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gst ndr2  (Carna Inc)


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    Structured Review

    Carna Inc gst ndr2
    NDR depletion abolishes mobility and metastasis properties in HBEC with RASSF1A depletion. HBEC-3 were transfected with non-silencing siRNA (siNeg), siRASSF1A and/or with siNDR1 or siNDR2. Experiences were performed 48 h after transfection. A549 cells were transfected with shcontrol, shNDR1 or shNDR2. a Wound healing assay of HBEC-3 cells on collagen IV coating were performed 48 h after transfection. Scale bar represents 100 μm. b Invasion capacity of HBEC-3 cells on BioCoat Matrigel Invasion Chamber. Relative invasion normalized to that of the cells transfected with siNeg. Scale bar represents 80 μm. c - d ShNDR1 or shNDR2-infected A549 cells suspension were injected subcutaneously in SCID −/− Beige mice. c Xenograft tumor size [length (L)/width (l)/thickness (e)]. NDR1 and <t>NDR2</t> mRNA levels of the injected cells, representative xenograft and NDR1 or NDR2 expression assayed by immunohistochemistry on xenografts are presented respectively on the left of, on the right of and below the xenografts growth curves. d Quantification of lung and liver microscopic nodules metastases for A549 cells expressing shNDR1, shNDR2 or shcontrol. Excised mice lung and liver as histologic photographs of the lung and liver metastases after injection with shNDR1, shNDR2 or shcontrol are presented below the quantification. Error bars indicate the standard error of the mean (SEM) ( n ≥ 3). * P < 0.05, ** P < 0.01 and *** P < 0.001, using an ANOVA test followed by Dunnett test
    Gst Ndr2, supplied by Carna Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/01-126/NDR2/pmc06461807-54-17-18
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    gst ndr2 - by Bioz Stars, 2026-09
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    Images

    1) Product Images from "NDR2 kinase contributes to cell invasion and cytokinesis defects induced by the inactivation of RASSF1A tumor-suppressor gene in lung cancer cells"

    Article Title: NDR2 kinase contributes to cell invasion and cytokinesis defects induced by the inactivation of RASSF1A tumor-suppressor gene in lung cancer cells

    Journal: Journal of Experimental & Clinical Cancer Research : CR

    doi: 10.1186/s13046-019-1145-8

    NDR depletion abolishes mobility and metastasis properties in HBEC with RASSF1A depletion. HBEC-3 were transfected with non-silencing siRNA (siNeg), siRASSF1A and/or with siNDR1 or siNDR2. Experiences were performed 48 h after transfection. A549 cells were transfected with shcontrol, shNDR1 or shNDR2. a Wound healing assay of HBEC-3 cells on collagen IV coating were performed 48 h after transfection. Scale bar represents 100 μm. b Invasion capacity of HBEC-3 cells on BioCoat Matrigel Invasion Chamber. Relative invasion normalized to that of the cells transfected with siNeg. Scale bar represents 80 μm. c - d ShNDR1 or shNDR2-infected A549 cells suspension were injected subcutaneously in SCID −/− Beige mice. c Xenograft tumor size [length (L)/width (l)/thickness (e)]. NDR1 and NDR2 mRNA levels of the injected cells, representative xenograft and NDR1 or NDR2 expression assayed by immunohistochemistry on xenografts are presented respectively on the left of, on the right of and below the xenografts growth curves. d Quantification of lung and liver microscopic nodules metastases for A549 cells expressing shNDR1, shNDR2 or shcontrol. Excised mice lung and liver as histologic photographs of the lung and liver metastases after injection with shNDR1, shNDR2 or shcontrol are presented below the quantification. Error bars indicate the standard error of the mean (SEM) ( n ≥ 3). * P < 0.05, ** P < 0.01 and *** P < 0.001, using an ANOVA test followed by Dunnett test
    Figure Legend Snippet: NDR depletion abolishes mobility and metastasis properties in HBEC with RASSF1A depletion. HBEC-3 were transfected with non-silencing siRNA (siNeg), siRASSF1A and/or with siNDR1 or siNDR2. Experiences were performed 48 h after transfection. A549 cells were transfected with shcontrol, shNDR1 or shNDR2. a Wound healing assay of HBEC-3 cells on collagen IV coating were performed 48 h after transfection. Scale bar represents 100 μm. b Invasion capacity of HBEC-3 cells on BioCoat Matrigel Invasion Chamber. Relative invasion normalized to that of the cells transfected with siNeg. Scale bar represents 80 μm. c - d ShNDR1 or shNDR2-infected A549 cells suspension were injected subcutaneously in SCID −/− Beige mice. c Xenograft tumor size [length (L)/width (l)/thickness (e)]. NDR1 and NDR2 mRNA levels of the injected cells, representative xenograft and NDR1 or NDR2 expression assayed by immunohistochemistry on xenografts are presented respectively on the left of, on the right of and below the xenografts growth curves. d Quantification of lung and liver microscopic nodules metastases for A549 cells expressing shNDR1, shNDR2 or shcontrol. Excised mice lung and liver as histologic photographs of the lung and liver metastases after injection with shNDR1, shNDR2 or shcontrol are presented below the quantification. Error bars indicate the standard error of the mean (SEM) ( n ≥ 3). * P < 0.05, ** P < 0.01 and *** P < 0.001, using an ANOVA test followed by Dunnett test

