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antibody against mst1r  (Santa Cruz Biotechnology)


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    Structured Review

    Santa Cruz Biotechnology antibody against mst1r
    Homozygous mutation in <t>MST1R</t> identified in a TOF family. ( a ) Pedigree of the family with two TOF probands carrying a homozygous missense mutation (c.2009T > G) in the MST1R gene. ( b ) Sanger sequencing results confirming a recessive homozygous missense mutation in the two probands; their patients were heterozygous carriers. ( c ) Evolutionary conservation of V670 in the MST1R protein in several species. ( d ) Prediction of the 3D structures of the MST1R protein using AlphaFold. The location of the V670G variant is indicated (black circle, green segment). The hydrophobic interaction between V670 (green) and M662 (magenta, bold text) residue is indicated (black rectangle)
    Antibody Against Mst1r, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 24 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ron%CE%B2/Ron+%CE%B2+Antibody/pmc11889330-66-9-17
    Average 93 stars, based on 24 article reviews
    antibody against mst1r - by Bioz Stars, 2026-08
    93/100 stars

    Images

    1) Product Images from "MST1R Gene Variants Predispose Individuals to Tetralogy of Fallot"

    Article Title: MST1R Gene Variants Predispose Individuals to Tetralogy of Fallot

    Journal: Phenomics

    doi: 10.1007/s43657-024-00175-9

    Homozygous mutation in MST1R identified in a TOF family. ( a ) Pedigree of the family with two TOF probands carrying a homozygous missense mutation (c.2009T > G) in the MST1R gene. ( b ) Sanger sequencing results confirming a recessive homozygous missense mutation in the two probands; their patients were heterozygous carriers. ( c ) Evolutionary conservation of V670 in the MST1R protein in several species. ( d ) Prediction of the 3D structures of the MST1R protein using AlphaFold. The location of the V670G variant is indicated (black circle, green segment). The hydrophobic interaction between V670 (green) and M662 (magenta, bold text) residue is indicated (black rectangle)
    Figure Legend Snippet: Homozygous mutation in MST1R identified in a TOF family. ( a ) Pedigree of the family with two TOF probands carrying a homozygous missense mutation (c.2009T > G) in the MST1R gene. ( b ) Sanger sequencing results confirming a recessive homozygous missense mutation in the two probands; their patients were heterozygous carriers. ( c ) Evolutionary conservation of V670 in the MST1R protein in several species. ( d ) Prediction of the 3D structures of the MST1R protein using AlphaFold. The location of the V670G variant is indicated (black circle, green segment). The hydrophobic interaction between V670 (green) and M662 (magenta, bold text) residue is indicated (black rectangle)

    Techniques Used: Mutagenesis, Sequencing, Variant Assay, Residue

    Decreased MST1R expression in cardiac tissues from TOF patients. Representative immunohistochemical staining images of MST1R in cardiac tissues from TOF patients and healthy controls. White arrow indicating MST1R in the Control, red arrow indicating MST1R in the TOF; Scale bars, 50 μm
    Figure Legend Snippet: Decreased MST1R expression in cardiac tissues from TOF patients. Representative immunohistochemical staining images of MST1R in cardiac tissues from TOF patients and healthy controls. White arrow indicating MST1R in the Control, red arrow indicating MST1R in the TOF; Scale bars, 50 μm

    Techniques Used: Expressing, Immunohistochemical staining, Staining, Control

    Comparison of rare variants in sporadic TOF patients and healthy controls
    Figure Legend Snippet: Comparison of rare variants in sporadic TOF patients and healthy controls

    Techniques Used: Comparison

    Genetic findings in TOF patients with  MST1R  variants
    Figure Legend Snippet: Genetic findings in TOF patients with MST1R variants

    Techniques Used: Variant Assay, Sequencing

    Clinical features of TOF patients with  MST1R  variants
    Figure Legend Snippet: Clinical features of TOF patients with MST1R variants

    Techniques Used:

