p75 ntr-knockout mice Search Results


mouse anti human ngfr  (Miltenyi Biotec)
95
Miltenyi Biotec mouse anti human ngfr
Design considerations for single and dual-receptor engineered T cells (A) Schematic representation of a DAP12-associated synthetic antigen receptor (DAP12-SAR) composed of an antigen binding domain fused to the hinge, transmembrane (TM) and intracellular (ICD) domains of a DAP12-associated activating receptor (created using BioRender). (B) Schematic diagram of cDNA encoding DAP12 and the SAR separated by a Thoseasigna virus 2A (T2A) sequence for co-expression. (C) SAR surface expression was determined by binding of a myc-tag specific mAb or HER2-Fc to T cells engineered with the IL13Rα2-KIR and HER2-KIR, respectively. Cells were gated as follows: lymphocytes > single cells > CD4/CD8 > <t>NGFR</t> + . Presented is SAR expression on the CD4 + NGFR + population (unfilled black = non-transduced; gray = SAR). (D) Representative cytotoxicity of IL13Rα2-KIR, HER2-KIR and non-specific SAR T cell products after 96-h co-culture with U-251 tumor cells in an Incucyte assay (E:T = 8:1). The experiment was performed in technical triplicates and error bars are standard error mean (SEM). (E) Schematic representation of dual-SAR constructs. (F) SAR surface expression on T cells engineered with single and dual SAR constructs, using anti-Myc tag mAb and HER2-Fc to detect binding of the IL13Rα2-KIR and HER2-KIR, respectively. Cells were gated as follows: lymphocytes > single cells > CD4/CD8 > NGFR + .
Mouse Anti Human Ngfr, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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p75 ntr-/- , exon iii knockout mice  (Jackson Laboratory)
90
Jackson Laboratory p75 ntr-/- , exon iii knockout mice
Deletion of <t>p75</t> NTR reduced the development of acellular capillaries in ischemic retinas. ( A , B ) Representative trypsin-digested and PASH-stained retinas of WT and p75 NTR-/- mice subjected to I/R. Bright field imaging showed an increased number of acellular capillaries (red arrows) in WT that was attenuated in p75 NTR-/- mice (20x magnification. ( C ) Statistical analysis using two-way ANOVA showed significant impact of disease condition (ischemia) and gene deletion on the number of acellular capillaries. I/R significantly increased the number of acellular capillaries in WT retinas when compared to shams. This effect was ameliorated in retinas of p75 NTR-/- mice (*, significant using two-way ANOVA, n = 4–5).
P75 Ntr / , Exon Iii Knockout Mice, supplied by Jackson Laboratory, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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p75 ntr knockout mice  (Jackson Laboratory)
90
Jackson Laboratory p75 ntr knockout mice
Deletion of <t>p75</t> NTR reduced the development of acellular capillaries in ischemic retinas. ( A , B ) Representative trypsin-digested and PASH-stained retinas of WT and p75 NTR-/- mice subjected to I/R. Bright field imaging showed an increased number of acellular capillaries (red arrows) in WT that was attenuated in p75 NTR-/- mice (20x magnification. ( C ) Statistical analysis using two-way ANOVA showed significant impact of disease condition (ischemia) and gene deletion on the number of acellular capillaries. I/R significantly increased the number of acellular capillaries in WT retinas when compared to shams. This effect was ameliorated in retinas of p75 NTR-/- mice (*, significant using two-way ANOVA, n = 4–5).
P75 Ntr Knockout Mice, supplied by Jackson Laboratory, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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wild-type mice  (Jackson Laboratory)
90
Jackson Laboratory wild-type mice
A summary of sources of antibodies used to detect protein expression using Western Blot.
Wild Type Mice, supplied by Jackson Laboratory, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Design considerations for single and dual-receptor engineered T cells (A) Schematic representation of a DAP12-associated synthetic antigen receptor (DAP12-SAR) composed of an antigen binding domain fused to the hinge, transmembrane (TM) and intracellular (ICD) domains of a DAP12-associated activating receptor (created using BioRender). (B) Schematic diagram of cDNA encoding DAP12 and the SAR separated by a Thoseasigna virus 2A (T2A) sequence for co-expression. (C) SAR surface expression was determined by binding of a myc-tag specific mAb or HER2-Fc to T cells engineered with the IL13Rα2-KIR and HER2-KIR, respectively. Cells were gated as follows: lymphocytes > single cells > CD4/CD8 > NGFR + . Presented is SAR expression on the CD4 + NGFR + population (unfilled black = non-transduced; gray = SAR). (D) Representative cytotoxicity of IL13Rα2-KIR, HER2-KIR and non-specific SAR T cell products after 96-h co-culture with U-251 tumor cells in an Incucyte assay (E:T = 8:1). The experiment was performed in technical triplicates and error bars are standard error mean (SEM). (E) Schematic representation of dual-SAR constructs. (F) SAR surface expression on T cells engineered with single and dual SAR constructs, using anti-Myc tag mAb and HER2-Fc to detect binding of the IL13Rα2-KIR and HER2-KIR, respectively. Cells were gated as follows: lymphocytes > single cells > CD4/CD8 > NGFR + .

