senescence associated β galactosidase sa βgal assay senescence associated β galactosidase  (Millipore)


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    Millipore senescence associated β galactosidase sa βgal assay senescence associated β galactosidase
    The treatment with IL6 and IL8 induces senescence in MCF-7 cells. a Representative images of MCF-7 cells treated with SCM during 10 days or ( c ) cytokines (50 ng/ml) during 5 days and stained for <t>SA-β-GAL.</t> Scale bar, 10 μm. b Gene expression profile of p16, p21 and p53 in MCF-7 cells stimulated with SCM or ( e ) cytokines, as indicated. The values were normalized to GADPH and relative to control cells ( dotted lines ). Error bars represent SEM. (* p
    Senescence Associated β Galactosidase Sa βgal Assay Senescence Associated β Galactosidase, supplied by Millipore, used in various techniques. Bioz Stars score: 91/100, based on 3042 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/senescence associated β galactosidase sa βgal assay senescence associated β galactosidase/product/Millipore
    Average 91 stars, based on 3042 article reviews
    Price from $9.99 to $1999.99
    senescence associated β galactosidase sa βgal assay senescence associated β galactosidase - by Bioz Stars, 2020-08
    91/100 stars

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    Images

    1) Product Images from "Senescence-associated IL-6 and IL-8 cytokines induce a self- and cross-reinforced senescence/inflammatory milieu strengthening tumorigenic capabilities in the MCF-7 breast cancer cell line"

    Article Title: Senescence-associated IL-6 and IL-8 cytokines induce a self- and cross-reinforced senescence/inflammatory milieu strengthening tumorigenic capabilities in the MCF-7 breast cancer cell line

    Journal: Cell Communication and Signaling : CCS

    doi: 10.1186/s12964-017-0172-3

    The treatment with IL6 and IL8 induces senescence in MCF-7 cells. a Representative images of MCF-7 cells treated with SCM during 10 days or ( c ) cytokines (50 ng/ml) during 5 days and stained for SA-β-GAL. Scale bar, 10 μm. b Gene expression profile of p16, p21 and p53 in MCF-7 cells stimulated with SCM or ( e ) cytokines, as indicated. The values were normalized to GADPH and relative to control cells ( dotted lines ). Error bars represent SEM. (* p
    Figure Legend Snippet: The treatment with IL6 and IL8 induces senescence in MCF-7 cells. a Representative images of MCF-7 cells treated with SCM during 10 days or ( c ) cytokines (50 ng/ml) during 5 days and stained for SA-β-GAL. Scale bar, 10 μm. b Gene expression profile of p16, p21 and p53 in MCF-7 cells stimulated with SCM or ( e ) cytokines, as indicated. The values were normalized to GADPH and relative to control cells ( dotted lines ). Error bars represent SEM. (* p

    Techniques Used: Staining, Expressing

    2) Product Images from "Heterotypic paracrine signaling drives fibroblast senescence and tumor progression of large cell carcinoma of the lung"

    Article Title: Heterotypic paracrine signaling drives fibroblast senescence and tumor progression of large cell carcinoma of the lung

    Journal: Oncotarget

    doi: 10.18632/oncotarget.10327

    Analysis of senescence markers in normal (cancer-naive) lung fibroblasts co-cultured with lung cancer cell lines derived from ADC, SCC and LCC patients A. Outline of the Transwell-based co-cultures. B. Representative phase contrast images of SA-βgal stainings of CCD-19Lu fibroblasts co-cultured with a panel of lung cancer cell lines. More images are shown in Supplementary Figure S2 . C. Average percentage of SA-βgal+ CCD-19Lu fibroblasts co-cultured with a panel of lung cancer cell lines. Bare Transwell inserts were used as negative control. All pair-wise comparisons were performed with respect to Bare. D. Average percentage of growth arrested CCD-19Lu fibroblasts co-cultured with a panel of lung cancer cell lines with 0% or 10% FBS. E. Average relative changes in growth arrested cells computed from data in (D) as in Figure 1G .
    Figure Legend Snippet: Analysis of senescence markers in normal (cancer-naive) lung fibroblasts co-cultured with lung cancer cell lines derived from ADC, SCC and LCC patients A. Outline of the Transwell-based co-cultures. B. Representative phase contrast images of SA-βgal stainings of CCD-19Lu fibroblasts co-cultured with a panel of lung cancer cell lines. More images are shown in Supplementary Figure S2 . C. Average percentage of SA-βgal+ CCD-19Lu fibroblasts co-cultured with a panel of lung cancer cell lines. Bare Transwell inserts were used as negative control. All pair-wise comparisons were performed with respect to Bare. D. Average percentage of growth arrested CCD-19Lu fibroblasts co-cultured with a panel of lung cancer cell lines with 0% or 10% FBS. E. Average relative changes in growth arrested cells computed from data in (D) as in Figure 1G .

