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nrg1β egf domain  (R&D Systems)


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    R&D Systems nrg1β egf domain
    H1047R and E545K knockin cells are hyper-responsive to neuregulin-1 beta 1 <t>(NRG1β)</t> treatment. A Parental SK-BR-3 cells treated with NRG1β and lapatinib show rescue from lapatinib at high concentrations of NRG1β, but only partial rescue when treated with low doses of NRG1β (2 ng/mL). B The H1047R cells show complete rescue from lapatinib with all doses of NRG1β, even at the highest dose of lapatinib, suggesting that the mutant cells are more responsive to ligand stimulation than their wildtype counterparts. C The E545K cells also show complete rescue from lapatinib inhibition by all doses of NRG1β. Value shown are median cell counts relative to untreated controls. Error bars are ± standard deviation
    Nrg1β Egf Domain, supplied by R&D Systems, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/nrg1%CE%B2+egf+domain/pmc08336338-59-0-3?v=R%26D+Systems
    Average 90 stars, based on 1 article reviews
    nrg1β egf domain - by Bioz Stars, 2026-07
    90/100 stars

    Images

    1) Product Images from "Sensitivity to targeted therapy differs between HER2-amplified breast cancer cells harboring kinase and helical domain mutations in PIK3CA"

    Article Title: Sensitivity to targeted therapy differs between HER2-amplified breast cancer cells harboring kinase and helical domain mutations in PIK3CA

    Journal: Breast Cancer Research : BCR

    doi: 10.1186/s13058-021-01457-0

    H1047R and E545K knockin cells are hyper-responsive to neuregulin-1 beta 1 (NRG1β) treatment. A Parental SK-BR-3 cells treated with NRG1β and lapatinib show rescue from lapatinib at high concentrations of NRG1β, but only partial rescue when treated with low doses of NRG1β (2 ng/mL). B The H1047R cells show complete rescue from lapatinib with all doses of NRG1β, even at the highest dose of lapatinib, suggesting that the mutant cells are more responsive to ligand stimulation than their wildtype counterparts. C The E545K cells also show complete rescue from lapatinib inhibition by all doses of NRG1β. Value shown are median cell counts relative to untreated controls. Error bars are ± standard deviation
    Figure Legend Snippet: H1047R and E545K knockin cells are hyper-responsive to neuregulin-1 beta 1 (NRG1β) treatment. A Parental SK-BR-3 cells treated with NRG1β and lapatinib show rescue from lapatinib at high concentrations of NRG1β, but only partial rescue when treated with low doses of NRG1β (2 ng/mL). B The H1047R cells show complete rescue from lapatinib with all doses of NRG1β, even at the highest dose of lapatinib, suggesting that the mutant cells are more responsive to ligand stimulation than their wildtype counterparts. C The E545K cells also show complete rescue from lapatinib inhibition by all doses of NRG1β. Value shown are median cell counts relative to untreated controls. Error bars are ± standard deviation