    Generation and characterization of MST1R -deficient hiPSCs. ( a ) Schematic illustrating the generation of MST1R hiPSCs using gRNAs for exon 6 targeting. ( b ) Western blot analysis of WT and MST1R -deficient clones. ( c ) Representative immunofluorescence images of pluripotency markers OCT4 (red) and SSEA4 (green) in WT and M7 clones with DAPI (blue) staining. Scale Bars, 200 μm. ( d ) Alkaline phosphatase staining of WT and M7 clones. Scale bars, 200 mm
    Figure Legend Snippet: Generation and characterization of MST1R -deficient hiPSCs. ( a ) Schematic illustrating the generation of MST1R hiPSCs using gRNAs for exon 6 targeting. ( b ) Western blot analysis of WT and MST1R -deficient clones. ( c ) Representative immunofluorescence images of pluripotency markers OCT4 (red) and SSEA4 (green) in WT and M7 clones with DAPI (blue) staining. Scale Bars, 200 μm. ( d ) Alkaline phosphatase staining of WT and M7 clones. Scale bars, 200 mm

    Techniques Used: Western Blot, Clone Assay, Immunofluorescence, Staining

    Phenotypic characterization of the MST1R -deficient CMs. ( a ) A schematic of the protocol for converting hiPSCs into CMs by modulating Wnt signaling activity. ( b ) Representative immunofluorescence images of WT-CMs and M7-CMs stained with ACTN2 (green), TNNT2 (red) and DAPI (blue). Scale Bars, 15 μm. ( c ) Quantification of irregularly organized sarcomeres in WT ( n = 25) and MST1R KO ( n = 27) day 15 differentiated cardiomyocytes. n = 25 (WT) and n = 27 ( MST1R KO) biological independent samples. *** p < 0.001 by Fisher’s exact. ( d ) Transmission electron microscopy of day 15 differentiated cardiomyocytes. Scale Bars, 500 nm. ( e ) Expression level of cardiomyocytes structural genes ( ACTN2 , MYH7 and MYL7 ) and contraction regulatory gene ( TNNT2 ). n = 3, ** p < 0.01, *** p < 0.001, **** p < 0.0001 by Student's t test
    Figure Legend Snippet: Phenotypic characterization of the MST1R -deficient CMs. ( a ) A schematic of the protocol for converting hiPSCs into CMs by modulating Wnt signaling activity. ( b ) Representative immunofluorescence images of WT-CMs and M7-CMs stained with ACTN2 (green), TNNT2 (red) and DAPI (blue). Scale Bars, 15 μm. ( c ) Quantification of irregularly organized sarcomeres in WT ( n = 25) and MST1R KO ( n = 27) day 15 differentiated cardiomyocytes. n = 25 (WT) and n = 27 ( MST1R KO) biological independent samples. *** p < 0.001 by Fisher’s exact. ( d ) Transmission electron microscopy of day 15 differentiated cardiomyocytes. Scale Bars, 500 nm. ( e ) Expression level of cardiomyocytes structural genes ( ACTN2 , MYH7 and MYL7 ) and contraction regulatory gene ( TNNT2 ). n = 3, ** p < 0.01, *** p < 0.001, **** p < 0.0001 by Student's t test

    Techniques Used: Activity Assay, Immunofluorescence, Staining, Transmission Assay, Electron Microscopy, Expressing



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    Homozygous mutation in <t>MST1R</t> identified in a TOF family. ( a ) Pedigree of the family with two TOF probands carrying a homozygous missense mutation (c.2009T > G) in the MST1R gene. ( b ) Sanger sequencing results confirming a recessive homozygous missense mutation in the two probands; their patients were heterozygous carriers. ( c ) Evolutionary conservation of V670 in the MST1R protein in several species. ( d ) Prediction of the 3D structures of the MST1R protein using AlphaFold. The location of the V670G variant is indicated (black circle, green segment). The hydrophobic interaction between V670 (green) and M662 (magenta, bold text) residue is indicated (black rectangle)
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    Image Search Results