Journal: iScience

Article Title: DAP12-associated synthetic antigen receptors enable multi-targeting of T cells with independent chimeric receptors in a small genetic payload

doi: 10.1016/j.isci.2025.112142

Figure Lengend Snippet: Design considerations for single and dual-receptor engineered T cells (A) Schematic representation of a DAP12-associated synthetic antigen receptor (DAP12-SAR) composed of an antigen binding domain fused to the hinge, transmembrane (TM) and intracellular (ICD) domains of a DAP12-associated activating receptor (created using BioRender). (B) Schematic diagram of cDNA encoding DAP12 and the SAR separated by a Thoseasigna virus 2A (T2A) sequence for co-expression. (C) SAR surface expression was determined by binding of a myc-tag specific mAb or HER2-Fc to T cells engineered with the IL13Rα2-KIR and HER2-KIR, respectively. Cells were gated as follows: lymphocytes > single cells > CD4/CD8 > NGFR + . Presented is SAR expression on the CD4 + NGFR + population (unfilled black = non-transduced; gray = SAR). (D) Representative cytotoxicity of IL13Rα2-KIR, HER2-KIR and non-specific SAR T cell products after 96-h co-culture with U-251 tumor cells in an Incucyte assay (E:T = 8:1). The experiment was performed in technical triplicates and error bars are standard error mean (SEM). (E) Schematic representation of dual-SAR constructs. (F) SAR surface expression on T cells engineered with single and dual SAR constructs, using anti-Myc tag mAb and HER2-Fc to detect binding of the IL13Rα2-KIR and HER2-KIR, respectively. Cells were gated as follows: lymphocytes > single cells > CD4/CD8 > NGFR + .

Article Snippet: Other phenotypic markers were detected with mouse anti-human CD4 AlexaFluor700 (Invitrogen), mouse anti-human CD8a PerCP-Cyanine5.5 (Invitrogen), mouse anti-human CD8 BV786 (BD Biosciences) and mouse anti-human NGFR (Miltenyi Biotec).

Techniques: Binding Assay, Virus, Sequencing, Expressing, Co-Culture Assay, Construct

Dual targeting of IL13Rα2 and HER2 can be achieved by expression of different synthetic DAP12-associated receptors (A) Schematic representation of various HER2-SAR constructs evaluated. (B) Receptor surface expression and transduction efficiency of various HER2-SAR constructs, determined by binding to HER2-Fc and tNGFR expression, respectively. (C) Cytotoxicity of HER2-SAR engineered T cells after 120 h co-culture with HCT-116 and U-251 tumor cells in an Incucyte assay. (D) Proliferation of respective HER2-SAR constructs after 72 h co-culture with HCT-116 or U-251 tumor cells at a 1:1 ratio. Absolute cell count was determined by flow cytometry using 123count eBeads. (E) Schematic diagram of cDNA encoding single and dual SAR constructs. (F) SAR surface expression of single and dual IL13Rα2/HER2 SAR T cells determined by binding of a myc-tag specific mAb or HER2-Fc to detect the IL13Rα2-KIR and HER2-TREM1 SARs, respectively. Cells were gated as follows: lymphocytes > single cells > CD4/CD8 > NGFR + . Presented is SAR expression on the CD4 + NGFR + population. (G) Mean fluorescence intensity (MFI) of respective SARs on single and dual-receptor engineered T cells. Data are from 4 experiments with 4 PBMC donors (each donor is represented by a unique symbol). (H) Cytotoxicity of single, dual, and non-transduced T cell products after 120-h co-culture with U-251 tumor cells in an Incucyte assay. All conditions were normalized to growth of tumor cells alone. Data are from 4 individual experiments with 3 PBMC donors. Error bars represent SEM of technical replicates. (I) Cytotoxicity of single, dual, and non-transduced T cell products after 120-h co-culture with U-251 IL13Rα2 KO and U-251 HER2 KO cells in an IncuCyte assay. Data are representative of 3 experiments with 3 PBMC donors. Error bars represent SEM. Statistical analysis for (G) and (H) were performed using a paired t test and two-way ANOVA with correction for multiple comparison (Tukey test), respectively (∗ p = ≤ 0.05, ∗∗ p = ≤ 0.01, ∗∗∗ p = ≤ 0.001, ∗∗∗∗ p = ≤ 0.0001).

Journal: iScience

Article Title: DAP12-associated synthetic antigen receptors enable multi-targeting of T cells with independent chimeric receptors in a small genetic payload

doi: 10.1016/j.isci.2025.112142

Figure Lengend Snippet: Dual targeting of IL13Rα2 and HER2 can be achieved by expression of different synthetic DAP12-associated receptors (A) Schematic representation of various HER2-SAR constructs evaluated. (B) Receptor surface expression and transduction efficiency of various HER2-SAR constructs, determined by binding to HER2-Fc and tNGFR expression, respectively. (C) Cytotoxicity of HER2-SAR engineered T cells after 120 h co-culture with HCT-116 and U-251 tumor cells in an Incucyte assay. (D) Proliferation of respective HER2-SAR constructs after 72 h co-culture with HCT-116 or U-251 tumor cells at a 1:1 ratio. Absolute cell count was determined by flow cytometry using 123count eBeads. (E) Schematic diagram of cDNA encoding single and dual SAR constructs. (F) SAR surface expression of single and dual IL13Rα2/HER2 SAR T cells determined by binding of a myc-tag specific mAb or HER2-Fc to detect the IL13Rα2-KIR and HER2-TREM1 SARs, respectively. Cells were gated as follows: lymphocytes > single cells > CD4/CD8 > NGFR + . Presented is SAR expression on the CD4 + NGFR + population. (G) Mean fluorescence intensity (MFI) of respective SARs on single and dual-receptor engineered T cells. Data are from 4 experiments with 4 PBMC donors (each donor is represented by a unique symbol). (H) Cytotoxicity of single, dual, and non-transduced T cell products after 120-h co-culture with U-251 tumor cells in an Incucyte assay. All conditions were normalized to growth of tumor cells alone. Data are from 4 individual experiments with 3 PBMC donors. Error bars represent SEM of technical replicates. (I) Cytotoxicity of single, dual, and non-transduced T cell products after 120-h co-culture with U-251 IL13Rα2 KO and U-251 HER2 KO cells in an IncuCyte assay. Data are representative of 3 experiments with 3 PBMC donors. Error bars represent SEM. Statistical analysis for (G) and (H) were performed using a paired t test and two-way ANOVA with correction for multiple comparison (Tukey test), respectively (∗ p = ≤ 0.05, ∗∗ p = ≤ 0.01, ∗∗∗ p = ≤ 0.001, ∗∗∗∗ p = ≤ 0.0001).

