCC)
    99
    ATCC bxpc 3
    Phospho-drug loaded-CPSNPs block pancreatic cancer cell proliferation In vitro growth of human PDAC cell lines <t>BxPC-3</t> and PANC-1 is effectively blocked by mPEG-dFdCMPs, with EC 50 values of 130 and 550 nM, respectively. BxPC-3 cells were more resistant to mPEG-FdUMP-CPSNPS than PANC-1 cells, which had an EC 50 of 1.3 μM. Empty mPEG-CPSNPs (light hatched), free drug (black) or drug-containing CPSNPs (shaded hatched) are expressed as relative proliferation (percent of vehicle, white). Values are the mean of 3–4 independent experiments; *** p
    Bxpc 3, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/bxpc 3/product/ATCC
    Average 99 stars, based on 1 article reviews
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    Image Search Results


    MAPK signaling and STAT activation are inversely correlated in human TNBC cell lines and basal-like patient samples. A: immunoblot analysis of HCC1143, HCC1954, and MDA-MB-231 cells grown in either base media or PMEC media treated with or without trametinib (50 nM; MEKi) for 48 h prior to lysis; B: immunoblot analysis of HCC1143 cells grown in RPMI media supplemented with EGF (20 ng/mL), hydrocortisone (0.5 μg/mL), or insulin (10 μg/mL) along with being treated with or without trametinib (50 nM; MEKi) for 48 h prior to lysis; C: transcriptional analysis of STAT1 and Ras/MAPK scores for 211 Basal-like breast cancers. MAPK: mitogen activated protein kinase; TNBC: triple negative breast cancer; MEKi: MEK inhibition

    Journal: Cancer drug resistance (Alhambra, Calif.)

    Article Title: MEK inhibition activates STAT signaling to increase breast cancer immunogenicity via MHC-I expression

    doi: 10.20517/cdr.2019.109

    Figure Lengend Snippet: MAPK signaling and STAT activation are inversely correlated in human TNBC cell lines and basal-like patient samples. A: immunoblot analysis of HCC1143, HCC1954, and MDA-MB-231 cells grown in either base media or PMEC media treated with or without trametinib (50 nM; MEKi) for 48 h prior to lysis; B: immunoblot analysis of HCC1143 cells grown in RPMI media supplemented with EGF (20 ng/mL), hydrocortisone (0.5 μg/mL), or insulin (10 μg/mL) along with being treated with or without trametinib (50 nM; MEKi) for 48 h prior to lysis; C: transcriptional analysis of STAT1 and Ras/MAPK scores for 211 Basal-like breast cancers. MAPK: mitogen activated protein kinase; TNBC: triple negative breast cancer; MEKi: MEK inhibition

    Article Snippet: Cell lines and treatmentHuman breast cancer cell lines MDA-MB-231 (DMEM + 10% fetal bovine serum; FBS), HCC1143 (RPMI + 10% FBS), and HCC1954 (RPMI + 10% FBS) were obtained from American Type Culture Collection (ATCC).

    Techniques: Activation Assay, Multiple Displacement Amplification, Lysis, Inhibition

    LPA-induced FOXM1 in other EOC cell lines and FOXM1C was the dominant form in CAOV3 cells A. LPA (10 μM and 6 hr) induced FOXM1 up-regulation in CAOV3 and OVCAR5 cells. CAOV3 and OVCAR5 cells expressed the FOXM1B with apparent MW of 80 KDa (Sigma, Cat. Log # AV39518). B. OVCA433 cells did not express FOXM1C, while CAOV3 cells expressed the FOXM1C with apparent MW of 100 KDa (Cell Signaling, Cat. Log # D12D5). C. CAOV3-FOXM1-KD cell line was established using shRNA against FOXM1 (detailed in Methods). The parental or control-shRNA transfected CAOV3 cells responded to LPA (10 μM, 6 hr) for FOXM1 up-regulation, which was blocked by KD-FOXM1. D. The dominant splicing form of FOXM1 in CAOV3 was FOXM1C. E. Comparison of the relative mRNA expression levels FOXM1 isoform in three EOC cell lines. F. KD-YAP and PTX inhibited LPA-induced FOXM1 up-regulation in CAOV3 cells. G. KD-FOXM1 inhibited LPA-induced cell migration and invasion. H. KD-FOXM1 inhibited FBS (2%)-induced cell proliferation. * P