    Techniques Used: Transfection, Wound Healing Assay, Infection, Suspension, Injection, Expressing, Immunohistochemistry

    NDR depletion abolishes YAP activation induced by RASSF1A silencing in HBEC cells. a - b HBEC-3 cells were transfected with siNeg, siRASSF1A and/or with siNDR1 or siNDR2. c - d Xenograft obtained after subcutaneous injection of shcontrol, shNDR1 or NDR2 H1299 cells. Nuclear YAP quantification by immunofluorescence ( a ) or by immunohistochemistry ( c ). b , d Quantification of CTGF (Bi, Di) & ANKRD1 (Bii, Dii) mRNA using actin as an internal control in HBEC-3 cells. Error bars indicate the SEM ( n ≥ 3). * P < 0.05, ** P < 0.01 and *** P < 0.001, using an ANOVA test followed by Dunnett’s test
    Figure Legend Snippet: NDR depletion abolishes YAP activation induced by RASSF1A silencing in HBEC cells. a - b HBEC-3 cells were transfected with siNeg, siRASSF1A and/or with siNDR1 or siNDR2. c - d Xenograft obtained after subcutaneous injection of shcontrol, shNDR1 or NDR2 H1299 cells. Nuclear YAP quantification by immunofluorescence ( a ) or by immunohistochemistry ( c ). b , d Quantification of CTGF (Bi, Di) & ANKRD1 (Bii, Dii) mRNA using actin as an internal control in HBEC-3 cells. Error bars indicate the SEM ( n ≥ 3). * P < 0.05, ** P < 0.01 and *** P < 0.001, using an ANOVA test followed by Dunnett’s test

    Techniques Used: Activation Assay, Transfection, Injection, Immunofluorescence, Immunohistochemistry