Article Snippet: Other phenotypic markers were detected with mouse anti-human CD4 AlexaFluor700 (Invitrogen), mouse anti-human CD8a PerCP-Cyanine5.5 (Invitrogen), mouse anti-human CD8 BV786 (BD Biosciences) and mouse anti-human NGFR (Miltenyi Biotec).

Techniques: Expressing, Construct, Transduction, Binding Assay, Co-Culture Assay, Cell Counting, Flow Cytometry, Fluorescence, Comparison

Combinatorial targeting of CD133 and HER2 can be achieved using the dual-SAR approach (A) Schematic diagram of cDNA encoding CD133-SAR constructs. (B) SAR surface expression on primary human T cells as determined by binding of a myc-tag specific mAb or HER2-Fc to detect the IL13Rα2-KIR and HER2-TREM1 SARs, respectively. Cells were gated as follows: lymphocytes > single cells > CD4/CD8 > NGFR + . (C) T cells were incubated with firefly luciferase-expressing HCT-116 tumor cells for 20 h at indicated effector:target ratios. Luminescence was read with an open filter upon addition of 0.15 mg/mL D-luciferin substrate and converted to % cytotoxicity. Error bars display standard deviation for technical replicates. (D) T cells were CTV-labeled and incubated for 72-h with HCT-116 tumor cells at a 1:1 ratio. T cell proliferation was measured by flow cytometry with live > CD3 + > CD4 + > NGFR+ cells presented. (E) Schematic diagram of cDNA encoding single and dual CD133/HER2 SAR constructs. (F) SAR surface expression of single and dual CD133/HER2 SAR T cells determined by binding of a FLAG tag specific mAb or HER2-Fc to detect the CD133-NKp44 and HER2-TREM1 SARs, respectively. Cells were gated as follows: lymphocytes > single cells > CD4/CD8 > NGFR + . Presented is SAR expression on the CD4 + NGFR + population. (G) Mean fluorescence intensity (MFI) of respective SARs on single and dual-receptor engineered T cells. Data are from 4 experiments with 4 PBMC donors (each donor is represented by a unique symbol). (H) Cytotoxicity of single, dual, and non-transduced T cell products after 72-h co-culture with HCT-116 tumor cells in an Incucyte assay. All conditions in were normalized to growth of tumor cells alone. Data are from 4 individual experiments with 3 PBMC donors. Error bars represent SEM. (I) Cytotoxicity of single, dual and non-transduced T cell products after 120-h co-culture with HCT-116 CD133 KO and HCT-116 HER2 KO cells in an IncuCyte assay. Data are representative of 3 experiments with 3 PBMC donors. Error bars represent SEM of technical replicates. Statistical analysis for (G) and (H) were performed using a paired t test and two-way ANOVA with correction for multiple comparison (Tukey test), respectively (∗ p = ≤ 0.05, ∗∗ p = ≤ 0.01, ∗∗∗ p = ≤ 0.001, ∗∗∗∗ p = ≤ 0.0001).

Journal: iScience

Article Title: DAP12-associated synthetic antigen receptors enable multi-targeting of T cells with independent chimeric receptors in a small genetic payload