    Homozygous mutation in MST1R identified in a TOF family. ( a ) Pedigree of the family with two TOF probands carrying a homozygous missense mutation (c.2009T > G) in the MST1R gene. ( b ) Sanger sequencing results confirming a recessive homozygous missense mutation in the two probands; their patients were heterozygous carriers. ( c ) Evolutionary conservation of V670 in the MST1R protein in several species. ( d ) Prediction of the 3D structures of the MST1R protein using AlphaFold. The location of the V670G variant is indicated (black circle, green segment). The hydrophobic interaction between V670 (green) and M662 (magenta, bold text) residue is indicated (black rectangle)

    Journal: Phenomics

    Article Title: MST1R Gene Variants Predispose Individuals to Tetralogy of Fallot

    doi: 10.1007/s43657-024-00175-9

    Figure Lengend Snippet: Homozygous mutation in MST1R identified in a TOF family. ( a ) Pedigree of the family with two TOF probands carrying a homozygous missense mutation (c.2009T > G) in the MST1R gene. ( b ) Sanger sequencing results confirming a recessive homozygous missense mutation in the two probands; their patients were heterozygous carriers. ( c ) Evolutionary conservation of V670 in the MST1R protein in several species. ( d ) Prediction of the 3D structures of the MST1R protein using AlphaFold. The location of the V670G variant is indicated (black circle, green segment). The hydrophobic interaction between V670 (green) and M662 (magenta, bold text) residue is indicated (black rectangle)

    Article Snippet: Briefly, the tissue sections were incubated with a primary antibody against MST1R at a dilution of 1:100 (Santa Cruz, sc-374,626) at room temperature for 30 min.

    Techniques: Mutagenesis, Sequencing, Variant Assay, Residue

    Decreased MST1R expression in cardiac tissues from TOF patients. Representative immunohistochemical staining images of MST1R in cardiac tissues from TOF patients and healthy controls. White arrow indicating MST1R in the Control, red arrow indicating MST1R in the TOF; Scale bars, 50 μm

    Journal: Phenomics

    Article Title: MST1R Gene Variants Predispose Individuals to Tetralogy of Fallot

    doi: 10.1007/s43657-024-00175-9

    Figure Lengend Snippet: Decreased MST1R expression in cardiac tissues from TOF patients. Representative immunohistochemical staining images of MST1R in cardiac tissues from TOF patients and healthy controls. White arrow indicating MST1R in the Control, red arrow indicating MST1R in the TOF; Scale bars, 50 μm

    Article Snippet: Briefly, the tissue sections were incubated with a primary antibody against MST1R at a dilution of 1:100 (Santa Cruz, sc-374,626) at room temperature for 30 min.

    Techniques: Expressing, Immunohistochemical staining, Staining, Control

    Comparison of rare variants in sporadic TOF patients and healthy controls

    Journal: Phenomics

    Article Title: MST1R Gene Variants Predispose Individuals to Tetralogy of Fallot

    doi: 10.1007/s43657-024-00175-9

    Figure Lengend Snippet: Comparison of rare variants in sporadic TOF patients and healthy controls

    Article Snippet: Briefly, the tissue sections were incubated with a primary antibody against MST1R at a dilution of 1:100 (Santa Cruz, sc-374,626) at room temperature for 30 min.

    Techniques: Comparison

    Genetic findings in TOF patients with  MST1R  variants

    Journal: Phenomics

    Article Title: MST1R Gene Variants Predispose Individuals to Tetralogy of Fallot

    doi: 10.1007/s43657-024-00175-9

    Figure Lengend Snippet: Genetic findings in TOF patients with MST1R variants

    Article Snippet: Briefly, the tissue sections were incubated with a primary antibody against MST1R at a dilution of 1:100 (Santa Cruz, sc-374,626) at room temperature for 30 min.

    Techniques: Variant Assay, Sequencing

    Clinical features of TOF patients with  MST1R  variants

    Journal: Phenomics

    Article Title: MST1R Gene Variants Predispose Individuals to Tetralogy of Fallot

    doi: 10.1007/s43657-024-00175-9

    Figure Lengend Snippet: Clinical features of TOF patients with MST1R variants

    Article Snippet: Briefly, the tissue sections were incubated with a primary antibody against MST1R at a dilution of 1:100 (Santa Cruz, sc-374,626) at room temperature for 30 min.