    NDR2 interacts and phosphorylates GEF-H1 in HBEC. HBEC-3 or H1299 cells were transfected with siNeg and/or siRASSF1A, siNDR1, siNDR2, siGEF-H1, pcDNA3-NDR1, pcDNA3-NDR2 or pcB6-GEF-H1. a GST-RBD pull-down assay in H1299 cells. b Ser885 phosphorylation from GEF-H1 assayed by western blot following λ-phosphatase pre-treatment of the total protein extract or not and normalized with total GEF-H1 expression in HBEC-3 cells. c GST-NDR1 or -NDR2 pull-down assay using siRNA & GEF-H1 plasmid as controls. NDR2 phosphorylation on Ser265-GEFGH1 link with phosphorylation on Ser-885-GEF-H1A was assayed. NDR2 activity on HBEC-3 cells extracts previously transfected with pcB6-GEF-H1 wild type, mutated on Ser265 (S265A), or on Ser885 (S885A) was assayed by quantifying ser885-GEF-H1 phosphorylation status by western blot following normalization by total GEF-H1 expression. Error bars indicate the SEM ( n ≥ 3). * P < 0.05, ** P < 0.01 and *** P < 0.001, using an ANOVA test followed by Dunnett’s test
    Figure Legend Snippet: NDR2 interacts and phosphorylates GEF-H1 in HBEC. HBEC-3 or H1299 cells were transfected with siNeg and/or siRASSF1A, siNDR1, siNDR2, siGEF-H1, pcDNA3-NDR1, pcDNA3-NDR2 or pcB6-GEF-H1. a GST-RBD pull-down assay in H1299 cells. b Ser885 phosphorylation from GEF-H1 assayed by western blot following λ-phosphatase pre-treatment of the total protein extract or not and normalized with total GEF-H1 expression in HBEC-3 cells. c GST-NDR1 or -NDR2 pull-down assay using siRNA & GEF-H1 plasmid as controls. NDR2 phosphorylation on Ser265-GEFGH1 link with phosphorylation on Ser-885-GEF-H1A was assayed. NDR2 activity on HBEC-3 cells extracts previously transfected with pcB6-GEF-H1 wild type, mutated on Ser265 (S265A), or on Ser885 (S885A) was assayed by quantifying ser885-GEF-H1 phosphorylation status by western blot following normalization by total GEF-H1 expression. Error bars indicate the SEM ( n ≥ 3). * P < 0.05, ** P < 0.01 and *** P < 0.001, using an ANOVA test followed by Dunnett’s test

    Techniques Used: Transfection, Pull Down Assay, Western Blot, Expressing, Plasmid Preparation, Activity Assay

    NDR2 and GEF-H1 are co-stained in HBEC-3 cells during both interphase and cell division. HBEC-3 cells were transfected with siNeg or siRASSF1A. a GEF-H1 and NDR2 co-staining assayed by immunofluorescence in HBEC-3 cells during interphase. b Representative images are shown for NDR2 and GEF-H1 during mitosis. Localization was identified by immunofluorescence and confocal microscopy. Costaining was evaluated by ImageJ software. HBEC-3 cells were also stained with DAPI for DNA and PSer885GEF-H1 during mitosis. Error bars indicate the SEM ( n ≥ 3). * P < 0.05, ** P < 0.01 and *** P < 0.001, using an ANOVA test followed by Dunnett’s test
    Figure Legend Snippet: NDR2 and GEF-H1 are co-stained in HBEC-3 cells during both interphase and cell division. HBEC-3 cells were transfected with siNeg or siRASSF1A. a GEF-H1 and NDR2 co-staining assayed by immunofluorescence in HBEC-3 cells during interphase. b Representative images are shown for NDR2 and GEF-H1 during mitosis. Localization was identified by immunofluorescence and confocal microscopy. Costaining was evaluated by ImageJ software. HBEC-3 cells were also stained with DAPI for DNA and PSer885GEF-H1 during mitosis. Error bars indicate the SEM ( n ≥ 3). * P < 0.05, ** P < 0.01 and *** P < 0.001, using an ANOVA test followed by Dunnett’s test

    Techniques Used: Staining, Transfection, Immunofluorescence, Confocal Microscopy, Software

    A proposal model for RASSF1A regulation of the NDR2/GEFH-1/RhoB/YAP axis
    Figure Legend Snippet: A proposal model for RASSF1A regulation of the NDR2/GEFH-1/RhoB/YAP axis

    Techniques Used:

    Related Articles

    Incubation:

    Article Title: NDR2 kinase contributes to cell invasion and cytokinesis defects induced by the inactivation of RASSF1A tumor-suppressor gene in lung cancer cells
    Article Snippet: .. For GTP-pulldown assays, cell lysates were incubated with beads glutathione-S-transferase (GST)-Rhotekin Rho binding domain (RBD), GST-NDR1 or GST-NDR2 (Carna Biosciences, Japan), then precipitates analyzed by Western blotting using anti-RhoB, anti-GEF-H1 or anti-S885phospho-GEF-H1 antibodies. .. Cells were grown on 35-mm coverglass bottom dishes (MatTek).