doi: 10.1016/j.isci.2025.112142

Figure Lengend Snippet: Combinatorial targeting of CD133 and HER2 can be achieved using the dual-SAR approach (A) Schematic diagram of cDNA encoding CD133-SAR constructs. (B) SAR surface expression on primary human T cells as determined by binding of a myc-tag specific mAb or HER2-Fc to detect the IL13Rα2-KIR and HER2-TREM1 SARs, respectively. Cells were gated as follows: lymphocytes > single cells > CD4/CD8 > NGFR + . (C) T cells were incubated with firefly luciferase-expressing HCT-116 tumor cells for 20 h at indicated effector:target ratios. Luminescence was read with an open filter upon addition of 0.15 mg/mL D-luciferin substrate and converted to % cytotoxicity. Error bars display standard deviation for technical replicates. (D) T cells were CTV-labeled and incubated for 72-h with HCT-116 tumor cells at a 1:1 ratio. T cell proliferation was measured by flow cytometry with live > CD3 + > CD4 + > NGFR+ cells presented. (E) Schematic diagram of cDNA encoding single and dual CD133/HER2 SAR constructs. (F) SAR surface expression of single and dual CD133/HER2 SAR T cells determined by binding of a FLAG tag specific mAb or HER2-Fc to detect the CD133-NKp44 and HER2-TREM1 SARs, respectively. Cells were gated as follows: lymphocytes > single cells > CD4/CD8 > NGFR + . Presented is SAR expression on the CD4 + NGFR + population. (G) Mean fluorescence intensity (MFI) of respective SARs on single and dual-receptor engineered T cells. Data are from 4 experiments with 4 PBMC donors (each donor is represented by a unique symbol). (H) Cytotoxicity of single, dual, and non-transduced T cell products after 72-h co-culture with HCT-116 tumor cells in an Incucyte assay. All conditions in were normalized to growth of tumor cells alone. Data are from 4 individual experiments with 3 PBMC donors. Error bars represent SEM. (I) Cytotoxicity of single, dual and non-transduced T cell products after 120-h co-culture with HCT-116 CD133 KO and HCT-116 HER2 KO cells in an IncuCyte assay. Data are representative of 3 experiments with 3 PBMC donors. Error bars represent SEM of technical replicates. Statistical analysis for (G) and (H) were performed using a paired t test and two-way ANOVA with correction for multiple comparison (Tukey test), respectively (∗ p = ≤ 0.05, ∗∗ p = ≤ 0.01, ∗∗∗ p = ≤ 0.001, ∗∗∗∗ p = ≤ 0.0001).

Article Snippet: Other phenotypic markers were detected with mouse anti-human CD4 AlexaFluor700 (Invitrogen), mouse anti-human CD8a PerCP-Cyanine5.5 (Invitrogen), mouse anti-human CD8 BV786 (BD Biosciences) and mouse anti-human NGFR (Miltenyi Biotec).

Techniques: Construct, Expressing, Binding Assay, Incubation, Luciferase, Standard Deviation, Labeling, Flow Cytometry, FLAG-tag, Fluorescence, Co-Culture Assay, Comparison

Expression of multiple receptors attenuates the production of inflammatory cytokines but not proliferation (A and D) Schematic representation of stimulation conditions for single- vs. dual-SAR engagement against (A) U-251 tumor cells or (D) HCT-116 tumor cells. (B and E) Intracellular cytokine production by (B) U-251 or (E) HCT-116 stimulated engineered T cells was measured by flow cytometry. Data are presented as percent NGFR+ CD4 and CD8 T cells producing respective cytokines. Data are from four independent experiments with 3 PBMC donors. Each donor is represented by a unique symbol. For the gating strategy see <xref ref-type=Figure S6 A. (C and F) Engineered T cells were labeled with CellTrace Violet (CTV) and stimulated with (C) U-251 or (F) HCT-116 tumor cells at a 1:1 ratio for 72 h. T cell proliferation and absolute cell count using 123count eBeads were measured by flow cytometry. Data are from three independent experiments with 2 T cell donors. Each donor is represented by a unique symbol. For the gating strategy see Figure S6 . Statistical analysis for (B), (C), (E), and (F) were performed using two-way ANOVA with correction for multiple comparison (Tukey test) (∗ p = ≤ 0.05, ∗∗ p = ≤ 0.01, ∗∗∗ p = ≤ 0.001, ∗∗∗∗ p = ≤ 0.0001, ns = not significant. " width="100%" height="100%">

Journal: iScience

Article Title: DAP12-associated synthetic antigen receptors enable multi-targeting of T cells with independent chimeric receptors in a small genetic payload

doi: 10.1016/j.isci.2025.112142

Figure Lengend Snippet: Expression of multiple receptors attenuates the production of inflammatory cytokines but not proliferation (A and D) Schematic representation of stimulation conditions for single- vs. dual-SAR engagement against (A) U-251 tumor cells or (D) HCT-116 tumor cells. (B and E) Intracellular cytokine production by (B) U-251 or (E) HCT-116 stimulated engineered T cells was measured by flow cytometry. Data are presented as percent NGFR+ CD4 and CD8 T cells producing respective cytokines. Data are from four independent experiments with 3 PBMC donors. Each donor is represented by a unique symbol. For the gating strategy see Figure S6 A. (C and F) Engineered T cells were labeled with CellTrace Violet (CTV) and stimulated with (C) U-251 or (F) HCT-116 tumor cells at a 1:1 ratio for 72 h. T cell proliferation and absolute cell count using 123count eBeads were measured by flow cytometry. Data are from three independent experiments with 2 T cell donors. Each donor is represented by a unique symbol. For the gating strategy see Figure S6 . Statistical analysis for (B), (C), (E), and (F) were performed using two-way ANOVA with correction for multiple comparison (Tukey test) (∗ p = ≤ 0.05, ∗∗ p = ≤ 0.01, ∗∗∗ p = ≤ 0.001, ∗∗∗∗ p = ≤ 0.0001, ns = not significant.

Article Snippet: Other phenotypic markers were detected with mouse anti-human CD4 AlexaFluor700 (Invitrogen), mouse anti-human CD8a PerCP-Cyanine5.5 (Invitrogen), mouse anti-human CD8 BV786 (BD Biosciences) and mouse anti-human NGFR (Miltenyi Biotec).

