mouse anti cd2 Search Results


93
Miltenyi Biotec anti cd2 antibody
Deletion of NSrp70 results in defective survival signals following TCR activation in CD69 + DP thymocytes. ( A ) KEGG T cell receptor signaling pathway. The blue asterisks (*) represent down-regulated genes from the RNA-seq analysis (Figure ). ( B ) Expression of TCRβ, CD3ϵ, and CD3ζ on CD69 + DP thymocytes from Nsrp1 f/f (WT) and Nsrp1 f/f CD4Cre (KO) mice. ( C ) A schematic model of gene regulation by NSrp70. NSrp70 sequesters splicing factors in the nuclear speckles. Disintegration of splicing factors by NSrp70 deletion induces abnormal gene regulation during thymocyte development. As one of the results, reduced TCR expression may cause impaired T cell maturation. ( D ) Calcium flux in DP thymocytes. Cells from (A) were stimulated with PMA and ionomycin (P/I) or anti-CD3/CD28 antibodies, and then calcium fluxes were measured by flow cytometry. ( E ) Western blot of ZAP70, PKCθ, Erk1/2, and p38 in DP cell lysates stimulated on anti-CD3/28 for 0, 5, and 20 min. β-actin served as the loading control. M, molecular mass (KDa). ( F ) In vitro thymocyte development assay. CD69 – DP thymocytes were stimulated on <t>anti-TCRβ/CD2</t> antibodies for 20 h (stimulation), or the cells were further incubated for 20 h in medium without stimulation (recovery). (G and H) Cells from (F) were stained for Ki-67 ( G ) or annexin V and 7ADD ( H ). Cells were analyzed by flow cytometry (F–H). The bar graphs indicate mean fluorescence intensities (MFI) (G). *, meaningful P -value; NC, non-coated; S, stimulation; R, recovery. The bar graphs indicate average ± standard deviation of apoptotic and dead thymocytes population (H). NS, non-significant P -value. All data shown are representative of three independent experiments.
Anti Cd2 Antibody, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Bio-Rad anti cd2
Deletion of NSrp70 results in defective survival signals following TCR activation in CD69 + DP thymocytes. ( A ) KEGG T cell receptor signaling pathway. The blue asterisks (*) represent down-regulated genes from the RNA-seq analysis (Figure ). ( B ) Expression of TCRβ, CD3ϵ, and CD3ζ on CD69 + DP thymocytes from Nsrp1 f/f (WT) and Nsrp1 f/f CD4Cre (KO) mice. ( C ) A schematic model of gene regulation by NSrp70. NSrp70 sequesters splicing factors in the nuclear speckles. Disintegration of splicing factors by NSrp70 deletion induces abnormal gene regulation during thymocyte development. As one of the results, reduced TCR expression may cause impaired T cell maturation. ( D ) Calcium flux in DP thymocytes. Cells from (A) were stimulated with PMA and ionomycin (P/I) or anti-CD3/CD28 antibodies, and then calcium fluxes were measured by flow cytometry. ( E ) Western blot of ZAP70, PKCθ, Erk1/2, and p38 in DP cell lysates stimulated on anti-CD3/28 for 0, 5, and 20 min. β-actin served as the loading control. M, molecular mass (KDa). ( F ) In vitro thymocyte development assay. CD69 – DP thymocytes were stimulated on <t>anti-TCRβ/CD2</t> antibodies for 20 h (stimulation), or the cells were further incubated for 20 h in medium without stimulation (recovery). (G and H) Cells from (F) were stained for Ki-67 ( G ) or annexin V and 7ADD ( H ). Cells were analyzed by flow cytometry (F–H). The bar graphs indicate mean fluorescence intensities (MFI) (G). *, meaningful P -value; NC, non-coated; S, stimulation; R, recovery. The bar graphs indicate average ± standard deviation of apoptotic and dead thymocytes population (H). NS, non-significant P -value. All data shown are representative of three independent experiments.