    Binding Assay:

    Article Title: NDR2 kinase contributes to cell invasion and cytokinesis defects induced by the inactivation of RASSF1A tumor-suppressor gene in lung cancer cells
    Article Snippet: .. For GTP-pulldown assays, cell lysates were incubated with beads glutathione-S-transferase (GST)-Rhotekin Rho binding domain (RBD), GST-NDR1 or GST-NDR2 (Carna Biosciences, Japan), then precipitates analyzed by Western blotting using anti-RhoB, anti-GEF-H1 or anti-S885phospho-GEF-H1 antibodies. .. Cells were grown on 35-mm coverglass bottom dishes (MatTek).

    Western Blot:

    Article Title: NDR2 kinase contributes to cell invasion and cytokinesis defects induced by the inactivation of RASSF1A tumor-suppressor gene in lung cancer cells
    Article Snippet: .. For GTP-pulldown assays, cell lysates were incubated with beads glutathione-S-transferase (GST)-Rhotekin Rho binding domain (RBD), GST-NDR1 or GST-NDR2 (Carna Biosciences, Japan), then precipitates analyzed by Western blotting using anti-RhoB, anti-GEF-H1 or anti-S885phospho-GEF-H1 antibodies. .. Cells were grown on 35-mm coverglass bottom dishes (MatTek).



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    Image Search Results


    Frequency of WT1 126 -specific CTLs in CD8 + T cells. a WT1 126 -specific CTLs were defined by flow cytometry as CD3 + , CD8 + , WT1 126 tetramer + , and lineage markers (CD4, CD14, CD16, CD19, and CD56)-negative cells. b Frequencies of WT1 126 -specific CTLs in CD8 + T cells. Bars indicate the median values of the frequencies. No significant difference was found in the frequencies. WT1; Wilms’ tumor protein 1; CTLs, cytotoxic T-lymphocytes; PTs, patients with WT1-expressing tumor; HVs, healthy volunteers; ns, not significant

    Journal: Cancer Immunology, Immunotherapy : CII

    Article Title: Spontaneous high clonal expansion of Wilms’ tumor gene 1-specific cytotoxic T-lymphocytes in patients with Wilms’ tumor gene 1-expressing solid tumor

    doi: 10.1007/s00262-024-03862-8

    Figure Lengend Snippet: Frequency of WT1 126 -specific CTLs in CD8 + T cells. a WT1 126 -specific CTLs were defined by flow cytometry as CD3 + , CD8 + , WT1 126 tetramer + , and lineage markers (CD4, CD14, CD16, CD19, and CD56)-negative cells. b Frequencies of WT1 126 -specific CTLs in CD8 + T cells. Bars indicate the median values of the frequencies. No significant difference was found in the frequencies. WT1; Wilms’ tumor protein 1; CTLs, cytotoxic T-lymphocytes; PTs, patients with WT1-expressing tumor; HVs, healthy volunteers; ns, not significant

    Article Snippet: The PE-labeled HLA-A*02:01 WT1 126-134 (RMFPNAPYL) tetramer (WT1 126 tetramer) was purchased from MBL Co., Ltd. (Nagoya, Japan).

    Techniques: Flow Cytometry, Wilms Tumor Assay, Expressing

    Phenotypes of WT1 126 -specific CTLs Phenotypes of WT1 126 -specific CTLs in seven PTs ( a ) and five HVs ( b ). WT1 126 -specific CTLs were classified into four distinct subtypes based on the four differentiation stages according to the cell surface expression of CD45RA and CCR7 as follows: (i) naïve cells, CD45RA + CCR7 + ; (ii) central memory, CD45RA − CCR7 + ; (iii) effector memory, CD45RA − CCR7 − ; and (iv) effector, CD45RA + CCR7 − . c Subtype frequency in WT1 126 -specific CTLs. Box plots represent median ± 25th percentile, with whiskers representing min/max values. Red boxplots: PTs; blue boxplots: HVs. P -values were obtained using a two-way ANOVA followed by Sidak’s multiple comparison test. d The exhaustion state of WT1 126 -specific CTLs in PT4, HV1, and HV3. * P < 0.05, *** P < 0.001. ns, not significant. WT1, Wilms’ tumor protein 1; CTLs, cytotoxic T-lymphocytes; PTs, patients with WT1-expressing tumor; HVs, healthy volunteers; N/A, not assessable (less than 10 cells)