Techniques: Expressing, Flow Cytometry, Labeling, Cell Counting, Comparison

Expression of multiple receptors attenuates the early signal strength of individual receptors (A and B) Intracellular phospho-specific staining of ERK. Cells were stimulated for 30 min with respective WT or KO tumor lines, fixed, methanol-permeabilized and stained for phosphorylated ERK 1/2 (pT202/pY204). (A) Representative plots from 1 of 4 independent experiments and (B) %pERK+ of single and dual-SAR T cells following stimulation with a single target antigen. Data are from 4 independent experiments and 3 T cell donors. (C) Cells were stimulated with HCT-116 CD133 KO or U251 IL13Rα2 KO tumor cells for 1–4 h. The cells were surface stained for viability, CD4, CD8, NGFR and CD69, fixed/permeabilized, and then stained intracellularly/intranuclearly for Nur77. Cells were gated as follows: lymphocytes > single cells > live > CD4/CD8 > NGFR + > Nur77/CD69. Presented is Nur77 and CD69 expression on the CD8 + NGFR + population. Data are generated with T cells from one donor. For the gating strategy, see <xref ref-type=Figure S6 C. " width="100%" height="100%">

Journal: iScience

Article Title: DAP12-associated synthetic antigen receptors enable multi-targeting of T cells with independent chimeric receptors in a small genetic payload

doi: 10.1016/j.isci.2025.112142

Figure Lengend Snippet: Expression of multiple receptors attenuates the early signal strength of individual receptors (A and B) Intracellular phospho-specific staining of ERK. Cells were stimulated for 30 min with respective WT or KO tumor lines, fixed, methanol-permeabilized and stained for phosphorylated ERK 1/2 (pT202/pY204). (A) Representative plots from 1 of 4 independent experiments and (B) %pERK+ of single and dual-SAR T cells following stimulation with a single target antigen. Data are from 4 independent experiments and 3 T cell donors. (C) Cells were stimulated with HCT-116 CD133 KO or U251 IL13Rα2 KO tumor cells for 1–4 h. The cells were surface stained for viability, CD4, CD8, NGFR and CD69, fixed/permeabilized, and then stained intracellularly/intranuclearly for Nur77. Cells were gated as follows: lymphocytes > single cells > live > CD4/CD8 > NGFR + > Nur77/CD69. Presented is Nur77 and CD69 expression on the CD8 + NGFR + population. Data are generated with T cells from one donor. For the gating strategy, see Figure S6 C.

Article Snippet: Other phenotypic markers were detected with mouse anti-human CD4 AlexaFluor700 (Invitrogen), mouse anti-human CD8a PerCP-Cyanine5.5 (Invitrogen), mouse anti-human CD8 BV786 (BD Biosciences) and mouse anti-human NGFR (Miltenyi Biotec).

Techniques: Expressing, Staining, Generated

Journal: iScience

Article Title: DAP12-associated synthetic antigen receptors enable multi-targeting of T cells with independent chimeric receptors in a small genetic payload

doi: 10.1016/j.isci.2025.112142

Figure Lengend Snippet:

Article Snippet: Other phenotypic markers were detected with mouse anti-human CD4 AlexaFluor700 (Invitrogen), mouse anti-human CD8a PerCP-Cyanine5.5 (Invitrogen), mouse anti-human CD8 BV786 (BD Biosciences) and mouse anti-human NGFR (Miltenyi Biotec).

Techniques: FLAG-tag, Control, Virus, Generated, Subcloning, Recombinant, Staining, Flow Cytometry, Selection, Gene Knockout, Plasmid Preparation, Cloning, Expressing, Software

Deletion of p75 NTR reduced the development of acellular capillaries in ischemic retinas. ( A , B ) Representative trypsin-digested and PASH-stained retinas of WT and p75 NTR-/- mice subjected to I/R. Bright field imaging showed an increased number of acellular capillaries (red arrows) in WT that was attenuated in p75 NTR-/- mice (20x magnification. ( C ) Statistical analysis using two-way ANOVA showed significant impact of disease condition (ischemia) and gene deletion on the number of acellular capillaries. I/R significantly increased the number of acellular capillaries in WT retinas when compared to shams. This effect was ameliorated in retinas of p75 NTR-/- mice (*, significant using two-way ANOVA, n = 4–5).

Journal: International Journal of Molecular Sciences

Article Title: Modulation of p75 NTR on Mesenchymal Stem Cells Increases Their Vascular Protection in Retinal Ischemia-Reperfusion Mouse Model

doi: 10.3390/ijms22020829

Figure Lengend Snippet: Deletion of p75 NTR reduced the development of acellular capillaries in ischemic retinas. ( A , B ) Representative trypsin-digested and PASH-stained retinas of WT and p75 NTR-/- mice subjected to I/R. Bright field imaging showed an increased number of acellular capillaries (red arrows) in WT that was attenuated in p75 NTR-/- mice (20x magnification. ( C ) Statistical analysis using two-way ANOVA showed significant impact of disease condition (ischemia) and gene deletion on the number of acellular capillaries. I/R significantly increased the number of acellular capillaries in WT retinas when compared to shams. This effect was ameliorated in retinas of p75 NTR-/- mice (*, significant using two-way ANOVA, n = 4–5).

Article Snippet: The p75 NTR , B6.129S4Ngfrtm1Jae /J (p75 NTR-/- , exon III knockout mice were obtained from Jackson Laboratories (Bar Harbor, Maine, USA) and crossed with C57BL6-J mice (Jackson Laboratories).