    Techniques Used: Cell Culture, Derivative Assay, Negative Control

    Analysis of myofibroblast and senescence markers in primary lung fibroblasts from major NSCLC subtypes (ADC, SCC and LCC) A. Representative fluorescence images of α-SMA stainings of cultured CFs and TAFs from a randomly selected patient of each histologic subtype. Patient number is indicated in the bottom-left of each image. Scale bar here and thereafter, 50 μm. B. Average fold α-SMA fluorescence intensity per cell of TAFs with respect to paired CFs for each subtype (6 ADC, 8 SCC, 3 LCC). Data shown as mean ± SE. C. Representative phase contrast images of SA-βgal stainings of cultured CFs and TAFs from a randomly selected patient of each histologic subtype. SA-βgal+ fibroblasts appear in blue. More images are shown in Supplementary Figure S1 . D. Box-plot of the percentage of SA-βgal+ fibroblasts in CFs and TAFs for each subtype from two independent collections (10 ADC, 8 SCC, 4 LCC). E. Average percentage of growth arrested fibroblasts (G0/G1 of the cell cycle) in CFs and TAFs for each subtype (4 ADC, 4 SCC, 3 LCC) cultured with 0% and 10% FBS. F. Average relative change in arrested fibroblasts at 10% versus 0% FBS computed from the data in G. All pair-wise comparisons were performed with respect to CFs except in (E). Mann–Whitney rank sum test was used in (D). *, P
    Figure Legend Snippet: Analysis of myofibroblast and senescence markers in primary lung fibroblasts from major NSCLC subtypes (ADC, SCC and LCC) A. Representative fluorescence images of α-SMA stainings of cultured CFs and TAFs from a randomly selected patient of each histologic subtype. Patient number is indicated in the bottom-left of each image. Scale bar here and thereafter, 50 μm. B. Average fold α-SMA fluorescence intensity per cell of TAFs with respect to paired CFs for each subtype (6 ADC, 8 SCC, 3 LCC). Data shown as mean ± SE. C. Representative phase contrast images of SA-βgal stainings of cultured CFs and TAFs from a randomly selected patient of each histologic subtype. SA-βgal+ fibroblasts appear in blue. More images are shown in Supplementary Figure S1 . D. Box-plot of the percentage of SA-βgal+ fibroblasts in CFs and TAFs for each subtype from two independent collections (10 ADC, 8 SCC, 4 LCC). E. Average percentage of growth arrested fibroblasts (G0/G1 of the cell cycle) in CFs and TAFs for each subtype (4 ADC, 4 SCC, 3 LCC) cultured with 0% and 10% FBS. F. Average relative change in arrested fibroblasts at 10% versus 0% FBS computed from the data in G. All pair-wise comparisons were performed with respect to CFs except in (E). Mann–Whitney rank sum test was used in (D). *, P