    Journal: Cancer Immunology, Immunotherapy : CII

    Article Title: Spontaneous high clonal expansion of Wilms’ tumor gene 1-specific cytotoxic T-lymphocytes in patients with Wilms’ tumor gene 1-expressing solid tumor

    doi: 10.1007/s00262-024-03862-8

    Figure Lengend Snippet: Phenotypes of WT1 126 -specific CTLs Phenotypes of WT1 126 -specific CTLs in seven PTs ( a ) and five HVs ( b ). WT1 126 -specific CTLs were classified into four distinct subtypes based on the four differentiation stages according to the cell surface expression of CD45RA and CCR7 as follows: (i) naïve cells, CD45RA + CCR7 + ; (ii) central memory, CD45RA − CCR7 + ; (iii) effector memory, CD45RA − CCR7 − ; and (iv) effector, CD45RA + CCR7 − . c Subtype frequency in WT1 126 -specific CTLs. Box plots represent median ± 25th percentile, with whiskers representing min/max values. Red boxplots: PTs; blue boxplots: HVs. P -values were obtained using a two-way ANOVA followed by Sidak’s multiple comparison test. d The exhaustion state of WT1 126 -specific CTLs in PT4, HV1, and HV3. * P < 0.05, *** P < 0.001. ns, not significant. WT1, Wilms’ tumor protein 1; CTLs, cytotoxic T-lymphocytes; PTs, patients with WT1-expressing tumor; HVs, healthy volunteers; N/A, not assessable (less than 10 cells)

    Article Snippet: The PE-labeled HLA-A*02:01 WT1 126-134 (RMFPNAPYL) tetramer (WT1 126 tetramer) was purchased from MBL Co., Ltd. (Nagoya, Japan).

    Techniques: Expressing, Comparison, Wilms Tumor Assay

    Characteristics of the patients and healthy volunteers

    Journal: Cancer Immunology, Immunotherapy : CII

    Article Title: Spontaneous high clonal expansion of Wilms’ tumor gene 1-specific cytotoxic T-lymphocytes in patients with Wilms’ tumor gene 1-expressing solid tumor

    doi: 10.1007/s00262-024-03862-8

    Figure Lengend Snippet: Characteristics of the patients and healthy volunteers

    Article Snippet: The PE-labeled HLA-A*02:01 WT1 126-134 (RMFPNAPYL) tetramer (WT1 126 tetramer) was purchased from MBL Co., Ltd. (Nagoya, Japan).

    Techniques:

    T-cell repertoire clonality of WT1 126 -specific CTLs (a) Schema of the concept of TCR repertoire clonality. In cases where only one WT1-CTL clone occupies the whole, the clonality is calculated to be infinitely close to 1.000 (0.9999) but not 1.0. A clonality of 0.000 indicates no clonal expansion. Clonality 0.500 includes various types of clonal expansion. The clonalities of WT1 126 -specific CTLs are shown in PTs (b) and HVs (c). Individual clones are shown in different colors. Sequences with clonally expanded clones in each donor are shown in the same color except light gray. Light gray indicates CTLs with unique amino acid residues, that is, unexpanded CTL clones. (d) Graphical representation of the clonality of WT1 126 -specific CTLs in PTs (n = 7) and HVs (n = 5). Bars indicate the median value of the clonality. Differences in clonality between PTs and HVs were significant (* P < 0.05). P -values were obtained using the Mann–Whitney U test. WT1; Wilms’ tumor protein 1; CTLs, cytotoxic T-lymphocytes. PTs, patients with WT1-expressing tumor; HVs, healthy volunteers; TCR, T-cell receptors