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Bio-Rad mouse α human cd2 mab
Deletion of NSrp70 results in defective survival signals following TCR activation in CD69 + DP thymocytes. ( A ) KEGG T cell receptor signaling pathway. The blue asterisks (*) represent down-regulated genes from the RNA-seq analysis (Figure ). ( B ) Expression of TCRβ, CD3ϵ, and CD3ζ on CD69 + DP thymocytes from Nsrp1 f/f (WT) and Nsrp1 f/f CD4Cre (KO) mice. ( C ) A schematic model of gene regulation by NSrp70. NSrp70 sequesters splicing factors in the nuclear speckles. Disintegration of splicing factors by NSrp70 deletion induces abnormal gene regulation during thymocyte development. As one of the results, reduced TCR expression may cause impaired T cell maturation. ( D ) Calcium flux in DP thymocytes. Cells from (A) were stimulated with PMA and ionomycin (P/I) or anti-CD3/CD28 antibodies, and then calcium fluxes were measured by flow cytometry. ( E ) Western blot of ZAP70, PKCθ, Erk1/2, and p38 in DP cell lysates stimulated on anti-CD3/28 for 0, 5, and 20 min. β-actin served as the loading control. M, molecular mass (KDa). ( F ) In vitro thymocyte development assay. CD69 – DP thymocytes were stimulated on <t>anti-TCRβ/CD2</t> antibodies for 20 h (stimulation), or the cells were further incubated for 20 h in medium without stimulation (recovery). (G and H) Cells from (F) were stained for Ki-67 ( G ) or annexin V and 7ADD ( H ). Cells were analyzed by flow cytometry (F–H). The bar graphs indicate mean fluorescence intensities (MFI) (G). *, meaningful P -value; NC, non-coated; S, stimulation; R, recovery. The bar graphs indicate average ± standard deviation of apoptotic and dead thymocytes population (H). NS, non-significant P -value. All data shown are representative of three independent experiments.
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Cedarlane anti rcd2 antibody
Deletion of NSrp70 results in defective survival signals following TCR activation in CD69 + DP thymocytes. ( A ) KEGG T cell receptor signaling pathway. The blue asterisks (*) represent down-regulated genes from the RNA-seq analysis (Figure ). ( B ) Expression of TCRβ, CD3ϵ, and CD3ζ on CD69 + DP thymocytes from Nsrp1 f/f (WT) and Nsrp1 f/f CD4Cre (KO) mice. ( C ) A schematic model of gene regulation by NSrp70. NSrp70 sequesters splicing factors in the nuclear speckles. Disintegration of splicing factors by NSrp70 deletion induces abnormal gene regulation during thymocyte development. As one of the results, reduced TCR expression may cause impaired T cell maturation. ( D ) Calcium flux in DP thymocytes. Cells from (A) were stimulated with PMA and ionomycin (P/I) or anti-CD3/CD28 antibodies, and then calcium fluxes were measured by flow cytometry. ( E ) Western blot of ZAP70, PKCθ, Erk1/2, and p38 in DP cell lysates stimulated on anti-CD3/28 for 0, 5, and 20 min. β-actin served as the loading control. M, molecular mass (KDa). ( F ) In vitro thymocyte development assay. CD69 – DP thymocytes were stimulated on <t>anti-TCRβ/CD2</t> antibodies for 20 h (stimulation), or the cells were further incubated for 20 h in medium without stimulation (recovery). (G and H) Cells from (F) were stained for Ki-67 ( G ) or annexin V and 7ADD ( H ). Cells were analyzed by flow cytometry (F–H). The bar graphs indicate mean fluorescence intensities (MFI) (G). *, meaningful P -value; NC, non-coated; S, stimulation; R, recovery. The bar graphs indicate average ± standard deviation of apoptotic and dead thymocytes population (H). NS, non-significant P -value. All data shown are representative of three independent experiments.