Techniques: Staining, Imaging

MSCs incorporate to ischemic retinal vasculature and decreased acellular capillaries in WT and p75 NTR-/- ischemic retinas. ( A , B ) Confocal images of retinal flat mounts stained with isolectin (red), showing incorporation of intravitreally-injected GFP-labeled MSCs (green) into WT retinas subjected to I/R (40x magnification). ( A ) Different regions of flat-mounted retina 3 days post injections showing some MSCs morphed into amoboid/satellite-like shape (green, left panel) and some MSCs picked up isolectin stain (yellow, right panel). ( B ) Different regions of flat-mounted retina 1 week post injection showing, in the left panel, that some of the MSCs appeared perivascular (green) wrapped around retinal capillaries (red) and some other MSCs (right panel) maintained satellite-like shape and co-stained with isolectin (yellow) within retinal capillaries (red), suggesting integration into retinal vasculature. ( C ) Representative trypsin-digested and PASH-stained retinas of WT and p75 NTR-/- mice subjected to I/R and receiving GFP-labeled MSCs. Bright field imaging showed decreased count for acellular capillaries (red arrows, 20x magnification). ( D ) Bar graph and statistical analysis for acellular capillaries count in WT and p75 NTR-/- retinas subjected to I/R and receiving GFP-labeled MSCs. Ischemic WT retinas still showed a significant increase in the count of acellular capillaries that was completely ameliorated in p75 NTR-/- retinas following MSCs injection (*, significant using two-way ANOVA, n = 7–11).

Journal: International Journal of Molecular Sciences

Article Title: Modulation of p75 NTR on Mesenchymal Stem Cells Increases Their Vascular Protection in Retinal Ischemia-Reperfusion Mouse Model

doi: 10.3390/ijms22020829

Figure Lengend Snippet: MSCs incorporate to ischemic retinal vasculature and decreased acellular capillaries in WT and p75 NTR-/- ischemic retinas. ( A , B ) Confocal images of retinal flat mounts stained with isolectin (red), showing incorporation of intravitreally-injected GFP-labeled MSCs (green) into WT retinas subjected to I/R (40x magnification). ( A ) Different regions of flat-mounted retina 3 days post injections showing some MSCs morphed into amoboid/satellite-like shape (green, left panel) and some MSCs picked up isolectin stain (yellow, right panel). ( B ) Different regions of flat-mounted retina 1 week post injection showing, in the left panel, that some of the MSCs appeared perivascular (green) wrapped around retinal capillaries (red) and some other MSCs (right panel) maintained satellite-like shape and co-stained with isolectin (yellow) within retinal capillaries (red), suggesting integration into retinal vasculature. ( C ) Representative trypsin-digested and PASH-stained retinas of WT and p75 NTR-/- mice subjected to I/R and receiving GFP-labeled MSCs. Bright field imaging showed decreased count for acellular capillaries (red arrows, 20x magnification). ( D ) Bar graph and statistical analysis for acellular capillaries count in WT and p75 NTR-/- retinas subjected to I/R and receiving GFP-labeled MSCs. Ischemic WT retinas still showed a significant increase in the count of acellular capillaries that was completely ameliorated in p75 NTR-/- retinas following MSCs injection (*, significant using two-way ANOVA, n = 7–11).

Article Snippet: The p75 NTR , B6.129S4Ngfrtm1Jae /J (p75 NTR-/- , exon III knockout mice were obtained from Jackson Laboratories (Bar Harbor, Maine, USA) and crossed with C57BL6-J mice (Jackson Laboratories).

Techniques: Staining, Injection, Labeling, Imaging

Silencing p75 NTR expression in MSCs increased vascular homing and protection in ischemic retinas. ( A ) Confocal images of ischemic WT retinal flat mounts stained with Isolectin-GS (red), showing numerous GFP-labeled MSCs (green) recruited to retinal capillaries (red) after silencing p75 NTR expression when compared to scrambled-MSCs (40x magnification). ( B ) Representative trypsin-digested and PASH-stained ischemic WT retinas showing decreased acellular capillaries (red arrows) in ischemic retinas receiving MSCs that do not express p75 NTR (20x magnification). ( C ) Bar graph and statistical analysis for acellular capillaries count in ischemic WT retinas receiving Scrambled mRNA-treated or siRNA-treated MSCs against p75 NTR . Number of acellular capillaries was significantly higher in retinas receiving p75 NTR -expressing MSCs but not p75 NTR -knocked down cells (*, significant using two-way ANOVA, n = 4).

Journal: International Journal of Molecular Sciences

Article Title: Modulation of p75 NTR on Mesenchymal Stem Cells Increases Their Vascular Protection in Retinal Ischemia-Reperfusion Mouse Model

doi: 10.3390/ijms22020829

Figure Lengend Snippet: Silencing p75 NTR expression in MSCs increased vascular homing and protection in ischemic retinas. ( A ) Confocal images of ischemic WT retinal flat mounts stained with Isolectin-GS (red), showing numerous GFP-labeled MSCs (green) recruited to retinal capillaries (red) after silencing p75 NTR expression when compared to scrambled-MSCs (40x magnification). ( B ) Representative trypsin-digested and PASH-stained ischemic WT retinas showing decreased acellular capillaries (red arrows) in ischemic retinas receiving MSCs that do not express p75 NTR (20x magnification). ( C ) Bar graph and statistical analysis for acellular capillaries count in ischemic WT retinas receiving Scrambled mRNA-treated or siRNA-treated MSCs against p75 NTR . Number of acellular capillaries was significantly higher in retinas receiving p75 NTR -expressing MSCs but not p75 NTR -knocked down cells (*, significant using two-way ANOVA, n = 4).