    Journal: Oncotarget

    Article Title: FOXM1 is a downstream target of LPA and YAP oncogenic signaling pathways in high grade serous ovarian cancer

    doi:

    Figure Lengend Snippet: LPA-induced FOXM1 in other EOC cell lines and FOXM1C was the dominant form in CAOV3 cells A. LPA (10 μM and 6 hr) induced FOXM1 up-regulation in CAOV3 and OVCAR5 cells. CAOV3 and OVCAR5 cells expressed the FOXM1B with apparent MW of 80 KDa (Sigma, Cat. Log # AV39518). B. OVCA433 cells did not express FOXM1C, while CAOV3 cells expressed the FOXM1C with apparent MW of 100 KDa (Cell Signaling, Cat. Log # D12D5). C. CAOV3-FOXM1-KD cell line was established using shRNA against FOXM1 (detailed in Methods). The parental or control-shRNA transfected CAOV3 cells responded to LPA (10 μM, 6 hr) for FOXM1 up-regulation, which was blocked by KD-FOXM1. D. The dominant splicing form of FOXM1 in CAOV3 was FOXM1C. E. Comparison of the relative mRNA expression levels FOXM1 isoform in three EOC cell lines. F. KD-YAP and PTX inhibited LPA-induced FOXM1 up-regulation in CAOV3 cells. G. KD-FOXM1 inhibited LPA-induced cell migration and invasion. H. KD-FOXM1 inhibited FBS (2%)-induced cell proliferation. * P

    Article Snippet: OVCA433 cells were cultured in RPMI 1640 with glutamine, 10% FBS (ATCC, Manassas, VA), and 100 μg/mL penicillin/streptomycin (P/S).

    Techniques: shRNA, Transfection, Expressing, Migration

    FOXM1 was functionally involved in cell proliferation, migration, and invasion in EOC cells OVCA433 cells were starved and pretreated with different doses of thiostrepton (a selective inhibitor of FOXM1) for 1 hr prior to LPA treatment (10 μM, 6 hr). Thiostrepton dose-dependently reduced LPA-induced FOXM1 expression A. and inhibited LPA-induced cell migration and invasion in OVCA433 cells B. FOXM1 down-regulation by shRNA C. reduced cell migration and invasion induced by LPA and cell proliferation induced by 2% FBS D. The results are from three independent experiments. FOXM1 was detected using the Sigma antibody (Cat. Log# AV39518). * P

    Journal: Oncotarget

    Article Title: FOXM1 is a downstream target of LPA and YAP oncogenic signaling pathways in high grade serous ovarian cancer

    doi:

    Figure Lengend Snippet: FOXM1 was functionally involved in cell proliferation, migration, and invasion in EOC cells OVCA433 cells were starved and pretreated with different doses of thiostrepton (a selective inhibitor of FOXM1) for 1 hr prior to LPA treatment (10 μM, 6 hr). Thiostrepton dose-dependently reduced LPA-induced FOXM1 expression A. and inhibited LPA-induced cell migration and invasion in OVCA433 cells B. FOXM1 down-regulation by shRNA C. reduced cell migration and invasion induced by LPA and cell proliferation induced by 2% FBS D. The results are from three independent experiments. FOXM1 was detected using the Sigma antibody (Cat. Log# AV39518). * P

    Article Snippet: OVCA433 cells were cultured in RPMI 1640 with glutamine, 10% FBS (ATCC, Manassas, VA), and 100 μg/mL penicillin/streptomycin (P/S).