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Cedarlane mouse anti cd2
Deletion of NSrp70 results in defective survival signals following TCR activation in CD69 + DP thymocytes. ( A ) KEGG T cell receptor signaling pathway. The blue asterisks (*) represent down-regulated genes from the RNA-seq analysis (Figure ). ( B ) Expression of TCRβ, CD3ϵ, and CD3ζ on CD69 + DP thymocytes from Nsrp1 f/f (WT) and Nsrp1 f/f CD4Cre (KO) mice. ( C ) A schematic model of gene regulation by NSrp70. NSrp70 sequesters splicing factors in the nuclear speckles. Disintegration of splicing factors by NSrp70 deletion induces abnormal gene regulation during thymocyte development. As one of the results, reduced TCR expression may cause impaired T cell maturation. ( D ) Calcium flux in DP thymocytes. Cells from (A) were stimulated with PMA and ionomycin (P/I) or anti-CD3/CD28 antibodies, and then calcium fluxes were measured by flow cytometry. ( E ) Western blot of ZAP70, PKCθ, Erk1/2, and p38 in DP cell lysates stimulated on anti-CD3/28 for 0, 5, and 20 min. β-actin served as the loading control. M, molecular mass (KDa). ( F ) In vitro thymocyte development assay. CD69 – DP thymocytes were stimulated on <t>anti-TCRβ/CD2</t> antibodies for 20 h (stimulation), or the cells were further incubated for 20 h in medium without stimulation (recovery). (G and H) Cells from (F) were stained for Ki-67 ( G ) or annexin V and 7ADD ( H ). Cells were analyzed by flow cytometry (F–H). The bar graphs indicate mean fluorescence intensities (MFI) (G). *, meaningful P -value; NC, non-coated; S, stimulation; R, recovery. The bar graphs indicate average ± standard deviation of apoptotic and dead thymocytes population (H). NS, non-significant P -value. All data shown are representative of three independent experiments.
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93
Bio-Rad anti bovine cd2 fitc
Deletion of NSrp70 results in defective survival signals following TCR activation in CD69 + DP thymocytes. ( A ) KEGG T cell receptor signaling pathway. The blue asterisks (*) represent down-regulated genes from the RNA-seq analysis (Figure ). ( B ) Expression of TCRβ, CD3ϵ, and CD3ζ on CD69 + DP thymocytes from Nsrp1 f/f (WT) and Nsrp1 f/f CD4Cre (KO) mice. ( C ) A schematic model of gene regulation by NSrp70. NSrp70 sequesters splicing factors in the nuclear speckles. Disintegration of splicing factors by NSrp70 deletion induces abnormal gene regulation during thymocyte development. As one of the results, reduced TCR expression may cause impaired T cell maturation. ( D ) Calcium flux in DP thymocytes. Cells from (A) were stimulated with PMA and ionomycin (P/I) or anti-CD3/CD28 antibodies, and then calcium fluxes were measured by flow cytometry. ( E ) Western blot of ZAP70, PKCθ, Erk1/2, and p38 in DP cell lysates stimulated on anti-CD3/28 for 0, 5, and 20 min. β-actin served as the loading control. M, molecular mass (KDa). ( F ) In vitro thymocyte development assay. CD69 – DP thymocytes were stimulated on <t>anti-TCRβ/CD2</t> antibodies for 20 h (stimulation), or the cells were further incubated for 20 h in medium without stimulation (recovery). (G and H) Cells from (F) were stained for Ki-67 ( G ) or annexin V and 7ADD ( H ). Cells were analyzed by flow cytometry (F–H). The bar graphs indicate mean fluorescence intensities (MFI) (G). *, meaningful P -value; NC, non-coated; S, stimulation; R, recovery. The bar graphs indicate average ± standard deviation of apoptotic and dead thymocytes population (H). NS, non-significant P -value. All data shown are representative of three independent experiments.