Article Snippet: The p75 NTR , B6.129S4Ngfrtm1Jae /J (p75 NTR-/- , exon III knockout mice were obtained from Jackson Laboratories (Bar Harbor, Maine, USA) and crossed with C57BL6-J mice (Jackson Laboratories).

Techniques: Expressing, Staining, Labeling

Silencing p75 NTR expression improves MSCs-secretome. Representative micrograph of Western blotting ( A ) and statistical analysis ( B – D ) of GFP-MSCs CM showed 1.8-Fold increase in SDF-1-a, 6-Fold increase in VEGF-A and 5.8-Fold increase in NGF, upon silencing the expression of p75 NTR (* p < 0.05, n = 3. Significance detected by unpaired student T-test).

Journal: International Journal of Molecular Sciences

Article Title: Modulation of p75 NTR on Mesenchymal Stem Cells Increases Their Vascular Protection in Retinal Ischemia-Reperfusion Mouse Model

doi: 10.3390/ijms22020829

Figure Lengend Snippet: Silencing p75 NTR expression improves MSCs-secretome. Representative micrograph of Western blotting ( A ) and statistical analysis ( B – D ) of GFP-MSCs CM showed 1.8-Fold increase in SDF-1-a, 6-Fold increase in VEGF-A and 5.8-Fold increase in NGF, upon silencing the expression of p75 NTR (* p < 0.05, n = 3. Significance detected by unpaired student T-test).

Article Snippet: The p75 NTR , B6.129S4Ngfrtm1Jae /J (p75 NTR-/- , exon III knockout mice were obtained from Jackson Laboratories (Bar Harbor, Maine, USA) and crossed with C57BL6-J mice (Jackson Laboratories).

Techniques: Expressing, Western Blot

Silencing p75 NTR expression on MSCs improves paracrine effect in HREs. RT-PCR analysis showed that treatment of HREs with CM of p75 NTR -silenced MSCs significantly increased gene expression of angiogenic and survival factor transcripts, including VEGF-A ( A ), Akt ( B ), Bcl-2 ( C ) and some of the apoptotic markers including BAX ( D ) , but no change was observed in p53 ( E ) or caspase-3 ( F ) transcripts when compared to HREs treated with CM of control cells. *, significant at p < 0.05; NS, not significant. Significance was detected by unpaired student T-test, n = 3.

Journal: International Journal of Molecular Sciences

Article Title: Modulation of p75 NTR on Mesenchymal Stem Cells Increases Their Vascular Protection in Retinal Ischemia-Reperfusion Mouse Model

doi: 10.3390/ijms22020829

Figure Lengend Snippet: Silencing p75 NTR expression on MSCs improves paracrine effect in HREs. RT-PCR analysis showed that treatment of HREs with CM of p75 NTR -silenced MSCs significantly increased gene expression of angiogenic and survival factor transcripts, including VEGF-A ( A ), Akt ( B ), Bcl-2 ( C ) and some of the apoptotic markers including BAX ( D ) , but no change was observed in p53 ( E ) or caspase-3 ( F ) transcripts when compared to HREs treated with CM of control cells. *, significant at p < 0.05; NS, not significant. Significance was detected by unpaired student T-test, n = 3.

Article Snippet: The p75 NTR , B6.129S4Ngfrtm1Jae /J (p75 NTR-/- , exon III knockout mice were obtained from Jackson Laboratories (Bar Harbor, Maine, USA) and crossed with C57BL6-J mice (Jackson Laboratories).

Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction, Gene Expression, Control

Silencing p75 NTR expression on MSCs improves angiogenic response in HREs. ( A , B ) Representative images and statistical analysis of HREs migration shows significant increase in HREs migration (distance marked from original plating line marked with blue pen) after 12 h treatment with CM of p75 NTR -silenced MSCs (*, significance using one-way ANOVA test, n = 5–7. ( C – E ) Representative phase contrast images ( C ) and statistical analysis for tube length ( D ) and number of tube junction ( E ) formed in vitro by HREs after 24 h treatment with conditioned medium of p75 NTR -silenced MSCs. Results showed significant increase in tube length and number of tube junctions (*, significance using one-way ANOVA test, n = 3).

Journal: International Journal of Molecular Sciences

Article Title: Modulation of p75 NTR on Mesenchymal Stem Cells Increases Their Vascular Protection in Retinal Ischemia-Reperfusion Mouse Model

doi: 10.3390/ijms22020829

Figure Lengend Snippet: Silencing p75 NTR expression on MSCs improves angiogenic response in HREs. ( A , B ) Representative images and statistical analysis of HREs migration shows significant increase in HREs migration (distance marked from original plating line marked with blue pen) after 12 h treatment with CM of p75 NTR -silenced MSCs (*, significance using one-way ANOVA test, n = 5–7. ( C – E ) Representative phase contrast images ( C ) and statistical analysis for tube length ( D ) and number of tube junction ( E ) formed in vitro by HREs after 24 h treatment with conditioned medium of p75 NTR -silenced MSCs. Results showed significant increase in tube length and number of tube junctions (*, significance using one-way ANOVA test, n = 3).

Article Snippet: The p75 NTR , B6.129S4Ngfrtm1Jae /J (p75 NTR-/- , exon III knockout mice were obtained from Jackson Laboratories (Bar Harbor, Maine, USA) and crossed with C57BL6-J mice (Jackson Laboratories).