    Journal: Cancer Immunology, Immunotherapy : CII

    Article Title: Spontaneous high clonal expansion of Wilms’ tumor gene 1-specific cytotoxic T-lymphocytes in patients with Wilms’ tumor gene 1-expressing solid tumor

    doi: 10.1007/s00262-024-03862-8

    Figure Lengend Snippet: T-cell repertoire clonality of WT1 126 -specific CTLs (a) Schema of the concept of TCR repertoire clonality. In cases where only one WT1-CTL clone occupies the whole, the clonality is calculated to be infinitely close to 1.000 (0.9999) but not 1.0. A clonality of 0.000 indicates no clonal expansion. Clonality 0.500 includes various types of clonal expansion. The clonalities of WT1 126 -specific CTLs are shown in PTs (b) and HVs (c). Individual clones are shown in different colors. Sequences with clonally expanded clones in each donor are shown in the same color except light gray. Light gray indicates CTLs with unique amino acid residues, that is, unexpanded CTL clones. (d) Graphical representation of the clonality of WT1 126 -specific CTLs in PTs (n = 7) and HVs (n = 5). Bars indicate the median value of the clonality. Differences in clonality between PTs and HVs were significant (* P < 0.05). P -values were obtained using the Mann–Whitney U test. WT1; Wilms’ tumor protein 1; CTLs, cytotoxic T-lymphocytes. PTs, patients with WT1-expressing tumor; HVs, healthy volunteers; TCR, T-cell receptors

    Article Snippet: The PE-labeled HLA-A*02:01 WT1 126-134 (RMFPNAPYL) tetramer (WT1 126 tetramer) was purchased from MBL Co., Ltd. (Nagoya, Japan).

    Techniques: Clone Assay, MANN-WHITNEY, Wilms Tumor Assay, Expressing

    Correlation between the subtype of WT1 126 -specific CTLs and clonality Correlation between the subtype of WT1 126 -specific CTLs and clonality is shown for PTs (n = 7) ( a ) and HVs (n = 5) ( b ). Small numbers represent patient numbers. Red circles represent the top three PTs in terms of clonality, and blue circles represent the remaining PTs. R 2 denotes Pearson’s correlation. P values were obtained using two-sided t tests. WT1; Wilms’ tumor protein 1; CTLs, cytotoxic T-lymphocytes. PTs, patients with WT1-expressing tumor; HVs, healthy volunteers; N, naïve (CD45RA + CCR7 + ); CM, central memory (CD45RA − CCR7 + ); EM, effector memory (CD45RA − CCR7 − ); E, effector (CD45RA + CCR7. − )

    Journal: Cancer Immunology, Immunotherapy : CII

    Article Title: Spontaneous high clonal expansion of Wilms’ tumor gene 1-specific cytotoxic T-lymphocytes in patients with Wilms’ tumor gene 1-expressing solid tumor

    doi: 10.1007/s00262-024-03862-8

    Figure Lengend Snippet: Correlation between the subtype of WT1 126 -specific CTLs and clonality Correlation between the subtype of WT1 126 -specific CTLs and clonality is shown for PTs (n = 7) ( a ) and HVs (n = 5) ( b ). Small numbers represent patient numbers. Red circles represent the top three PTs in terms of clonality, and blue circles represent the remaining PTs. R 2 denotes Pearson’s correlation. P values were obtained using two-sided t tests. WT1; Wilms’ tumor protein 1; CTLs, cytotoxic T-lymphocytes. PTs, patients with WT1-expressing tumor; HVs, healthy volunteers; N, naïve (CD45RA + CCR7 + ); CM, central memory (CD45RA − CCR7 + ); EM, effector memory (CD45RA − CCR7 − ); E, effector (CD45RA + CCR7. − )

    Article Snippet: The PE-labeled HLA-A*02:01 WT1 126-134 (RMFPNAPYL) tetramer (WT1 126 tetramer) was purchased from MBL Co., Ltd. (Nagoya, Japan).

    Techniques: Wilms Tumor Assay, Expressing