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91
Miltenyi Biotec cd2 rea959 fitc
Deletion of NSrp70 results in defective survival signals following TCR activation in CD69 + DP thymocytes. ( A ) KEGG T cell receptor signaling pathway. The blue asterisks (*) represent down-regulated genes from the RNA-seq analysis (Figure ). ( B ) Expression of TCRβ, CD3ϵ, and CD3ζ on CD69 + DP thymocytes from Nsrp1 f/f (WT) and Nsrp1 f/f CD4Cre (KO) mice. ( C ) A schematic model of gene regulation by NSrp70. NSrp70 sequesters splicing factors in the nuclear speckles. Disintegration of splicing factors by NSrp70 deletion induces abnormal gene regulation during thymocyte development. As one of the results, reduced TCR expression may cause impaired T cell maturation. ( D ) Calcium flux in DP thymocytes. Cells from (A) were stimulated with PMA and ionomycin (P/I) or anti-CD3/CD28 antibodies, and then calcium fluxes were measured by flow cytometry. ( E ) Western blot of ZAP70, PKCθ, Erk1/2, and p38 in DP cell lysates stimulated on anti-CD3/28 for 0, 5, and 20 min. β-actin served as the loading control. M, molecular mass (KDa). ( F ) In vitro thymocyte development assay. CD69 – DP thymocytes were stimulated on <t>anti-TCRβ/CD2</t> antibodies for 20 h (stimulation), or the cells were further incubated for 20 h in medium without stimulation (recovery). (G and H) Cells from (F) were stained for Ki-67 ( G ) or annexin V and 7ADD ( H ). Cells were analyzed by flow cytometry (F–H). The bar graphs indicate mean fluorescence intensities (MFI) (G). *, meaningful P -value; NC, non-coated; S, stimulation; R, recovery. The bar graphs indicate average ± standard deviation of apoptotic and dead thymocytes population (H). NS, non-significant P -value. All data shown are representative of three independent experiments.
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80
Cedarlane mouse monoclonal anti rat cd2 igg thymocyte
Deletion of NSrp70 results in defective survival signals following TCR activation in CD69 + DP thymocytes. ( A ) KEGG T cell receptor signaling pathway. The blue asterisks (*) represent down-regulated genes from the RNA-seq analysis (Figure ). ( B ) Expression of TCRβ, CD3ϵ, and CD3ζ on CD69 + DP thymocytes from Nsrp1 f/f (WT) and Nsrp1 f/f CD4Cre (KO) mice. ( C ) A schematic model of gene regulation by NSrp70. NSrp70 sequesters splicing factors in the nuclear speckles. Disintegration of splicing factors by NSrp70 deletion induces abnormal gene regulation during thymocyte development. As one of the results, reduced TCR expression may cause impaired T cell maturation. ( D ) Calcium flux in DP thymocytes. Cells from (A) were stimulated with PMA and ionomycin (P/I) or anti-CD3/CD28 antibodies, and then calcium fluxes were measured by flow cytometry. ( E ) Western blot of ZAP70, PKCθ, Erk1/2, and p38 in DP cell lysates stimulated on anti-CD3/28 for 0, 5, and 20 min. β-actin served as the loading control. M, molecular mass (KDa). ( F ) In vitro thymocyte development assay. CD69 – DP thymocytes were stimulated on <t>anti-TCRβ/CD2</t> antibodies for 20 h (stimulation), or the cells were further incubated for 20 h in medium without stimulation (recovery). (G and H) Cells from (F) were stained for Ki-67 ( G ) or annexin V and 7ADD ( H ). Cells were analyzed by flow cytometry (F–H). The bar graphs indicate mean fluorescence intensities (MFI) (G). *, meaningful P -value; NC, non-coated; S, stimulation; R, recovery. The bar graphs indicate average ± standard deviation of apoptotic and dead thymocytes population (H). NS, non-significant P -value. All data shown are representative of three independent experiments.