    Techniques:

    Generation and characterization of MST1R -deficient hiPSCs. ( a ) Schematic illustrating the generation of MST1R hiPSCs using gRNAs for exon 6 targeting. ( b ) Western blot analysis of WT and MST1R -deficient clones. ( c ) Representative immunofluorescence images of pluripotency markers OCT4 (red) and SSEA4 (green) in WT and M7 clones with DAPI (blue) staining. Scale Bars, 200 μm. ( d ) Alkaline phosphatase staining of WT and M7 clones. Scale bars, 200 mm

    Journal: Phenomics

    Article Title: MST1R Gene Variants Predispose Individuals to Tetralogy of Fallot

    doi: 10.1007/s43657-024-00175-9

    Figure Lengend Snippet: Generation and characterization of MST1R -deficient hiPSCs. ( a ) Schematic illustrating the generation of MST1R hiPSCs using gRNAs for exon 6 targeting. ( b ) Western blot analysis of WT and MST1R -deficient clones. ( c ) Representative immunofluorescence images of pluripotency markers OCT4 (red) and SSEA4 (green) in WT and M7 clones with DAPI (blue) staining. Scale Bars, 200 μm. ( d ) Alkaline phosphatase staining of WT and M7 clones. Scale bars, 200 mm

    Article Snippet: Briefly, the tissue sections were incubated with a primary antibody against MST1R at a dilution of 1:100 (Santa Cruz, sc-374,626) at room temperature for 30 min.

    Techniques: Western Blot, Clone Assay, Immunofluorescence, Staining

    Phenotypic characterization of the MST1R -deficient CMs. ( a ) A schematic of the protocol for converting hiPSCs into CMs by modulating Wnt signaling activity. ( b ) Representative immunofluorescence images of WT-CMs and M7-CMs stained with ACTN2 (green), TNNT2 (red) and DAPI (blue). Scale Bars, 15 μm. ( c ) Quantification of irregularly organized sarcomeres in WT ( n = 25) and MST1R KO ( n = 27) day 15 differentiated cardiomyocytes. n = 25 (WT) and n = 27 ( MST1R KO) biological independent samples. *** p < 0.001 by Fisher’s exact. ( d ) Transmission electron microscopy of day 15 differentiated cardiomyocytes. Scale Bars, 500 nm. ( e ) Expression level of cardiomyocytes structural genes ( ACTN2 , MYH7 and MYL7 ) and contraction regulatory gene ( TNNT2 ). n = 3, ** p < 0.01, *** p < 0.001, **** p < 0.0001 by Student's t test

    Journal: Phenomics

    Article Title: MST1R Gene Variants Predispose Individuals to Tetralogy of Fallot

    doi: 10.1007/s43657-024-00175-9

    Figure Lengend Snippet: Phenotypic characterization of the MST1R -deficient CMs. ( a ) A schematic of the protocol for converting hiPSCs into CMs by modulating Wnt signaling activity. ( b ) Representative immunofluorescence images of WT-CMs and M7-CMs stained with ACTN2 (green), TNNT2 (red) and DAPI (blue). Scale Bars, 15 μm. ( c ) Quantification of irregularly organized sarcomeres in WT ( n = 25) and MST1R KO ( n = 27) day 15 differentiated cardiomyocytes. n = 25 (WT) and n = 27 ( MST1R KO) biological independent samples. *** p < 0.001 by Fisher’s exact. ( d ) Transmission electron microscopy of day 15 differentiated cardiomyocytes. Scale Bars, 500 nm. ( e ) Expression level of cardiomyocytes structural genes ( ACTN2 , MYH7 and MYL7 ) and contraction regulatory gene ( TNNT2 ). n = 3, ** p < 0.01, *** p < 0.001, **** p < 0.0001 by Student's t test

    Article Snippet: Briefly, the tissue sections were incubated with a primary antibody against MST1R at a dilution of 1:100 (Santa Cruz, sc-374,626) at room temperature for 30 min.

    Techniques: Activity Assay, Immunofluorescence, Staining, Transmission Assay, Electron Microscopy, Expressing

    Homozygous mutation in MST1R identified in a TOF family. ( a ) Pedigree of the family with two TOF probands carrying a homozygous missense mutation (c.2009T > G) in the MST1R gene. ( b ) Sanger sequencing results confirming a recessive homozygous missense mutation in the two probands; their patients were heterozygous carriers. ( c ) Evolutionary conservation of V670 in the MST1R protein in several species. ( d ) Prediction of the 3D structures of the MST1R protein using AlphaFold. The location of the V670G variant is indicated (black circle, green segment). The hydrophobic interaction between V670 (green) and M662 (magenta, bold text) residue is indicated (black rectangle)

    Journal: Phenomics

    Article Title: MST1R Gene Variants Predispose Individuals to Tetralogy of Fallot

    doi: 10.1007/s43657-024-00175-9

    Figure Lengend Snippet: Homozygous mutation in MST1R identified in a TOF family. ( a ) Pedigree of the family with two TOF probands carrying a homozygous missense mutation (c.2009T > G) in the MST1R gene. ( b ) Sanger sequencing results confirming a recessive homozygous missense mutation in the two probands; their patients were heterozygous carriers. ( c ) Evolutionary conservation of V670 in the MST1R protein in several species. ( d ) Prediction of the 3D structures of the MST1R protein using AlphaFold. The location of the V670G variant is indicated (black circle, green segment). The hydrophobic interaction between V670 (green) and M662 (magenta, bold text) residue is indicated (black rectangle)

    Article Snippet: The membranes were blocked with 5% non-fat milk in TBST (Beyotime, ST673) at room temperature for 1 h and then incubated overnight at 4 °C with primary antibodies against MST1R (Santa Cruz, sc-374,626) at 1:500 and Glyceraldehyde-3-Phosphate Dehydrogenase (GAPDH) (Proteintech, 10494-1-AP) at 1:10000.

    Techniques: Mutagenesis, Sequencing, Variant Assay, Residue

    Decreased MST1R expression in cardiac tissues from TOF patients. Representative immunohistochemical staining images of MST1R in cardiac tissues from TOF patients and healthy controls. White arrow indicating MST1R in the Control, red arrow indicating MST1R in the TOF; Scale bars, 50 μm

    Journal: Phenomics

    Article Title: MST1R Gene Variants Predispose Individuals to Tetralogy of Fallot

    doi: 10.1007/s43657-024-00175-9

    Figure Lengend Snippet: Decreased MST1R expression in cardiac tissues from TOF patients. Representative immunohistochemical staining images of MST1R in cardiac tissues from TOF patients and healthy controls. White arrow indicating MST1R in the Control, red arrow indicating MST1R in the TOF; Scale bars, 50 μm

    Article Snippet: The membranes were blocked with 5% non-fat milk in TBST (Beyotime, ST673) at room temperature for 1 h and then incubated overnight at 4 °C with primary antibodies against MST1R (Santa Cruz, sc-374,626) at 1:500 and Glyceraldehyde-3-Phosphate Dehydrogenase (GAPDH) (Proteintech, 10494-1-AP) at 1:10000.

    Techniques: Expressing, Immunohistochemical staining, Staining, Control

    Comparison of rare variants in sporadic TOF patients and healthy controls

    Journal: Phenomics

    Article Title: MST1R Gene Variants Predispose Individuals to Tetralogy of Fallot

    doi: 10.1007/s43657-024-00175-9

    Figure Lengend Snippet: Comparison of rare variants in sporadic TOF patients and healthy controls

    Article Snippet: The membranes were blocked with 5% non-fat milk in TBST (Beyotime, ST673) at room temperature for 1 h and then incubated overnight at 4 °C with primary antibodies against MST1R (Santa Cruz, sc-374,626) at 1:500 and Glyceraldehyde-3-Phosphate Dehydrogenase (GAPDH) (Proteintech, 10494-1-AP) at 1:10000.

    Techniques: Comparison

    Genetic findings in TOF patients with  MST1R  variants

    Journal: Phenomics

    Article Title: MST1R Gene Variants Predispose Individuals to Tetralogy of Fallot

    doi: 10.1007/s43657-024-00175-9

    Figure Lengend Snippet: Genetic findings in TOF patients with MST1R variants

    Article Snippet: The membranes were blocked with 5% non-fat milk in TBST (Beyotime, ST673) at room temperature for 1 h and then incubated overnight at 4 °C with primary antibodies against MST1R (Santa Cruz, sc-374,626) at 1:500 and Glyceraldehyde-3-Phosphate Dehydrogenase (GAPDH) (Proteintech, 10494-1-AP) at 1:10000.

    Techniques: Variant Assay, Sequencing

    Clinical features of TOF patients with  MST1R  variants

    Journal: Phenomics

    Article Title: MST1R Gene Variants Predispose Individuals to Tetralogy of Fallot

    doi: 10.1007/s43657-024-00175-9

    Figure Lengend Snippet: Clinical features of TOF patients with MST1R variants

    Article Snippet: The membranes were blocked with 5% non-fat milk in TBST (Beyotime, ST673) at room temperature for 1 h and then incubated overnight at 4 °C with primary antibodies against MST1R (Santa Cruz, sc-374,626) at 1:500 and Glyceraldehyde-3-Phosphate Dehydrogenase (GAPDH) (Proteintech, 10494-1-AP) at 1:10000.

    Techniques:

    Generation and characterization of MST1R -deficient hiPSCs. ( a ) Schematic illustrating the generation of MST1R hiPSCs using gRNAs for exon 6 targeting. ( b ) Western blot analysis of WT and MST1R -deficient clones. ( c ) Representative immunofluorescence images of pluripotency markers OCT4 (red) and SSEA4 (green) in WT and M7 clones with DAPI (blue) staining. Scale Bars, 200 μm. ( d ) Alkaline phosphatase staining of WT and M7 clones. Scale bars, 200 mm

    Journal: Phenomics

    Article Title: MST1R Gene Variants Predispose Individuals to Tetralogy of Fallot

    doi: 10.1007/s43657-024-00175-9

    Figure Lengend Snippet: Generation and characterization of MST1R -deficient hiPSCs. ( a ) Schematic illustrating the generation of MST1R hiPSCs using gRNAs for exon 6 targeting. ( b ) Western blot analysis of WT and MST1R -deficient clones. ( c ) Representative immunofluorescence images of pluripotency markers OCT4 (red) and SSEA4 (green) in WT and M7 clones with DAPI (blue) staining. Scale Bars, 200 μm. ( d ) Alkaline phosphatase staining of WT and M7 clones. Scale bars, 200 mm

    Article Snippet: The membranes were blocked with 5% non-fat milk in TBST (Beyotime, ST673) at room temperature for 1 h and then incubated overnight at 4 °C with primary antibodies against MST1R (Santa Cruz, sc-374,626) at 1:500 and Glyceraldehyde-3-Phosphate Dehydrogenase (GAPDH) (Proteintech, 10494-1-AP) at 1:10000.

    Techniques: Western Blot, Clone Assay, Immunofluorescence, Staining

    Phenotypic characterization of the MST1R -deficient CMs. ( a ) A schematic of the protocol for converting hiPSCs into CMs by modulating Wnt signaling activity. ( b ) Representative immunofluorescence images of WT-CMs and M7-CMs stained with ACTN2 (green), TNNT2 (red) and DAPI (blue). Scale Bars, 15 μm. ( c ) Quantification of irregularly organized sarcomeres in WT ( n = 25) and MST1R KO ( n = 27) day 15 differentiated cardiomyocytes. n = 25 (WT) and n = 27 ( MST1R KO) biological independent samples. *** p < 0.001 by Fisher’s exact. ( d ) Transmission electron microscopy of day 15 differentiated cardiomyocytes. Scale Bars, 500 nm. ( e ) Expression level of cardiomyocytes structural genes ( ACTN2 , MYH7 and MYL7 ) and contraction regulatory gene ( TNNT2 ). n = 3, ** p < 0.01, *** p < 0.001, **** p < 0.0001 by Student's t test

    Journal: Phenomics

    Article Title: MST1R Gene Variants Predispose Individuals to Tetralogy of Fallot

    doi: 10.1007/s43657-024-00175-9

    Figure Lengend Snippet: Phenotypic characterization of the MST1R -deficient CMs. ( a ) A schematic of the protocol for converting hiPSCs into CMs by modulating Wnt signaling activity. ( b ) Representative immunofluorescence images of WT-CMs and M7-CMs stained with ACTN2 (green), TNNT2 (red) and DAPI (blue). Scale Bars, 15 μm. ( c ) Quantification of irregularly organized sarcomeres in WT ( n = 25) and MST1R KO ( n = 27) day 15 differentiated cardiomyocytes. n = 25 (WT) and n = 27 ( MST1R KO) biological independent samples. *** p < 0.001 by Fisher’s exact. ( d ) Transmission electron microscopy of day 15 differentiated cardiomyocytes. Scale Bars, 500 nm. ( e ) Expression level of cardiomyocytes structural genes ( ACTN2 , MYH7 and MYL7 ) and contraction regulatory gene ( TNNT2 ). n = 3, ** p < 0.01, *** p < 0.001, **** p < 0.0001 by Student's t test

    Article Snippet: The membranes were blocked with 5% non-fat milk in TBST (Beyotime, ST673) at room temperature for 1 h and then incubated overnight at 4 °C with primary antibodies against MST1R (Santa Cruz, sc-374,626) at 1:500 and Glyceraldehyde-3-Phosphate Dehydrogenase (GAPDH) (Proteintech, 10494-1-AP) at 1:10000.

    Techniques: Activity Assay, Immunofluorescence, Staining, Transmission Assay, Electron Microscopy, Expressing

    Journal: eLife

    Article Title: EGFR transactivates RON to drive oncogenic crosstalk

    doi: 10.7554/eLife.63678

    Figure Lengend Snippet:

    Article Snippet: antibody , Anti- RONβ (Mouse monoclonal) , Santa Cruz Biotechnology , Cat# sc-74588 RRID: AB_2235711 , Clone E-3 WB (1:500) Used with the PY1238/39 RON antibody (R&D Systems Cat# AF1947).

    Techniques: Stable Transfection, Transfection, Plasmid Preparation, Construct, Generated, Cytometry, Kinase Assay, Recombinant, Sequencing, Ligation, Mutagenesis, Bicinchoninic Acid Protein Assay, Expressing, Software, Magnetic Beads

    Journal: eLife

    Article Title: EGFR transactivates RON to drive oncogenic crosstalk

    doi: 10.7554/eLife.63678

    Figure Lengend Snippet:

    Article Snippet: antibody , Anti-RONβ (Rabbit polyclonal) , Santa Cruz Biotechnology , Cat# sc-322 RRID: AB_677390 , Clone C-20 WB (1:500) EM (1:20) Discontinued antibody; remainder of experiments done with Cell Signaling Technology Cat# 2,654.

    Techniques: Stable Transfection, Transfection, Plasmid Preparation, Construct, Generated, Cytometry, Kinase Assay, Recombinant, Sequencing, Ligation, Mutagenesis, Bicinchoninic Acid Protein Assay, Expressing, Software, Magnetic Beads

    Journal: eLife

    Article Title: EGFR transactivates RON to drive oncogenic crosstalk

    doi: 10.7554/eLife.63678

    Figure Lengend Snippet:

    Article Snippet: antibody , Anti- RONβ (Rabbit monoclonal) , Cell Signaling Technology , Cat# 2654 RRID: AB_2298153 , Clone C81H9 WB (1:2000).

    Techniques: Stable Transfection, Transfection, Plasmid Preparation, Construct, Generated, Cytometry, Kinase Assay, Recombinant, Sequencing, Ligation, Mutagenesis, Bicinchoninic Acid Protein Assay, Expressing, Software, Magnetic Beads