    Techniques: Migration, Expressing, shRNA

    Phospho-drug loaded-CPSNPs block pancreatic cancer cell proliferation In vitro growth of human PDAC cell lines BxPC-3 and PANC-1 is effectively blocked by mPEG-dFdCMPs, with EC 50 values of 130 and 550 nM, respectively. BxPC-3 cells were more resistant to mPEG-FdUMP-CPSNPS than PANC-1 cells, which had an EC 50 of 1.3 μM. Empty mPEG-CPSNPs (light hatched), free drug (black) or drug-containing CPSNPs (shaded hatched) are expressed as relative proliferation (percent of vehicle, white). Values are the mean of 3–4 independent experiments; *** p

    Journal: Nanomedicine : nanotechnology, biology, and medicine

    Article Title: Effective Encapsulation and Biological Activity of Phosphorylated Chemotherapeutics in Calcium Phosphosilicate Nanoparticles for the Treatment of Pancreatic Cancer

    doi: 10.1016/j.nano.2017.06.017

    Figure Lengend Snippet: Phospho-drug loaded-CPSNPs block pancreatic cancer cell proliferation In vitro growth of human PDAC cell lines BxPC-3 and PANC-1 is effectively blocked by mPEG-dFdCMPs, with EC 50 values of 130 and 550 nM, respectively. BxPC-3 cells were more resistant to mPEG-FdUMP-CPSNPS than PANC-1 cells, which had an EC 50 of 1.3 μM. Empty mPEG-CPSNPs (light hatched), free drug (black) or drug-containing CPSNPs (shaded hatched) are expressed as relative proliferation (percent of vehicle, white). Values are the mean of 3–4 independent experiments; *** p

    Article Snippet: PANC-1 (in Dulbecco’s modified Eagle medium/10% fetal bovine serum) and BxPC-3 (in RPMI medium/10% fetal bovine serum) cells (ATCC) were seeded onto 96-well plates at 5,000 cells/well.

    Techniques: Blocking Assay, In Vitro

    CPSNP-encapsulated FdUMP inactivates TS Immunoblots of the FdUMP target enzyme thymidylate synthase (TS) from PANC-1 (upper panel) or BxPC-3 (lower panel) cells treated with (Lane 3) 250 μM free FdUMP or (Lane 5) 2 μM mPEG-FdUMP-CPSNPs. Both cell lines showed significant ( > 80%) conversion of TS to an inactive ternary complex (TS:FdUMP) with free drug and with mPEG-FdUMP-CPSNP treatment. Controls that received (Lane 1) no treatment, (Lane 2) vehicle or (Lane 4) mPEG-CPSNPs exhibited only active TS with no evidence of TS:FdUMP ternary complex formation.

    Journal: Nanomedicine : nanotechnology, biology, and medicine

    Article Title: Effective Encapsulation and Biological Activity of Phosphorylated Chemotherapeutics in Calcium Phosphosilicate Nanoparticles for the Treatment of Pancreatic Cancer

    doi: 10.1016/j.nano.2017.06.017

    Figure Lengend Snippet: CPSNP-encapsulated FdUMP inactivates TS Immunoblots of the FdUMP target enzyme thymidylate synthase (TS) from PANC-1 (upper panel) or BxPC-3 (lower panel) cells treated with (Lane 3) 250 μM free FdUMP or (Lane 5) 2 μM mPEG-FdUMP-CPSNPs. Both cell lines showed significant ( > 80%) conversion of TS to an inactive ternary complex (TS:FdUMP) with free drug and with mPEG-FdUMP-CPSNP treatment. Controls that received (Lane 1) no treatment, (Lane 2) vehicle or (Lane 4) mPEG-CPSNPs exhibited only active TS with no evidence of TS:FdUMP ternary complex formation.

    Article Snippet: PANC-1 (in Dulbecco’s modified Eagle medium/10% fetal bovine serum) and BxPC-3 (in RPMI medium/10% fetal bovine serum) cells (ATCC) were seeded onto 96-well plates at 5,000 cells/well.

    Techniques: Western Blot