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93
Cytek Biosciences pe anti cd209
Deletion of NSrp70 results in defective survival signals following TCR activation in CD69 + DP thymocytes. ( A ) KEGG T cell receptor signaling pathway. The blue asterisks (*) represent down-regulated genes from the RNA-seq analysis (Figure ). ( B ) Expression of TCRβ, CD3ϵ, and CD3ζ on CD69 + DP thymocytes from Nsrp1 f/f (WT) and Nsrp1 f/f CD4Cre (KO) mice. ( C ) A schematic model of gene regulation by NSrp70. NSrp70 sequesters splicing factors in the nuclear speckles. Disintegration of splicing factors by NSrp70 deletion induces abnormal gene regulation during thymocyte development. As one of the results, reduced TCR expression may cause impaired T cell maturation. ( D ) Calcium flux in DP thymocytes. Cells from (A) were stimulated with PMA and ionomycin (P/I) or anti-CD3/CD28 antibodies, and then calcium fluxes were measured by flow cytometry. ( E ) Western blot of ZAP70, PKCθ, Erk1/2, and p38 in DP cell lysates stimulated on anti-CD3/28 for 0, 5, and 20 min. β-actin served as the loading control. M, molecular mass (KDa). ( F ) In vitro thymocyte development assay. CD69 – DP thymocytes were stimulated on <t>anti-TCRβ/CD2</t> antibodies for 20 h (stimulation), or the cells were further incubated for 20 h in medium without stimulation (recovery). (G and H) Cells from (F) were stained for Ki-67 ( G ) or annexin V and 7ADD ( H ). Cells were analyzed by flow cytometry (F–H). The bar graphs indicate mean fluorescence intensities (MFI) (G). *, meaningful P -value; NC, non-coated; S, stimulation; R, recovery. The bar graphs indicate average ± standard deviation of apoptotic and dead thymocytes population (H). NS, non-significant P -value. All data shown are representative of three independent experiments.
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90
Becton Dickinson mouse anti-human cd2-apc
Deletion of NSrp70 results in defective survival signals following TCR activation in CD69 + DP thymocytes. ( A ) KEGG T cell receptor signaling pathway. The blue asterisks (*) represent down-regulated genes from the RNA-seq analysis (Figure ). ( B ) Expression of TCRβ, CD3ϵ, and CD3ζ on CD69 + DP thymocytes from Nsrp1 f/f (WT) and Nsrp1 f/f CD4Cre (KO) mice. ( C ) A schematic model of gene regulation by NSrp70. NSrp70 sequesters splicing factors in the nuclear speckles. Disintegration of splicing factors by NSrp70 deletion induces abnormal gene regulation during thymocyte development. As one of the results, reduced TCR expression may cause impaired T cell maturation. ( D ) Calcium flux in DP thymocytes. Cells from (A) were stimulated with PMA and ionomycin (P/I) or anti-CD3/CD28 antibodies, and then calcium fluxes were measured by flow cytometry. ( E ) Western blot of ZAP70, PKCθ, Erk1/2, and p38 in DP cell lysates stimulated on anti-CD3/28 for 0, 5, and 20 min. β-actin served as the loading control. M, molecular mass (KDa). ( F ) In vitro thymocyte development assay. CD69 – DP thymocytes were stimulated on <t>anti-TCRβ/CD2</t> antibodies for 20 h (stimulation), or the cells were further incubated for 20 h in medium without stimulation (recovery). (G and H) Cells from (F) were stained for Ki-67 ( G ) or annexin V and 7ADD ( H ). Cells were analyzed by flow cytometry (F–H). The bar graphs indicate mean fluorescence intensities (MFI) (G). *, meaningful P -value; NC, non-coated; S, stimulation; R, recovery. The bar graphs indicate average ± standard deviation of apoptotic and dead thymocytes population (H). NS, non-significant P -value. All data shown are representative of three independent experiments.
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Serotech Inc cd81
Deletion of NSrp70 results in defective survival signals following TCR activation in CD69 + DP thymocytes. ( A ) KEGG T cell receptor signaling pathway. The blue asterisks (*) represent down-regulated genes from the RNA-seq analysis (Figure ). ( B ) Expression of TCRβ, CD3ϵ, and CD3ζ on CD69 + DP thymocytes from Nsrp1 f/f (WT) and Nsrp1 f/f CD4Cre (KO) mice. ( C ) A schematic model of gene regulation by NSrp70. NSrp70 sequesters splicing factors in the nuclear speckles. Disintegration of splicing factors by NSrp70 deletion induces abnormal gene regulation during thymocyte development. As one of the results, reduced TCR expression may cause impaired T cell maturation. ( D ) Calcium flux in DP thymocytes. Cells from (A) were stimulated with PMA and ionomycin (P/I) or anti-CD3/CD28 antibodies, and then calcium fluxes were measured by flow cytometry. ( E ) Western blot of ZAP70, PKCθ, Erk1/2, and p38 in DP cell lysates stimulated on anti-CD3/28 for 0, 5, and 20 min. β-actin served as the loading control. M, molecular mass (KDa). ( F ) In vitro thymocyte development assay. CD69 – DP thymocytes were stimulated on <t>anti-TCRβ/CD2</t> antibodies for 20 h (stimulation), or the cells were further incubated for 20 h in medium without stimulation (recovery). (G and H) Cells from (F) were stained for Ki-67 ( G ) or annexin V and 7ADD ( H ). Cells were analyzed by flow cytometry (F–H). The bar graphs indicate mean fluorescence intensities (MFI) (G). *, meaningful P -value; NC, non-coated; S, stimulation; R, recovery. The bar graphs indicate average ± standard deviation of apoptotic and dead thymocytes population (H). NS, non-significant P -value. All data shown are representative of three independent experiments.
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Becton Dickinson fluorescein isothiocyanate-conjugated mouse anti-human cd2
Deletion of NSrp70 results in defective survival signals following TCR activation in CD69 + DP thymocytes. ( A ) KEGG T cell receptor signaling pathway. The blue asterisks (*) represent down-regulated genes from the RNA-seq analysis (Figure ). ( B ) Expression of TCRβ, CD3ϵ, and CD3ζ on CD69 + DP thymocytes from Nsrp1 f/f (WT) and Nsrp1 f/f CD4Cre (KO) mice. ( C ) A schematic model of gene regulation by NSrp70. NSrp70 sequesters splicing factors in the nuclear speckles. Disintegration of splicing factors by NSrp70 deletion induces abnormal gene regulation during thymocyte development. As one of the results, reduced TCR expression may cause impaired T cell maturation. ( D ) Calcium flux in DP thymocytes. Cells from (A) were stimulated with PMA and ionomycin (P/I) or anti-CD3/CD28 antibodies, and then calcium fluxes were measured by flow cytometry. ( E ) Western blot of ZAP70, PKCθ, Erk1/2, and p38 in DP cell lysates stimulated on anti-CD3/28 for 0, 5, and 20 min. β-actin served as the loading control. M, molecular mass (KDa). ( F ) In vitro thymocyte development assay. CD69 – DP thymocytes were stimulated on <t>anti-TCRβ/CD2</t> antibodies for 20 h (stimulation), or the cells were further incubated for 20 h in medium without stimulation (recovery). (G and H) Cells from (F) were stained for Ki-67 ( G ) or annexin V and 7ADD ( H ). Cells were analyzed by flow cytometry (F–H). The bar graphs indicate mean fluorescence intensities (MFI) (G). *, meaningful P -value; NC, non-coated; S, stimulation; R, recovery. The bar graphs indicate average ± standard deviation of apoptotic and dead thymocytes population (H). NS, non-significant P -value. All data shown are representative of three independent experiments.
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Image Search Results


Deletion of NSrp70 results in defective survival signals following TCR activation in CD69 + DP thymocytes. ( A ) KEGG T cell receptor signaling pathway. The blue asterisks (*) represent down-regulated genes from the RNA-seq analysis (Figure ). ( B ) Expression of TCRβ, CD3ϵ, and CD3ζ on CD69 + DP thymocytes from Nsrp1 f/f (WT) and Nsrp1 f/f CD4Cre (KO) mice. ( C ) A schematic model of gene regulation by NSrp70. NSrp70 sequesters splicing factors in the nuclear speckles. Disintegration of splicing factors by NSrp70 deletion induces abnormal gene regulation during thymocyte development. As one of the results, reduced TCR expression may cause impaired T cell maturation. ( D ) Calcium flux in DP thymocytes. Cells from (A) were stimulated with PMA and ionomycin (P/I) or anti-CD3/CD28 antibodies, and then calcium fluxes were measured by flow cytometry. ( E ) Western blot of ZAP70, PKCθ, Erk1/2, and p38 in DP cell lysates stimulated on anti-CD3/28 for 0, 5, and 20 min. β-actin served as the loading control. M, molecular mass (KDa). ( F ) In vitro thymocyte development assay. CD69 – DP thymocytes were stimulated on anti-TCRβ/CD2 antibodies for 20 h (stimulation), or the cells were further incubated for 20 h in medium without stimulation (recovery). (G and H) Cells from (F) were stained for Ki-67 ( G ) or annexin V and 7ADD ( H ). Cells were analyzed by flow cytometry (F–H). The bar graphs indicate mean fluorescence intensities (MFI) (G). *, meaningful P -value; NC, non-coated; S, stimulation; R, recovery. The bar graphs indicate average ± standard deviation of apoptotic and dead thymocytes population (H). NS, non-significant P -value. All data shown are representative of three independent experiments.

Journal: Nucleic Acids Research

Article Title: NSrp70 is a lymphocyte-essential splicing factor that controls thymocyte development

doi: 10.1093/nar/gkab389

Figure Lengend Snippet: Deletion of NSrp70 results in defective survival signals following TCR activation in CD69 + DP thymocytes. ( A ) KEGG T cell receptor signaling pathway. The blue asterisks (*) represent down-regulated genes from the RNA-seq analysis (Figure ). ( B ) Expression of TCRβ, CD3ϵ, and CD3ζ on CD69 + DP thymocytes from Nsrp1 f/f (WT) and Nsrp1 f/f CD4Cre (KO) mice. ( C ) A schematic model of gene regulation by NSrp70. NSrp70 sequesters splicing factors in the nuclear speckles. Disintegration of splicing factors by NSrp70 deletion induces abnormal gene regulation during thymocyte development. As one of the results, reduced TCR expression may cause impaired T cell maturation. ( D ) Calcium flux in DP thymocytes. Cells from (A) were stimulated with PMA and ionomycin (P/I) or anti-CD3/CD28 antibodies, and then calcium fluxes were measured by flow cytometry. ( E ) Western blot of ZAP70, PKCθ, Erk1/2, and p38 in DP cell lysates stimulated on anti-CD3/28 for 0, 5, and 20 min. β-actin served as the loading control. M, molecular mass (KDa). ( F ) In vitro thymocyte development assay. CD69 – DP thymocytes were stimulated on anti-TCRβ/CD2 antibodies for 20 h (stimulation), or the cells were further incubated for 20 h in medium without stimulation (recovery). (G and H) Cells from (F) were stained for Ki-67 ( G ) or annexin V and 7ADD ( H ). Cells were analyzed by flow cytometry (F–H). The bar graphs indicate mean fluorescence intensities (MFI) (G). *, meaningful P -value; NC, non-coated; S, stimulation; R, recovery. The bar graphs indicate average ± standard deviation of apoptotic and dead thymocytes population (H). NS, non-significant P -value. All data shown are representative of three independent experiments.

Article Snippet: Anti-CD2 antibody (130-100-617) was purchased from Miltenyi Biotec (Bergisch Gladbach, Germany).

Techniques: Activation Assay, RNA Sequencing, Expressing, Flow Cytometry, Western Blot, Control, In Vitro, Incubation, Staining, Fluorescence, Standard Deviation