    Techniques Used: Knock-In, Mutagenesis, Inhibition, Standard Deviation

    Addition of NRG1β de-sensitizes cells to lapatinib, co-treatment with AKT inhibitor or pertuzumab overcomes this effect. A Parental SKBR3 cells or PIK3CA mutant clones treated with lapatinib, AKT inhibitor GSK690693, or combination of the two drugs at a fixed molar ratio in the absence or presence of NRG1β for 72 h. Only H1047R knockin mutant cells show decreased sensitivity to lapatinib at baseline, consistent with results shown in Fig. . Treatment with NRG1β makes cells more resistant to lapatinib, and response is partially restored by co-treatment with GSK690693. The efficacy of the combination is greatest in the H1047R mutant cells as measured by the GR max response. Significant synergistic interactions are marked with an *. B Parental SKBR3 cells or PIK3CA mutant clones treated with lapatinib, pertuzumab, or combination of the two drugs at a fixed molar ratio in the absence or presence of NRG1β for 72 h. Combination of drugs resulted in synergistic growth inhibition at low doses in all three cell lines, but offered no benefit over lapatinib alone at higher doses. Addition of NRG1β-induced resistance to lapatinib in all three cell lines was abrogated with the addition of pertuzumab. Note that synergy could not be accurately calculated by the combination index method for these curves since it requires fitting dose-response curves and pertuzumab did not have any effect on the growth of cells as a monotherapy
    Figure Legend Snippet: Addition of NRG1β de-sensitizes cells to lapatinib, co-treatment with AKT inhibitor or pertuzumab overcomes this effect. A Parental SKBR3 cells or PIK3CA mutant clones treated with lapatinib, AKT inhibitor GSK690693, or combination of the two drugs at a fixed molar ratio in the absence or presence of NRG1β for 72 h. Only H1047R knockin mutant cells show decreased sensitivity to lapatinib at baseline, consistent with results shown in Fig. . Treatment with NRG1β makes cells more resistant to lapatinib, and response is partially restored by co-treatment with GSK690693. The efficacy of the combination is greatest in the H1047R mutant cells as measured by the GR max response. Significant synergistic interactions are marked with an *. B Parental SKBR3 cells or PIK3CA mutant clones treated with lapatinib, pertuzumab, or combination of the two drugs at a fixed molar ratio in the absence or presence of NRG1β for 72 h. Combination of drugs resulted in synergistic growth inhibition at low doses in all three cell lines, but offered no benefit over lapatinib alone at higher doses. Addition of NRG1β-induced resistance to lapatinib in all three cell lines was abrogated with the addition of pertuzumab. Note that synergy could not be accurately calculated by the combination index method for these curves since it requires fitting dose-response curves and pertuzumab did not have any effect on the growth of cells as a monotherapy

    Techniques Used: Mutagenesis, Clone Assay, Knock-In, Inhibition



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    H1047R and E545K knockin cells are hyper-responsive to neuregulin-1 beta 1 <t>(NRG1β)</t> treatment. A Parental SK-BR-3 cells treated with NRG1β and lapatinib show rescue from lapatinib at high concentrations of NRG1β, but only partial rescue when treated with low doses of NRG1β (2 ng/mL). B The H1047R cells show complete rescue from lapatinib with all doses of NRG1β, even at the highest dose of lapatinib, suggesting that the mutant cells are more responsive to ligand stimulation than their wildtype counterparts. C The E545K cells also show complete rescue from lapatinib inhibition by all doses of NRG1β. Value shown are median cell counts relative to untreated controls. Error bars are ± standard deviation
    Nrg1β Egf Domain, supplied by R&D Systems, 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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    (A) Endogenous ErbB4 in MCF7 cells was stimulated using saturating levels of <t>NRG1β</t> (25 nM/ 200 ng/ml) or NRG1α (1 μM/ 7 μg/ml). Activating phosphorylation of ErbB4 and ERK1/2, as well as total ErbB4 and ERK levels, were monitored by immunoblotting total cell lysates. Grb2 was used as a loading control. Blots are representative of at least three independent experiments. Statistical significance of differences was assessed using the Bonferroni-Dunn method (alpha = 0.05), with datasets for each point analyzed individually without assuming consistent SD.
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    nrg1β r d systems  (R&D Systems)
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    (A) Isolated TNCCs plated on Boyden inserts in the presence of different molecular gradients. Data is internally normalized to control. All gradients tested except NGF were significantly different than control (p<0.05 by paired t-test; n=circles on graph/experimental dates). GDNF, glial cell-derived neurotrophic factor. Red line, 100% of control. (B) Isolated TNCC plated on FN slides were filmed with or without 200ng/ml of NRG1. Total migrated distance and Euclidean distance were normalized showing increased migration after <t>NRG1</t> treatment (p<0.07 and p<0.02 respectively. N=3 experiments, N of cells =86). (C) Velocity of cells in B was measured, with NRG1 treated cells moving twice as fast as control cells (p<0.017). (D–I) NT explants cultured in Boyden chambers with an NRG1β gradient (−/+), no NRG1β (−/−), or homogenous NRG1β (+/+). (D–G) Representative HNK1 staining of chemotaxis filters showing a higher percent TNCCs on the bottom side in −/+ versus −/− chambers. Top of filter in focus (D,E); bottom in focus (F,G). Bar, 25 μm. (H) Percent HNK1-positive and percent HNK1-negative transmigrated cells. n=7 experimental dates (>33 NT explants per treatment). p<0.0001 for HNK1-positive −/− versus −/+ treatments, 1-tailed Dunnett’s. (I) Combined TNCC density from top and bottom sample areas. All t-tests described: no multiple testing adjustments made. Bar graphs show means +/− SEM.
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    Image Search Results


    H1047R and E545K knockin cells are hyper-responsive to neuregulin-1 beta 1 (NRG1β) treatment. A Parental SK-BR-3 cells treated with NRG1β and lapatinib show rescue from lapatinib at high concentrations of NRG1β, but only partial rescue when treated with low doses of NRG1β (2 ng/mL). B The H1047R cells show complete rescue from lapatinib with all doses of NRG1β, even at the highest dose of lapatinib, suggesting that the mutant cells are more responsive to ligand stimulation than their wildtype counterparts. C The E545K cells also show complete rescue from lapatinib inhibition by all doses of NRG1β. Value shown are median cell counts relative to untreated controls. Error bars are ± standard deviation

    Journal: Breast Cancer Research : BCR

    Article Title: Sensitivity to targeted therapy differs between HER2-amplified breast cancer cells harboring kinase and helical domain mutations in PIK3CA

    doi: 10.1186/s13058-021-01457-0

    Figure Lengend Snippet: H1047R and E545K knockin cells are hyper-responsive to neuregulin-1 beta 1 (NRG1β) treatment. A Parental SK-BR-3 cells treated with NRG1β and lapatinib show rescue from lapatinib at high concentrations of NRG1β, but only partial rescue when treated with low doses of NRG1β (2 ng/mL). B The H1047R cells show complete rescue from lapatinib with all doses of NRG1β, even at the highest dose of lapatinib, suggesting that the mutant cells are more responsive to ligand stimulation than their wildtype counterparts. C The E545K cells also show complete rescue from lapatinib inhibition by all doses of NRG1β. Value shown are median cell counts relative to untreated controls. Error bars are ± standard deviation

    Article Snippet: NRG1β EGF Domain (R&D Systems (Minneapolis, MN)) was added 24 h after cell plating, followed immediately by treatment with vehicle or lapatinib at four different concentrations (50, 100, 250, or 500 nM).

    Techniques: Knock-In, Mutagenesis, Inhibition, Standard Deviation

    Addition of NRG1β de-sensitizes cells to lapatinib, co-treatment with AKT inhibitor or pertuzumab overcomes this effect. A Parental SKBR3 cells or PIK3CA mutant clones treated with lapatinib, AKT inhibitor GSK690693, or combination of the two drugs at a fixed molar ratio in the absence or presence of NRG1β for 72 h. Only H1047R knockin mutant cells show decreased sensitivity to lapatinib at baseline, consistent with results shown in Fig. . Treatment with NRG1β makes cells more resistant to lapatinib, and response is partially restored by co-treatment with GSK690693. The efficacy of the combination is greatest in the H1047R mutant cells as measured by the GR max response. Significant synergistic interactions are marked with an *. B Parental SKBR3 cells or PIK3CA mutant clones treated with lapatinib, pertuzumab, or combination of the two drugs at a fixed molar ratio in the absence or presence of NRG1β for 72 h. Combination of drugs resulted in synergistic growth inhibition at low doses in all three cell lines, but offered no benefit over lapatinib alone at higher doses. Addition of NRG1β-induced resistance to lapatinib in all three cell lines was abrogated with the addition of pertuzumab. Note that synergy could not be accurately calculated by the combination index method for these curves since it requires fitting dose-response curves and pertuzumab did not have any effect on the growth of cells as a monotherapy

    Journal: Breast Cancer Research : BCR

    Article Title: Sensitivity to targeted therapy differs between HER2-amplified breast cancer cells harboring kinase and helical domain mutations in PIK3CA

    doi: 10.1186/s13058-021-01457-0

    Figure Lengend Snippet: Addition of NRG1β de-sensitizes cells to lapatinib, co-treatment with AKT inhibitor or pertuzumab overcomes this effect. A Parental SKBR3 cells or PIK3CA mutant clones treated with lapatinib, AKT inhibitor GSK690693, or combination of the two drugs at a fixed molar ratio in the absence or presence of NRG1β for 72 h. Only H1047R knockin mutant cells show decreased sensitivity to lapatinib at baseline, consistent with results shown in Fig. . Treatment with NRG1β makes cells more resistant to lapatinib, and response is partially restored by co-treatment with GSK690693. The efficacy of the combination is greatest in the H1047R mutant cells as measured by the GR max response. Significant synergistic interactions are marked with an *. B Parental SKBR3 cells or PIK3CA mutant clones treated with lapatinib, pertuzumab, or combination of the two drugs at a fixed molar ratio in the absence or presence of NRG1β for 72 h. Combination of drugs resulted in synergistic growth inhibition at low doses in all three cell lines, but offered no benefit over lapatinib alone at higher doses. Addition of NRG1β-induced resistance to lapatinib in all three cell lines was abrogated with the addition of pertuzumab. Note that synergy could not be accurately calculated by the combination index method for these curves since it requires fitting dose-response curves and pertuzumab did not have any effect on the growth of cells as a monotherapy

    Article Snippet: NRG1β EGF Domain (R&D Systems (Minneapolis, MN)) was added 24 h after cell plating, followed immediately by treatment with vehicle or lapatinib at four different concentrations (50, 100, 250, or 500 nM).

    Techniques: Mutagenesis, Clone Assay, Knock-In, Inhibition

    (A) Endogenous ErbB4 in MCF7 cells was stimulated using saturating levels of NRG1β (25 nM/ 200 ng/ml) or NRG1α (1 μM/ 7 μg/ml). Activating phosphorylation of ErbB4 and ERK1/2, as well as total ErbB4 and ERK levels, were monitored by immunoblotting total cell lysates. Grb2 was used as a loading control. Blots are representative of at least three independent experiments. Statistical significance of differences was assessed using the Bonferroni-Dunn method (alpha = 0.05), with datasets for each point analyzed individually without assuming consistent SD.

    Journal: Science signaling

    Article Title: Kinetics of receptor tyrosine kinase activation define ERK signaling dynamics *

    doi: 10.1126/scisignal.aaz5267

    Figure Lengend Snippet: (A) Endogenous ErbB4 in MCF7 cells was stimulated using saturating levels of NRG1β (25 nM/ 200 ng/ml) or NRG1α (1 μM/ 7 μg/ml). Activating phosphorylation of ErbB4 and ERK1/2, as well as total ErbB4 and ERK levels, were monitored by immunoblotting total cell lysates. Grb2 was used as a loading control. Blots are representative of at least three independent experiments. Statistical significance of differences was assessed using the Bonferroni-Dunn method (alpha = 0.05), with datasets for each point analyzed individually without assuming consistent SD.

    Article Snippet: Recombinant human NRG1α (Cat. #296-HR) and NRG1β (Cat. #396-HB/CF) were obtained from R&D Systems.

    Techniques: Phospho-proteomics, Western Blot, Control

    (A) Isolated TNCCs plated on Boyden inserts in the presence of different molecular gradients. Data is internally normalized to control. All gradients tested except NGF were significantly different than control (p<0.05 by paired t-test; n=circles on graph/experimental dates). GDNF, glial cell-derived neurotrophic factor. Red line, 100% of control. (B) Isolated TNCC plated on FN slides were filmed with or without 200ng/ml of NRG1. Total migrated distance and Euclidean distance were normalized showing increased migration after NRG1 treatment (p<0.07 and p<0.02 respectively. N=3 experiments, N of cells =86). (C) Velocity of cells in B was measured, with NRG1 treated cells moving twice as fast as control cells (p<0.017). (D–I) NT explants cultured in Boyden chambers with an NRG1β gradient (−/+), no NRG1β (−/−), or homogenous NRG1β (+/+). (D–G) Representative HNK1 staining of chemotaxis filters showing a higher percent TNCCs on the bottom side in −/+ versus −/− chambers. Top of filter in focus (D,E); bottom in focus (F,G). Bar, 25 μm. (H) Percent HNK1-positive and percent HNK1-negative transmigrated cells. n=7 experimental dates (>33 NT explants per treatment). p<0.0001 for HNK1-positive −/− versus −/+ treatments, 1-tailed Dunnett’s. (I) Combined TNCC density from top and bottom sample areas. All t-tests described: no multiple testing adjustments made. Bar graphs show means +/− SEM.

    Journal: Developmental dynamics : an official publication of the American Association of Anatomists

    Article Title: Neuregulin-1 is a chemoattractant and chemokinetic molecule for trunk neural crest cells

    doi: 10.1002/dvdy.24625

    Figure Lengend Snippet: (A) Isolated TNCCs plated on Boyden inserts in the presence of different molecular gradients. Data is internally normalized to control. All gradients tested except NGF were significantly different than control (p<0.05 by paired t-test; n=circles on graph/experimental dates). GDNF, glial cell-derived neurotrophic factor. Red line, 100% of control. (B) Isolated TNCC plated on FN slides were filmed with or without 200ng/ml of NRG1. Total migrated distance and Euclidean distance were normalized showing increased migration after NRG1 treatment (p<0.07 and p<0.02 respectively. N=3 experiments, N of cells =86). (C) Velocity of cells in B was measured, with NRG1 treated cells moving twice as fast as control cells (p<0.017). (D–I) NT explants cultured in Boyden chambers with an NRG1β gradient (−/+), no NRG1β (−/−), or homogenous NRG1β (+/+). (D–G) Representative HNK1 staining of chemotaxis filters showing a higher percent TNCCs on the bottom side in −/+ versus −/− chambers. Top of filter in focus (D,E); bottom in focus (F,G). Bar, 25 μm. (H) Percent HNK1-positive and percent HNK1-negative transmigrated cells. n=7 experimental dates (>33 NT explants per treatment). p<0.0001 for HNK1-positive −/− versus −/+ treatments, 1-tailed Dunnett’s. (I) Combined TNCC density from top and bottom sample areas. All t-tests described: no multiple testing adjustments made. Bar graphs show means +/− SEM.

    Article Snippet: Amplification was done over 35 cycles (95°C 5minutes, 94°C 30 seconds, 58°C 30 seconds, 72°C 1 minute) for RT-PCR (Eppendorf master cycler gradient). table ft1 table-wrap mode="anchored" t5 REAGENT or RESOURCE SOURCE IDENTIFIER Antibodies Mouse HNK-1 IgM DSHB Cat#1C10 Alexa 488 anti-mouse IgM Invitrogen Cat# A-21042 Mouse anti-c-erbB-4 IgG1 Thermo Scientific Cat#MS270P0 Rabbit anti-GFP IgG Life Technologies Cat# A-11122 Rhodamine Red-X anti-mouse IgM Jackson ImmunoResearch, West Grove, PA Cat#115-295-075 594 F(ab′)2 fragment of anti-mouse IgG ThermoFisher Cat#A-11020 488 anti-rabbit IgG ThermoFisher Cat#A-11034 594 anti-rabbit IgG ThermoFisher Cat# {"type":"entrez-nucleotide","attrs":{"text":"A11037","term_id":"492397","term_text":"A11037"}} A11037 647 anti-mouse IgM ThermoFisher Cat#A-21238 Bacterial and Virus Strains pcDNA3-DNerbB4 Rio et al. 1997 pcDNA3-EGFP Addgene #13031 Biological Samples Chicken embryos (Gallus gallus) AA Laboratories, Westminster, CA Quail embryos (Coturnix coturnix) McIntyre Poultry, Lakeside CA Chemicals, Peptides, and Recombinant Proteins Children’s Oncology Group Cell Culture and Xenograft Repository http://cogcell.org/ NRG1-EGF Domains NRG1α R&D Systems Cat#296-HR-050 BSA ThermoFisher Cat#BP-1600-100 NRG1β R&D Systems Cat#396-HB-050/CF Tryphostin AG 1478 Enzo Cat #ALX-270-036-M001 BPE BD Cat# 356123 Live Cell Imaging Solution Life Technologies Cat# A14291DJ Critical Commercial Assays Boyden Chamber Assay BD Immulon 4 ELISA well Dynatech Laboratories, Chantilly, VA microchips Caltech Microfluidic Foundry www.kni.caltech.edu/foundry Modified Zigmond Chamber Assay Walheim et al., 2012 Deposited Data Experimental Models: Cell Lines Experimental Models: Organisms/Strains Oligonucleotides Recombinant DNA Software and Algorithms Excel Microsoft https://products.office.com/en-us/excel SPSS IBM https://www.ibm.com/us-en/marketplace/spss-statistics ImageJ Manual Tracking ImageJ https://imagej.nih.gov/ij/plugins/track/track.html ImageJ Chemotaxis and Migration Tool ImageJ http://ibidi.com/software/chemotaxis_and_migration_tool AxioVision Rel.

    Techniques: Isolation, Control, Derivative Assay, Migration, Cell Culture, Staining, Chemotaxis Assay

    A NT explant (darker tissue) was plated within a region of an ELISA well pre-coated with NRG1α and filmed for 18 h as TNCCs emigrated from the NT explant and were confronted by the coat border (red curved line). A–C: Numerous emigrating cells can be seen migrating freely outside a PBS area (arrows). D–F: Numerous emigrating cells can be seen excessively lingering near the NRG1α border and/or preferentially migrating to open spaces still within the NRG1-coated region not occupied by other cells before migrating outside the coated region (arrows).

    Journal: Developmental dynamics : an official publication of the American Association of Anatomists

    Article Title: Neuregulin-1 is a chemoattractant and chemokinetic molecule for trunk neural crest cells

    doi: 10.1002/dvdy.24625

    Figure Lengend Snippet: A NT explant (darker tissue) was plated within a region of an ELISA well pre-coated with NRG1α and filmed for 18 h as TNCCs emigrated from the NT explant and were confronted by the coat border (red curved line). A–C: Numerous emigrating cells can be seen migrating freely outside a PBS area (arrows). D–F: Numerous emigrating cells can be seen excessively lingering near the NRG1α border and/or preferentially migrating to open spaces still within the NRG1-coated region not occupied by other cells before migrating outside the coated region (arrows).

    Article Snippet: Amplification was done over 35 cycles (95°C 5minutes, 94°C 30 seconds, 58°C 30 seconds, 72°C 1 minute) for RT-PCR (Eppendorf master cycler gradient). table ft1 table-wrap mode="anchored" t5 REAGENT or RESOURCE SOURCE IDENTIFIER Antibodies Mouse HNK-1 IgM DSHB Cat#1C10 Alexa 488 anti-mouse IgM Invitrogen Cat# A-21042 Mouse anti-c-erbB-4 IgG1 Thermo Scientific Cat#MS270P0 Rabbit anti-GFP IgG Life Technologies Cat# A-11122 Rhodamine Red-X anti-mouse IgM Jackson ImmunoResearch, West Grove, PA Cat#115-295-075 594 F(ab′)2 fragment of anti-mouse IgG ThermoFisher Cat#A-11020 488 anti-rabbit IgG ThermoFisher Cat#A-11034 594 anti-rabbit IgG ThermoFisher Cat# {"type":"entrez-nucleotide","attrs":{"text":"A11037","term_id":"492397","term_text":"A11037"}} A11037 647 anti-mouse IgM ThermoFisher Cat#A-21238 Bacterial and Virus Strains pcDNA3-DNerbB4 Rio et al. 1997 pcDNA3-EGFP Addgene #13031 Biological Samples Chicken embryos (Gallus gallus) AA Laboratories, Westminster, CA Quail embryos (Coturnix coturnix) McIntyre Poultry, Lakeside CA Chemicals, Peptides, and Recombinant Proteins Children’s Oncology Group Cell Culture and Xenograft Repository http://cogcell.org/ NRG1-EGF Domains NRG1α R&D Systems Cat#296-HR-050 BSA ThermoFisher Cat#BP-1600-100 NRG1β R&D Systems Cat#396-HB-050/CF Tryphostin AG 1478 Enzo Cat #ALX-270-036-M001 BPE BD Cat# 356123 Live Cell Imaging Solution Life Technologies Cat# A14291DJ Critical Commercial Assays Boyden Chamber Assay BD Immulon 4 ELISA well Dynatech Laboratories, Chantilly, VA microchips Caltech Microfluidic Foundry www.kni.caltech.edu/foundry Modified Zigmond Chamber Assay Walheim et al., 2012 Deposited Data Experimental Models: Cell Lines Experimental Models: Organisms/Strains Oligonucleotides Recombinant DNA Software and Algorithms Excel Microsoft https://products.office.com/en-us/excel SPSS IBM https://www.ibm.com/us-en/marketplace/spss-statistics ImageJ Manual Tracking ImageJ https://imagej.nih.gov/ij/plugins/track/track.html ImageJ Chemotaxis and Migration Tool ImageJ http://ibidi.com/software/chemotaxis_and_migration_tool AxioVision Rel.

    Techniques: Enzyme-linked Immunosorbent Assay

    RT-PCR analysis

    Journal: Developmental dynamics : an official publication of the American Association of Anatomists

    Article Title: Neuregulin-1 is a chemoattractant and chemokinetic molecule for trunk neural crest cells

    doi: 10.1002/dvdy.24625

    Figure Lengend Snippet: RT-PCR analysis

    Article Snippet: Amplification was done over 35 cycles (95°C 5minutes, 94°C 30 seconds, 58°C 30 seconds, 72°C 1 minute) for RT-PCR (Eppendorf master cycler gradient). table ft1 table-wrap mode="anchored" t5 REAGENT or RESOURCE SOURCE IDENTIFIER Antibodies Mouse HNK-1 IgM DSHB Cat#1C10 Alexa 488 anti-mouse IgM Invitrogen Cat# A-21042 Mouse anti-c-erbB-4 IgG1 Thermo Scientific Cat#MS270P0 Rabbit anti-GFP IgG Life Technologies Cat# A-11122 Rhodamine Red-X anti-mouse IgM Jackson ImmunoResearch, West Grove, PA Cat#115-295-075 594 F(ab′)2 fragment of anti-mouse IgG ThermoFisher Cat#A-11020 488 anti-rabbit IgG ThermoFisher Cat#A-11034 594 anti-rabbit IgG ThermoFisher Cat# {"type":"entrez-nucleotide","attrs":{"text":"A11037","term_id":"492397","term_text":"A11037"}} A11037 647 anti-mouse IgM ThermoFisher Cat#A-21238 Bacterial and Virus Strains pcDNA3-DNerbB4 Rio et al. 1997 pcDNA3-EGFP Addgene #13031 Biological Samples Chicken embryos (Gallus gallus) AA Laboratories, Westminster, CA Quail embryos (Coturnix coturnix) McIntyre Poultry, Lakeside CA Chemicals, Peptides, and Recombinant Proteins Children’s Oncology Group Cell Culture and Xenograft Repository http://cogcell.org/ NRG1-EGF Domains NRG1α R&D Systems Cat#296-HR-050 BSA ThermoFisher Cat#BP-1600-100 NRG1β R&D Systems Cat#396-HB-050/CF Tryphostin AG 1478 Enzo Cat #ALX-270-036-M001 BPE BD Cat# 356123 Live Cell Imaging Solution Life Technologies Cat# A14291DJ Critical Commercial Assays Boyden Chamber Assay BD Immulon 4 ELISA well Dynatech Laboratories, Chantilly, VA microchips Caltech Microfluidic Foundry www.kni.caltech.edu/foundry Modified Zigmond Chamber Assay Walheim et al., 2012 Deposited Data Experimental Models: Cell Lines Experimental Models: Organisms/Strains Oligonucleotides Recombinant DNA Software and Algorithms Excel Microsoft https://products.office.com/en-us/excel SPSS IBM https://www.ibm.com/us-en/marketplace/spss-statistics ImageJ Manual Tracking ImageJ https://imagej.nih.gov/ij/plugins/track/track.html ImageJ Chemotaxis and Migration Tool ImageJ http://ibidi.com/software/chemotaxis_and_migration_tool AxioVision Rel.

    Techniques: Virus, Recombinant, Cell Culture, Live Cell Imaging, Boyden Chamber Assay, Enzyme-linked Immunosorbent Assay, Modification, Software, Chemotaxis Assay, Migration