    Techniques Used: Fluorescence, Cell Culture, MANN-WHITNEY

    Effect of oxidative stress and exogenous TGF-β1 on fibroblast senescence induction by LCC cells A. Average percentage of SA-βgal+ CCD-19Lu fibroblasts co-cultured with H460 in the presence of increasing doses of the antioxidant NAC or vehicle. B, C. Average percentage of SA-βgal+ CCD-19Lu fibroblasts in response to direct or indirect oxidative stress elicited by (B) 2h treatment of H 2 O 2 followed by 4 days of recovery or (C) 9 day treatment with bleomycin (BLM). D. Average percentage of SA-βgal+ CCD-19Lu fibroblasts daily treated with TGF-β1-continuously or intermitently for 4h/day as in [ 8 ]- for 2 weeks. E. Average percentage of SA-βgal+ CCD-19Lu fibroblasts co-cultured with H460 in the presence 5 μM of the TGF-β pathway inhibitor SB505124 for 9 days. All results correspond to two replicates from at least three independent experiments. All pair-wise comparisons were performed with respect to Bare or vehicle.
    Figure Legend Snippet: Effect of oxidative stress and exogenous TGF-β1 on fibroblast senescence induction by LCC cells A. Average percentage of SA-βgal+ CCD-19Lu fibroblasts co-cultured with H460 in the presence of increasing doses of the antioxidant NAC or vehicle. B, C. Average percentage of SA-βgal+ CCD-19Lu fibroblasts in response to direct or indirect oxidative stress elicited by (B) 2h treatment of H 2 O 2 followed by 4 days of recovery or (C) 9 day treatment with bleomycin (BLM). D. Average percentage of SA-βgal+ CCD-19Lu fibroblasts daily treated with TGF-β1-continuously or intermitently for 4h/day as in [ 8 ]- for 2 weeks. E. Average percentage of SA-βgal+ CCD-19Lu fibroblasts co-cultured with H460 in the presence 5 μM of the TGF-β pathway inhibitor SB505124 for 9 days. All results correspond to two replicates from at least three independent experiments. All pair-wise comparisons were performed with respect to Bare or vehicle.

    Techniques Used: Cell Culture

    3) Product Images from "Chronic Low Dose Rate Ionizing Radiation Exposure Induces Premature Senescence in Human Fibroblasts that Correlates with Up Regulation of Proteins Involved in Protection against Oxidative Stress"

    Article Title: Chronic Low Dose Rate Ionizing Radiation Exposure Induces Premature Senescence in Human Fibroblasts that Correlates with Up Regulation of Proteins Involved in Protection against Oxidative Stress

    Journal: Proteomes

    doi: 10.3390/proteomes2030341

    Panel ( A ): Growth rate kinetics of VH10 cells in response to chronic dose of 5 (□) and 15 ( × ) mGy/h γ-rays as well as for non-exposed cells (■). The results are based on 3 independent experiments ( n = 3) for each dose rate that were started from passage 12. The slopes of growth rate for each experiment have been calculated and used to test the significance between the growth rates of non-exposed and exposed cells; Panel ( B ): The senescence-associated β-galactosidase staining of VH10 cells. Fibroblasts at early (20 days of culture), late and senescent passages (days of culture as shown in C ) were subjected to in situ SA-βgal staining at pH 6 and examined by bright field microscopy. Cellular senescence is evident by flattened cell morphology, growth arrest and augmented senescence-associated β-galactosidase activity (numbers in brackets represent percent of β-galactosidase active cells); Panel ( C ): Western blots showing the expression of p53, p21 and p16. VH10 cells were harvested at early-, late-passages and senescent stages. Total protein extract were subjected to SDS-PAGE and Western blotting. The membranes were developed with antibodies for p53, p21, p16 and actin as control. Data are representative of two independent experiments.
    Figure Legend Snippet: Panel ( A ): Growth rate kinetics of VH10 cells in response to chronic dose of 5 (□) and 15 ( × ) mGy/h γ-rays as well as for non-exposed cells (■). The results are based on 3 independent experiments ( n = 3) for each dose rate that were started from passage 12. The slopes of growth rate for each experiment have been calculated and used to test the significance between the growth rates of non-exposed and exposed cells; Panel ( B ): The senescence-associated β-galactosidase staining of VH10 cells. Fibroblasts at early (20 days of culture), late and senescent passages (days of culture as shown in C ) were subjected to in situ SA-βgal staining at pH 6 and examined by bright field microscopy. Cellular senescence is evident by flattened cell morphology, growth arrest and augmented senescence-associated β-galactosidase activity (numbers in brackets represent percent of β-galactosidase active cells); Panel ( C ): Western blots showing the expression of p53, p21 and p16. VH10 cells were harvested at early-, late-passages and senescent stages. Total protein extract were subjected to SDS-PAGE and Western blotting. The membranes were developed with antibodies for p53, p21, p16 and actin as control. Data are representative of two independent experiments.

    Techniques Used: Staining, In Situ, Microscopy, Activity Assay, Western Blot, Expressing, SDS Page

    4) Product Images from "HIV and drug abuse mediate astrocyte senescence in a β‐catenin‐dependent manner leading to neuronal toxicity"

    Article Title: HIV and drug abuse mediate astrocyte senescence in a β‐catenin‐dependent manner leading to neuronal toxicity

    Journal: Aging Cell

    doi: 10.1111/acel.12593

    Meth and HIV infection decrease β‐catenin signaling. A) HFA s were transfected with TOP flash and treated daily with 300 μ m of meth. At 48 h post‐transfection, luciferase activities were measured. The value of arbitrary units per μg of cellular protein in the control was set at 100%. B‐C) HFA s were infected with VSVG ‐ HIV . Cell lysates were collected postinfection at 0, 24, 48, and 72 h. Western analysis was used for the detection of total β‐catenin and active β‐catenin, normalized to GAPDH . * denotes P
    Figure Legend Snippet: Meth and HIV infection decrease β‐catenin signaling. A) HFA s were transfected with TOP flash and treated daily with 300 μ m of meth. At 48 h post‐transfection, luciferase activities were measured. The value of arbitrary units per μg of cellular protein in the control was set at 100%. B‐C) HFA s were infected with VSVG ‐ HIV . Cell lysates were collected postinfection at 0, 24, 48, and 72 h. Western analysis was used for the detection of total β‐catenin and active β‐catenin, normalized to GAPDH . * denotes P

    Techniques Used: Infection, Transfection, Luciferase, Western Blot

    Suppression of β‐catenin induces HFA senescence (A, B). A) HFA s were transfected with scrambled control si RNA or β‐catenin si RNA . At day 3, cell lysates were harvested for analysis of β‐catenin levels by Western blotting, using GAPDH as control. B) In parallel experiments, si RNA ‐transfected HFA s were treated with 1x PBS vehicle or 300 μ m of meth daily. At day 6, cells were fixed and stained for SA ‐βGal. * denotes P
    Figure Legend Snippet: Suppression of β‐catenin induces HFA senescence (A, B). A) HFA s were transfected with scrambled control si RNA or β‐catenin si RNA . At day 3, cell lysates were harvested for analysis of β‐catenin levels by Western blotting, using GAPDH as control. B) In parallel experiments, si RNA ‐transfected HFA s were treated with 1x PBS vehicle or 300 μ m of meth daily. At day 6, cells were fixed and stained for SA ‐βGal. * denotes P

    Techniques Used: Transfection, Western Blot, Staining

    5) Product Images from "Chronic Low Dose Rate Ionizing Radiation Exposure Induces Premature Senescence in Human Fibroblasts that Correlates with Up Regulation of Proteins Involved in Protection against Oxidative Stress"

    Article Title: Chronic Low Dose Rate Ionizing Radiation Exposure Induces Premature Senescence in Human Fibroblasts that Correlates with Up Regulation of Proteins Involved in Protection against Oxidative Stress

    Journal: Proteomes

    doi: 10.3390/proteomes2030341

    Panel ( A ): Growth rate kinetics of human fibroblast deficient in GS in response to chronic dose of 5 (□) and 15 (×) mGy/h γ-rays as well as for non-exposed cells (■). The results are based on 3 independent experiments ( n = 3) for each dose rate; Panel ( B ): The quantification of SA-βgal staining in GS deficient fibroblast after 3 weeks of chronic exposure to γ-rays are based on 3 independent experiments ( n = 3). The exposed cells were subjected to in situ SA-βgal staining at pH 6 and examined by bright field phase microscopy. The SA-βgal positive cells are presented as % of total number of the investigated cells.
    Figure Legend Snippet: Panel ( A ): Growth rate kinetics of human fibroblast deficient in GS in response to chronic dose of 5 (□) and 15 (×) mGy/h γ-rays as well as for non-exposed cells (■). The results are based on 3 independent experiments ( n = 3) for each dose rate; Panel ( B ): The quantification of SA-βgal staining in GS deficient fibroblast after 3 weeks of chronic exposure to γ-rays are based on 3 independent experiments ( n = 3). The exposed cells were subjected to in situ SA-βgal staining at pH 6 and examined by bright field phase microscopy. The SA-βgal positive cells are presented as % of total number of the investigated cells.

    Techniques Used: Staining, In Situ, Microscopy

    Panel ( A ): Growth rate kinetics of VH10 cells in response to chronic dose of 5 (□) and 15 ( × ) mGy/h γ-rays as well as for non-exposed cells (■). The results are based on 3 independent experiments ( n = 3) for each dose rate that were started from passage 12. The slopes of growth rate for each experiment have been calculated and used to test the significance between the growth rates of non-exposed and exposed cells; Panel ( B ): The senescence-associated β-galactosidase staining of VH10 cells. Fibroblasts at early (20 days of culture), late and senescent passages (days of culture as shown in C ) were subjected to in situ SA-βgal staining at pH 6 and examined by bright field microscopy. Cellular senescence is evident by flattened cell morphology, growth arrest and augmented senescence-associated β-galactosidase activity (numbers in brackets represent percent of β-galactosidase active cells); Panel ( C ): Western blots showing the expression of p53, p21 and p16. VH10 cells were harvested at early-, late-passages and senescent stages. Total protein extract were subjected to SDS-PAGE and Western blotting. The membranes were developed with antibodies for p53, p21, p16 and actin as control. Data are representative of two independent experiments.
    Figure Legend Snippet: Panel ( A ): Growth rate kinetics of VH10 cells in response to chronic dose of 5 (□) and 15 ( × ) mGy/h γ-rays as well as for non-exposed cells (■). The results are based on 3 independent experiments ( n = 3) for each dose rate that were started from passage 12. The slopes of growth rate for each experiment have been calculated and used to test the significance between the growth rates of non-exposed and exposed cells; Panel ( B ): The senescence-associated β-galactosidase staining of VH10 cells. Fibroblasts at early (20 days of culture), late and senescent passages (days of culture as shown in C ) were subjected to in situ SA-βgal staining at pH 6 and examined by bright field microscopy. Cellular senescence is evident by flattened cell morphology, growth arrest and augmented senescence-associated β-galactosidase activity (numbers in brackets represent percent of β-galactosidase active cells); Panel ( C ): Western blots showing the expression of p53, p21 and p16. VH10 cells were harvested at early-, late-passages and senescent stages. Total protein extract were subjected to SDS-PAGE and Western blotting. The membranes were developed with antibodies for p53, p21, p16 and actin as control. Data are representative of two independent experiments.

    Techniques Used: Staining, In Situ, Microscopy, Activity Assay, Western Blot, Expressing, SDS Page

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    Article Snippet: .. The following primary antibodies were used: anti-phosphorylated myosin light chain 2 (Thr18/Ser19; Cell Signaling Technology), anti-phosphorylated myosin light chain 2 (Ser19) produced in rabbit or in mouse (both obtained from Cell Signaling Technology), anti-GAPDH (Sigma-Aldrich, St. Louis, MO), mouse anti-MLCK (Sigma-Aldrich, St. Louis, MO) and rabbit anti-MLCK (abcam), anti-ROCK 2 (Sigma-Aldrich, St. Louis, MO), anti-Myc tag (Cell Signaling Technology), and anti-ROCK1 (Cell Signaling Technology). .. The following secondaries were used: IRDye 800 Goat anti-mouse IgG, IRDye 700 Goat anti-rabbit IgG (Licor), and HRP-conjugated anti-mouse (Life Technologies).

    Incubation:

    Article Title: Specific Alterations in Astrocyte Properties via the GluA2-GAPDH Complex Associated with Multiple Sclerosis
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    Article Snippet: .. For immunodetection, membranes were blocked in 5% BSA in TBS with 0.1% Tween-20 (TBST) and incubated in TBST with eNOS and phosphorylated-eNOS(Ser1177) antibodies (Cell life signaling, Danvers, MA, USA) (1:100 dilution), anti-EDN1 antibody (Sigma-Aldrich, St. Louis, MO, USA) (1:500), anti- NFκB (p65) antibody, and anti-phosphorylated NFκB (p65) at Ser536 position (St. John’s Laboratory, London, UK) (1:500), and anti-GAPDH antibody (Sigma-Aldrich, St. Louis, MO, USA) (1:1000) with chemiluminescent detection. .. Blots were incubated with peroxidase-labeled anti-rabbit or anti-mouse IgG secondary antibody (1:20,000; cat# PI-1000 (Rabbit), PI-2000 (mouse), Vector Labs, Burlingame, CA, USA) at room temperature, followed by enhanced chemiluminescence detection (Immobilon Western HRP substrate Luminol Reagent, Millipore, Billerica, MA, USA).

    Immunodetection:

    Article Title: Downregulation of endothelial nitric oxide synthase (eNOS) and endothelin-1 (ET-1) in a co-culture system with human stimulated X-linked CGD neutrophils
    Article Snippet: .. For immunodetection, membranes were blocked in 5% BSA in TBS with 0.1% Tween-20 (TBST) and incubated in TBST with eNOS and phosphorylated-eNOS(Ser1177) antibodies (Cell life signaling, Danvers, MA, USA) (1:100 dilution), anti-EDN1 antibody (Sigma-Aldrich, St. Louis, MO, USA) (1:500), anti- NFκB (p65) antibody, and anti-phosphorylated NFκB (p65) at Ser536 position (St. John’s Laboratory, London, UK) (1:500), and anti-GAPDH antibody (Sigma-Aldrich, St. Louis, MO, USA) (1:1000) with chemiluminescent detection. .. Blots were incubated with peroxidase-labeled anti-rabbit or anti-mouse IgG secondary antibody (1:20,000; cat# PI-1000 (Rabbit), PI-2000 (mouse), Vector Labs, Burlingame, CA, USA) at room temperature, followed by enhanced chemiluminescence detection (Immobilon Western HRP substrate Luminol Reagent, Millipore, Billerica, MA, USA).

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    • senescence associated β galactosidase sa βgal assay senescence associated β galactosidase  (Millipore)
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    Millipore senescence associated β galactosidase sa βgal assay senescence associated β galactosidase
    The treatment with IL6 and IL8 induces senescence in MCF-7 cells. a Representative images of MCF-7 cells treated with SCM during 10 days or ( c ) cytokines (50 ng/ml) during 5 days and stained for <t>SA-β-GAL.</t> Scale bar, 10 μm. b Gene expression profile of p16, p21 and p53 in MCF-7 cells stimulated with SCM or ( e ) cytokines, as indicated. The values were normalized to GADPH and relative to control cells ( dotted lines ). Error bars represent SEM. (* p
    Senescence Associated β Galactosidase Sa βgal Assay Senescence Associated β Galactosidase, supplied by Millipore, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/senescence associated β galactosidase sa βgal assay senescence associated β galactosidase/product/Millipore
    Average 91 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    senescence associated β galactosidase sa βgal assay senescence associated β galactosidase - by Bioz Stars, 2020-08
    91/100 stars
    		  Buy from Supplier

    Image Search Results


    The treatment with IL6 and IL8 induces senescence in MCF-7 cells. a Representative images of MCF-7 cells treated with SCM during 10 days or ( c ) cytokines (50 ng/ml) during 5 days and stained for SA-β-GAL. Scale bar, 10 μm. b Gene expression profile of p16, p21 and p53 in MCF-7 cells stimulated with SCM or ( e ) cytokines, as indicated. The values were normalized to GADPH and relative to control cells ( dotted lines ). Error bars represent SEM. (* p

    Journal: Cell Communication and Signaling : CCS

    Article Title: Senescence-associated IL-6 and IL-8 cytokines induce a self- and cross-reinforced senescence/inflammatory milieu strengthening tumorigenic capabilities in the MCF-7 breast cancer cell line

    doi: 10.1186/s12964-017-0172-3

    Figure Lengend Snippet: The treatment with IL6 and IL8 induces senescence in MCF-7 cells. a Representative images of MCF-7 cells treated with SCM during 10 days or ( c ) cytokines (50 ng/ml) during 5 days and stained for SA-β-GAL. Scale bar, 10 μm. b Gene expression profile of p16, p21 and p53 in MCF-7 cells stimulated with SCM or ( e ) cytokines, as indicated. The values were normalized to GADPH and relative to control cells ( dotted lines ). Error bars represent SEM. (* p

    Article Snippet: Senescence-associated β-galactosidase (SA-βGAL) assay Senescence-associated β-galactosidase (SA-βGAL) activity was evaluated in senescent- and young fibroblasts after 2 days of culture by using the cellular senescence assay kit (KAA002, Millipore).

    Techniques: Staining, Expressing