Techniques: Expressing, Migration, In Vitro

Modulating p75 NTR on MSCs using LM11A-31 improved their secretome and improved paracrine effect in HREs. Representative Western blotting ( A ) and statistical analysis of MSCs secretome treated with the pharmacologic modulator of p75 NTR ; LM11A-31. ( B – D ) showing ~14.9-Fold increase in SDF-1a ( B ), 1.6-Fold increase in VEGF-A ( C ) and ~4-Fold increase in NGF ( D ). * p < 0.05, Significance was detected by unpaired Student t-test, n = 3. RT-PCR analysis showed that treatment of HREs with CM of LM11A-31-treated MSCs significantly increased gene expression of the survival factor transcripts VEGF-A ( E ), Akt ( F ), Bcl-2 ( G ) and some of the apoptotic markers, such as Bax ( H ), but not p53 ( I ). *, Significant at p < 0.05; NS, not significant. Significance was detected by unpaired Student t-test, n = 3.

Journal: International Journal of Molecular Sciences

Article Title: Modulation of p75 NTR on Mesenchymal Stem Cells Increases Their Vascular Protection in Retinal Ischemia-Reperfusion Mouse Model

doi: 10.3390/ijms22020829

Figure Lengend Snippet: Modulating p75 NTR on MSCs using LM11A-31 improved their secretome and improved paracrine effect in HREs. Representative Western blotting ( A ) and statistical analysis of MSCs secretome treated with the pharmacologic modulator of p75 NTR ; LM11A-31. ( B – D ) showing ~14.9-Fold increase in SDF-1a ( B ), 1.6-Fold increase in VEGF-A ( C ) and ~4-Fold increase in NGF ( D ). * p < 0.05, Significance was detected by unpaired Student t-test, n = 3. RT-PCR analysis showed that treatment of HREs with CM of LM11A-31-treated MSCs significantly increased gene expression of the survival factor transcripts VEGF-A ( E ), Akt ( F ), Bcl-2 ( G ) and some of the apoptotic markers, such as Bax ( H ), but not p53 ( I ). *, Significant at p < 0.05; NS, not significant. Significance was detected by unpaired Student t-test, n = 3.

Article Snippet: The p75 NTR , B6.129S4Ngfrtm1Jae /J (p75 NTR-/- , exon III knockout mice were obtained from Jackson Laboratories (Bar Harbor, Maine, USA) and crossed with C57BL6-J mice (Jackson Laboratories).

Techniques: Western Blot, Reverse Transcription Polymerase Chain Reaction, Gene Expression

The sequence of the PCR primers used in the mRNA quantification experiments.

Journal: International Journal of Molecular Sciences

Article Title: Modulation of p75 NTR on Mesenchymal Stem Cells Increases Their Vascular Protection in Retinal Ischemia-Reperfusion Mouse Model

doi: 10.3390/ijms22020829

Figure Lengend Snippet: The sequence of the PCR primers used in the mRNA quantification experiments.

Article Snippet: The p75 NTR , B6.129S4Ngfrtm1Jae /J (p75 NTR-/- , exon III knockout mice were obtained from Jackson Laboratories (Bar Harbor, Maine, USA) and crossed with C57BL6-J mice (Jackson Laboratories).

Techniques: Sequencing

A summary of sources of antibodies used to detect protein expression using Western Blot.

Journal: Journal of diabetes, metabolic disorders & control

Article Title: Deletion of the Neurotrophin Receptor p75 NTR Prevents Diabetes-Induced Retinal Acellular Capillaries in Streptozotocin-Induced Mouse Diabetic Model

doi: 10.15406/jdmdc.2017.04.00129

Figure Lengend Snippet: A summary of sources of antibodies used to detect protein expression using Western Blot.

Article Snippet: Male 8-week old littermates of wild-type and p75 NTR knockout mice (~25g) from our colony with founders originally purchased from Jackson laboratory (Bar Harbor, ME, USA).

Techniques: Expressing, Western Blot

Genetic deletion of p75NTR mitigated diabetes-induced acellular capillaries. (C–F): Representative images of trypsinized-retina from WT or p75NTR KO controls or diabetic mice. (G): Quantitative data showing significant increase in retinal acellular capillaries after 6-month of diabetes in WT-diabetic but not in p75 KO-diabetic animals compared to respective controls. (A–B): Representative images of a typical occluded (acellular) capillary in a trypsinized retina of diabetic animals double-labelled with anti-Collagen IV (Green) and CD31 (Red).

Journal: Journal of diabetes, metabolic disorders & control

Article Title: Deletion of the Neurotrophin Receptor p75 NTR Prevents Diabetes-Induced Retinal Acellular Capillaries in Streptozotocin-Induced Mouse Diabetic Model

doi: 10.15406/jdmdc.2017.04.00129

Figure Lengend Snippet: Genetic deletion of p75NTR mitigated diabetes-induced acellular capillaries. (C–F): Representative images of trypsinized-retina from WT or p75NTR KO controls or diabetic mice. (G): Quantitative data showing significant increase in retinal acellular capillaries after 6-month of diabetes in WT-diabetic but not in p75 KO-diabetic animals compared to respective controls. (A–B): Representative images of a typical occluded (acellular) capillary in a trypsinized retina of diabetic animals double-labelled with anti-Collagen IV (Green) and CD31 (Red).

Article Snippet: Male 8-week old littermates of wild-type and p75 NTR knockout mice (~25g) from our colony with founders originally purchased from Jackson laboratory (Bar Harbor, ME, USA).

Techniques: