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melanocyte growth kit  (ATCC)


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    ATCC melanocyte growth kit
    A. Genetic variants fine-mapped for the melanoma GWAS are annotated, along with Bayesian fine-mapped variant credible sets (CS) from SuSiE and DAP-G for human primary <t>melanocyte</t> eQTLs for RAPGEF1 and UCK1 . Roadmap chromatin states (ChromHMM) from primary melanocytes are shown; red and orange denote annotated promoter, yellow and light green enhancer. Chromatin accessibility from DNAse I hypersensitivity sequencing (DHS) and ATAC-sequencing (ATAC) of melanocytes and melanoma cell models is shown. Chromatin interactions between the entire region of association (Capture-HiC baits) in human melanocytes is shown, as are separately only those interactions between fine-mapped variants and gene promoters; fine-mapped variants interact with the promoters of both RAPGEF1 , UCK1 , and NTNG2 (not shown on figure). B . Zoomed in view of the fine-mapped variants. The locations of small guide RNAs used for CRISPR-inhibition (CRISPRi sgRNAs) experiments are shown. Chromatin interactions between regoins harboring fine-mapped variants and gene promoters in human melanocytes are shown. C . CRISPR-inhibition (CRISPRi) validation of RAPGEF1 and UCK1 as cis -regulatory targets at 9q34.13. Guide RNAs were designed to target three fine-mapped variants within an ~11.3 kb interval. Each guide was individually tested for effects on RAPGEF1 and UCK1 expression relative to the average of two non-targeting guides in immortalized melanocytes stably expressing dCas9-KRAB via a TaqMan quantitative RT-PCR assay. Whiskers show minimum and maximum values. P -values were calculated using a two-sample two-sided paired t-test comparing 2^ (delta-Ct) values from individual guides to those from the average of the two non-targeting guides with 10 biological replicates in total.
    Melanocyte Growth Kit, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 66 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    melanocyte growth kit - by Bioz Stars, 2026-10
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    1) Product Images from "Functional characterization of the 9q34.13 locus identifies RAPGEF1 as a candidate gene modulating risk for melanoma and nevi via RAS activation"

    Article Title: Functional characterization of the 9q34.13 locus identifies RAPGEF1 as a candidate gene modulating risk for melanoma and nevi via RAS activation

    Journal: American journal of human genetics

    doi: 10.1016/j.ajhg.2026.08.014

    A. Genetic variants fine-mapped for the melanoma GWAS are annotated, along with Bayesian fine-mapped variant credible sets (CS) from SuSiE and DAP-G for human primary melanocyte eQTLs for RAPGEF1 and UCK1 . Roadmap chromatin states (ChromHMM) from primary melanocytes are shown; red and orange denote annotated promoter, yellow and light green enhancer. Chromatin accessibility from DNAse I hypersensitivity sequencing (DHS) and ATAC-sequencing (ATAC) of melanocytes and melanoma cell models is shown. Chromatin interactions between the entire region of association (Capture-HiC baits) in human melanocytes is shown, as are separately only those interactions between fine-mapped variants and gene promoters; fine-mapped variants interact with the promoters of both RAPGEF1 , UCK1 , and NTNG2 (not shown on figure). B . Zoomed in view of the fine-mapped variants. The locations of small guide RNAs used for CRISPR-inhibition (CRISPRi sgRNAs) experiments are shown. Chromatin interactions between regoins harboring fine-mapped variants and gene promoters in human melanocytes are shown. C . CRISPR-inhibition (CRISPRi) validation of RAPGEF1 and UCK1 as cis -regulatory targets at 9q34.13. Guide RNAs were designed to target three fine-mapped variants within an ~11.3 kb interval. Each guide was individually tested for effects on RAPGEF1 and UCK1 expression relative to the average of two non-targeting guides in immortalized melanocytes stably expressing dCas9-KRAB via a TaqMan quantitative RT-PCR assay. Whiskers show minimum and maximum values. P -values were calculated using a two-sample two-sided paired t-test comparing 2^ (delta-Ct) values from individual guides to those from the average of the two non-targeting guides with 10 biological replicates in total.
    Figure Legend Snippet: A. Genetic variants fine-mapped for the melanoma GWAS are annotated, along with Bayesian fine-mapped variant credible sets (CS) from SuSiE and DAP-G for human primary melanocyte eQTLs for RAPGEF1 and UCK1 . Roadmap chromatin states (ChromHMM) from primary melanocytes are shown; red and orange denote annotated promoter, yellow and light green enhancer. Chromatin accessibility from DNAse I hypersensitivity sequencing (DHS) and ATAC-sequencing (ATAC) of melanocytes and melanoma cell models is shown. Chromatin interactions between the entire region of association (Capture-HiC baits) in human melanocytes is shown, as are separately only those interactions between fine-mapped variants and gene promoters; fine-mapped variants interact with the promoters of both RAPGEF1 , UCK1 , and NTNG2 (not shown on figure). B . Zoomed in view of the fine-mapped variants. The locations of small guide RNAs used for CRISPR-inhibition (CRISPRi sgRNAs) experiments are shown. Chromatin interactions between regoins harboring fine-mapped variants and gene promoters in human melanocytes are shown. C . CRISPR-inhibition (CRISPRi) validation of RAPGEF1 and UCK1 as cis -regulatory targets at 9q34.13. Guide RNAs were designed to target three fine-mapped variants within an ~11.3 kb interval. Each guide was individually tested for effects on RAPGEF1 and UCK1 expression relative to the average of two non-targeting guides in immortalized melanocytes stably expressing dCas9-KRAB via a TaqMan quantitative RT-PCR assay. Whiskers show minimum and maximum values. P -values were calculated using a two-sample two-sided paired t-test comparing 2^ (delta-Ct) values from individual guides to those from the average of the two non-targeting guides with 10 biological replicates in total.

    Techniques Used: Variant Assay, Sequencing, CRISPR, Inhibition, Biomarker Discovery, Expressing, Stable Transfection, Quantitative RT-PCR

    A . Crystal violet assays following RAPGEF1 knockdown in immortalized melanocytes. Equal numbers of cells either infected with two RAPGEF1 shRNAs or vector control were seeded after infection and drug selection. Cells were fixed and stained with crystal violet at multiple timepoints after seeding. Crystal violet was then solubilized from stained cells and measured by OD560. OD560 values were normalized to the reading at D1, and the mean of six biological replicates and SEM were plotted. P -value was calculated from two-way ANOVA; B . Quantitative RT-PCR for RAPGEF1 in immortalized melanocytes following infection with shRNAs targeting RAPGEF1 relative to empty vector control. RNA was collected and assayed at D5 after infection. C . FACS analysis of immortalized melanocytes infected with either empty vector or RAPGEF1 shRNA at D5 after infection. BrdU and 7-AAD staining were used to characterize the cell cycle status of different cells. The images shown here are from a representative experiment from three biological replicates. D . Crystal violet assays following UCK1 knockdown in immortalized melanocytes. Equal numbers of cells either infected with two UCK1 shRNAs or vector control were seeded after infection and drug selection. Cells were fixed and stained with crystal violet at multiple timepoints after seeding. Crystal violet was then solubilized from stained cells and measured by OD560. OD560 values were normalized to the reading at D1, and the mean of six biological replicates and SEM were plotted. P -value was calculated from two-way ANOVA. E . Quantitative RT-PCR for UCK1 in immortalized melanocytes following infection with shRNAs targeting UCK1 relative to empty vector control. RNA was collected and assayed at D7 after infection F . FACS analysis of immortalized melanocytes infected with either empty vector or UCK1 shRNA at D7 after infection. BrdU and 7-AAD staining were used to characterize the cell cycle status of different cells. The images shown here are from a representative experiment from three biological replicates. G . Immortalized melanocytes infected with a dox-inducible vector (pCW57.1) to express RAPGEF1 were seeded after infection and drug selection. Dox-treated cells were treated with 200ng/mL dox at seeding (D0) and cells were fixed and stained with crystal violet at multiple timepoints after seeding. Crystal violet was then solubilized from stained cells and measured by OD560. OD560 values were normalized to the reading of D1 and the mean of 12 biological replicates and SEM were plotted. P -value was calculated using two-way ANOVA. H . Western blot for RAPGEF1 in dox-treated immortalized melanocytes. Whole cell extract was collected 48 hours post-dox treatment at D7 after infection.
    Figure Legend Snippet: A . Crystal violet assays following RAPGEF1 knockdown in immortalized melanocytes. Equal numbers of cells either infected with two RAPGEF1 shRNAs or vector control were seeded after infection and drug selection. Cells were fixed and stained with crystal violet at multiple timepoints after seeding. Crystal violet was then solubilized from stained cells and measured by OD560. OD560 values were normalized to the reading at D1, and the mean of six biological replicates and SEM were plotted. P -value was calculated from two-way ANOVA; B . Quantitative RT-PCR for RAPGEF1 in immortalized melanocytes following infection with shRNAs targeting RAPGEF1 relative to empty vector control. RNA was collected and assayed at D5 after infection. C . FACS analysis of immortalized melanocytes infected with either empty vector or RAPGEF1 shRNA at D5 after infection. BrdU and 7-AAD staining were used to characterize the cell cycle status of different cells. The images shown here are from a representative experiment from three biological replicates. D . Crystal violet assays following UCK1 knockdown in immortalized melanocytes. Equal numbers of cells either infected with two UCK1 shRNAs or vector control were seeded after infection and drug selection. Cells were fixed and stained with crystal violet at multiple timepoints after seeding. Crystal violet was then solubilized from stained cells and measured by OD560. OD560 values were normalized to the reading at D1, and the mean of six biological replicates and SEM were plotted. P -value was calculated from two-way ANOVA. E . Quantitative RT-PCR for UCK1 in immortalized melanocytes following infection with shRNAs targeting UCK1 relative to empty vector control. RNA was collected and assayed at D7 after infection F . FACS analysis of immortalized melanocytes infected with either empty vector or UCK1 shRNA at D7 after infection. BrdU and 7-AAD staining were used to characterize the cell cycle status of different cells. The images shown here are from a representative experiment from three biological replicates. G . Immortalized melanocytes infected with a dox-inducible vector (pCW57.1) to express RAPGEF1 were seeded after infection and drug selection. Dox-treated cells were treated with 200ng/mL dox at seeding (D0) and cells were fixed and stained with crystal violet at multiple timepoints after seeding. Crystal violet was then solubilized from stained cells and measured by OD560. OD560 values were normalized to the reading of D1 and the mean of 12 biological replicates and SEM were plotted. P -value was calculated using two-way ANOVA. H . Western blot for RAPGEF1 in dox-treated immortalized melanocytes. Whole cell extract was collected 48 hours post-dox treatment at D7 after infection.

    Techniques Used: Knockdown, Infection, Plasmid Preparation, Control, Selection, Staining, Quantitative RT-PCR, Analysis, shRNA, Western Blot

    A . Immortalized melanocytes (p’mel cells) expressing constitutively active BRAF p.Val600Glu were infected with empty pLX304 vector or constructs expressing different proteins and seeded in soft-agar plates after blasticidin selection. Images were taken between week 4-5 after plating, and colonies were counted from two sets of triplicates ( n = 6), with counts from each individual replicate shown as a dot. Whiskers show mean with SEM. P -values were calculated using two-tailed, unpaired Student’s t-test. Significance is shown only for comparisons with the empty vector control and RAPGEF1 overexpression. B . Representative images of colonies are shown. The same magnification (4x) was applied for all the images.
    Figure Legend Snippet: A . Immortalized melanocytes (p’mel cells) expressing constitutively active BRAF p.Val600Glu were infected with empty pLX304 vector or constructs expressing different proteins and seeded in soft-agar plates after blasticidin selection. Images were taken between week 4-5 after plating, and colonies were counted from two sets of triplicates ( n = 6), with counts from each individual replicate shown as a dot. Whiskers show mean with SEM. P -values were calculated using two-tailed, unpaired Student’s t-test. Significance is shown only for comparisons with the empty vector control and RAPGEF1 overexpression. B . Representative images of colonies are shown. The same magnification (4x) was applied for all the images.

    Techniques Used: Colony Assay, Stable Transfection, Expressing, Infection, Plasmid Preparation, Construct, Selection, Two Tailed Test, Control, Over Expression

    C283T immortalized melanocytes with doxycycline-inducible expression of RAPGEF1 were grown in supplement-free medium for 24hrs and subsequently treated with human EGF (hEGF) protein for the indicated time. A . Active GTP-bound RAP1 was pulled down by RalGDS-RBD beads from whole-cell extract. Pull-down and whole-cell (total RAP) fractions were compared by Western blotting with an antibody against RAP1. B . Active GTP-bound RAS was pulled down by Raf-RBD beads, with the pull-down and whole-cell (total RAS) fractions compared by Western blotting with an antibody against RAS. Active and total AKT and ERK were compared via Western blotting. The intensity of the phospho- versus total-AKT and ERK was determined by the ratio of the band intensity. Figures are representative experiments from three biological replicates.
    Figure Legend Snippet: C283T immortalized melanocytes with doxycycline-inducible expression of RAPGEF1 were grown in supplement-free medium for 24hrs and subsequently treated with human EGF (hEGF) protein for the indicated time. A . Active GTP-bound RAP1 was pulled down by RalGDS-RBD beads from whole-cell extract. Pull-down and whole-cell (total RAP) fractions were compared by Western blotting with an antibody against RAP1. B . Active GTP-bound RAS was pulled down by Raf-RBD beads, with the pull-down and whole-cell (total RAS) fractions compared by Western blotting with an antibody against RAS. Active and total AKT and ERK were compared via Western blotting. The intensity of the phospho- versus total-AKT and ERK was determined by the ratio of the band intensity. Figures are representative experiments from three biological replicates.

    Techniques Used: Activation Assay, Expressing, Pull Down Assay, Western Blot

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    A. Genetic variants fine-mapped for the melanoma GWAS are annotated, along with Bayesian fine-mapped variant credible sets (CS) from SuSiE and DAP-G for human primary <t>melanocyte</t> eQTLs for RAPGEF1 and UCK1 . Roadmap chromatin states (ChromHMM) from primary melanocytes are shown; red and orange denote annotated promoter, yellow and light green enhancer. Chromatin accessibility from DNAse I hypersensitivity sequencing (DHS) and ATAC-sequencing (ATAC) of melanocytes and melanoma cell models is shown. Chromatin interactions between the entire region of association (Capture-HiC baits) in human melanocytes is shown, as are separately only those interactions between fine-mapped variants and gene promoters; fine-mapped variants interact with the promoters of both RAPGEF1 , UCK1 , and NTNG2 (not shown on figure). B . Zoomed in view of the fine-mapped variants. The locations of small guide RNAs used for CRISPR-inhibition (CRISPRi sgRNAs) experiments are shown. Chromatin interactions between regoins harboring fine-mapped variants and gene promoters in human melanocytes are shown. C . CRISPR-inhibition (CRISPRi) validation of RAPGEF1 and UCK1 as cis -regulatory targets at 9q34.13. Guide RNAs were designed to target three fine-mapped variants within an ~11.3 kb interval. Each guide was individually tested for effects on RAPGEF1 and UCK1 expression relative to the average of two non-targeting guides in immortalized melanocytes stably expressing dCas9-KRAB via a TaqMan quantitative RT-PCR assay. Whiskers show minimum and maximum values. P -values were calculated using a two-sample two-sided paired t-test comparing 2^ (delta-Ct) values from individual guides to those from the average of the two non-targeting guides with 10 biological replicates in total.
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    A. Genetic variants fine-mapped for the melanoma GWAS are annotated, along with Bayesian fine-mapped variant credible sets (CS) from SuSiE and DAP-G for human primary melanocyte eQTLs for RAPGEF1 and UCK1 . Roadmap chromatin states (ChromHMM) from primary melanocytes are shown; red and orange denote annotated promoter, yellow and light green enhancer. Chromatin accessibility from DNAse I hypersensitivity sequencing (DHS) and ATAC-sequencing (ATAC) of melanocytes and melanoma cell models is shown. Chromatin interactions between the entire region of association (Capture-HiC baits) in human melanocytes is shown, as are separately only those interactions between fine-mapped variants and gene promoters; fine-mapped variants interact with the promoters of both RAPGEF1 , UCK1 , and NTNG2 (not shown on figure). B . Zoomed in view of the fine-mapped variants. The locations of small guide RNAs used for CRISPR-inhibition (CRISPRi sgRNAs) experiments are shown. Chromatin interactions between regoins harboring fine-mapped variants and gene promoters in human melanocytes are shown. C . CRISPR-inhibition (CRISPRi) validation of RAPGEF1 and UCK1 as cis -regulatory targets at 9q34.13. Guide RNAs were designed to target three fine-mapped variants within an ~11.3 kb interval. Each guide was individually tested for effects on RAPGEF1 and UCK1 expression relative to the average of two non-targeting guides in immortalized melanocytes stably expressing dCas9-KRAB via a TaqMan quantitative RT-PCR assay. Whiskers show minimum and maximum values. P -values were calculated using a two-sample two-sided paired t-test comparing 2^ (delta-Ct) values from individual guides to those from the average of the two non-targeting guides with 10 biological replicates in total.

    Journal: American journal of human genetics

    Article Title: Functional characterization of the 9q34.13 locus identifies RAPGEF1 as a candidate gene modulating risk for melanoma and nevi via RAS activation

    doi: 10.1016/j.ajhg.2026.08.014

    Figure Lengend Snippet: A. Genetic variants fine-mapped for the melanoma GWAS are annotated, along with Bayesian fine-mapped variant credible sets (CS) from SuSiE and DAP-G for human primary melanocyte eQTLs for RAPGEF1 and UCK1 . Roadmap chromatin states (ChromHMM) from primary melanocytes are shown; red and orange denote annotated promoter, yellow and light green enhancer. Chromatin accessibility from DNAse I hypersensitivity sequencing (DHS) and ATAC-sequencing (ATAC) of melanocytes and melanoma cell models is shown. Chromatin interactions between the entire region of association (Capture-HiC baits) in human melanocytes is shown, as are separately only those interactions between fine-mapped variants and gene promoters; fine-mapped variants interact with the promoters of both RAPGEF1 , UCK1 , and NTNG2 (not shown on figure). B . Zoomed in view of the fine-mapped variants. The locations of small guide RNAs used for CRISPR-inhibition (CRISPRi sgRNAs) experiments are shown. Chromatin interactions between regoins harboring fine-mapped variants and gene promoters in human melanocytes are shown. C . CRISPR-inhibition (CRISPRi) validation of RAPGEF1 and UCK1 as cis -regulatory targets at 9q34.13. Guide RNAs were designed to target three fine-mapped variants within an ~11.3 kb interval. Each guide was individually tested for effects on RAPGEF1 and UCK1 expression relative to the average of two non-targeting guides in immortalized melanocytes stably expressing dCas9-KRAB via a TaqMan quantitative RT-PCR assay. Whiskers show minimum and maximum values. P -values were calculated using a two-sample two-sided paired t-test comparing 2^ (delta-Ct) values from individual guides to those from the average of the two non-targeting guides with 10 biological replicates in total.

    Article Snippet: Melanocytes were grown in Dermal Cell Basal Medium (American Type Culture Collection/ATCC PCS-200-030) supplemented with Melanocyte Growth Kit (ATCC PCS-200-041) and 1% amphotericin B/penicillin/streptomycin (120-096-711, Quality Biological) at 37°C with 5% CO 2 .

    Techniques: Variant Assay, Sequencing, CRISPR, Inhibition, Biomarker Discovery, Expressing, Stable Transfection, Quantitative RT-PCR

    A . Crystal violet assays following RAPGEF1 knockdown in immortalized melanocytes. Equal numbers of cells either infected with two RAPGEF1 shRNAs or vector control were seeded after infection and drug selection. Cells were fixed and stained with crystal violet at multiple timepoints after seeding. Crystal violet was then solubilized from stained cells and measured by OD560. OD560 values were normalized to the reading at D1, and the mean of six biological replicates and SEM were plotted. P -value was calculated from two-way ANOVA; B . Quantitative RT-PCR for RAPGEF1 in immortalized melanocytes following infection with shRNAs targeting RAPGEF1 relative to empty vector control. RNA was collected and assayed at D5 after infection. C . FACS analysis of immortalized melanocytes infected with either empty vector or RAPGEF1 shRNA at D5 after infection. BrdU and 7-AAD staining were used to characterize the cell cycle status of different cells. The images shown here are from a representative experiment from three biological replicates. D . Crystal violet assays following UCK1 knockdown in immortalized melanocytes. Equal numbers of cells either infected with two UCK1 shRNAs or vector control were seeded after infection and drug selection. Cells were fixed and stained with crystal violet at multiple timepoints after seeding. Crystal violet was then solubilized from stained cells and measured by OD560. OD560 values were normalized to the reading at D1, and the mean of six biological replicates and SEM were plotted. P -value was calculated from two-way ANOVA. E . Quantitative RT-PCR for UCK1 in immortalized melanocytes following infection with shRNAs targeting UCK1 relative to empty vector control. RNA was collected and assayed at D7 after infection F . FACS analysis of immortalized melanocytes infected with either empty vector or UCK1 shRNA at D7 after infection. BrdU and 7-AAD staining were used to characterize the cell cycle status of different cells. The images shown here are from a representative experiment from three biological replicates. G . Immortalized melanocytes infected with a dox-inducible vector (pCW57.1) to express RAPGEF1 were seeded after infection and drug selection. Dox-treated cells were treated with 200ng/mL dox at seeding (D0) and cells were fixed and stained with crystal violet at multiple timepoints after seeding. Crystal violet was then solubilized from stained cells and measured by OD560. OD560 values were normalized to the reading of D1 and the mean of 12 biological replicates and SEM were plotted. P -value was calculated using two-way ANOVA. H . Western blot for RAPGEF1 in dox-treated immortalized melanocytes. Whole cell extract was collected 48 hours post-dox treatment at D7 after infection.

    Journal: American journal of human genetics

    Article Title: Functional characterization of the 9q34.13 locus identifies RAPGEF1 as a candidate gene modulating risk for melanoma and nevi via RAS activation

    doi: 10.1016/j.ajhg.2026.08.014

    Figure Lengend Snippet: A . Crystal violet assays following RAPGEF1 knockdown in immortalized melanocytes. Equal numbers of cells either infected with two RAPGEF1 shRNAs or vector control were seeded after infection and drug selection. Cells were fixed and stained with crystal violet at multiple timepoints after seeding. Crystal violet was then solubilized from stained cells and measured by OD560. OD560 values were normalized to the reading at D1, and the mean of six biological replicates and SEM were plotted. P -value was calculated from two-way ANOVA; B . Quantitative RT-PCR for RAPGEF1 in immortalized melanocytes following infection with shRNAs targeting RAPGEF1 relative to empty vector control. RNA was collected and assayed at D5 after infection. C . FACS analysis of immortalized melanocytes infected with either empty vector or RAPGEF1 shRNA at D5 after infection. BrdU and 7-AAD staining were used to characterize the cell cycle status of different cells. The images shown here are from a representative experiment from three biological replicates. D . Crystal violet assays following UCK1 knockdown in immortalized melanocytes. Equal numbers of cells either infected with two UCK1 shRNAs or vector control were seeded after infection and drug selection. Cells were fixed and stained with crystal violet at multiple timepoints after seeding. Crystal violet was then solubilized from stained cells and measured by OD560. OD560 values were normalized to the reading at D1, and the mean of six biological replicates and SEM were plotted. P -value was calculated from two-way ANOVA. E . Quantitative RT-PCR for UCK1 in immortalized melanocytes following infection with shRNAs targeting UCK1 relative to empty vector control. RNA was collected and assayed at D7 after infection F . FACS analysis of immortalized melanocytes infected with either empty vector or UCK1 shRNA at D7 after infection. BrdU and 7-AAD staining were used to characterize the cell cycle status of different cells. The images shown here are from a representative experiment from three biological replicates. G . Immortalized melanocytes infected with a dox-inducible vector (pCW57.1) to express RAPGEF1 were seeded after infection and drug selection. Dox-treated cells were treated with 200ng/mL dox at seeding (D0) and cells were fixed and stained with crystal violet at multiple timepoints after seeding. Crystal violet was then solubilized from stained cells and measured by OD560. OD560 values were normalized to the reading of D1 and the mean of 12 biological replicates and SEM were plotted. P -value was calculated using two-way ANOVA. H . Western blot for RAPGEF1 in dox-treated immortalized melanocytes. Whole cell extract was collected 48 hours post-dox treatment at D7 after infection.

    Article Snippet: Melanocytes were grown in Dermal Cell Basal Medium (American Type Culture Collection/ATCC PCS-200-030) supplemented with Melanocyte Growth Kit (ATCC PCS-200-041) and 1% amphotericin B/penicillin/streptomycin (120-096-711, Quality Biological) at 37°C with 5% CO 2 .

    Techniques: Knockdown, Infection, Plasmid Preparation, Control, Selection, Staining, Quantitative RT-PCR, Analysis, shRNA, Western Blot

    A . Immortalized melanocytes (p’mel cells) expressing constitutively active BRAF p.Val600Glu were infected with empty pLX304 vector or constructs expressing different proteins and seeded in soft-agar plates after blasticidin selection. Images were taken between week 4-5 after plating, and colonies were counted from two sets of triplicates ( n = 6), with counts from each individual replicate shown as a dot. Whiskers show mean with SEM. P -values were calculated using two-tailed, unpaired Student’s t-test. Significance is shown only for comparisons with the empty vector control and RAPGEF1 overexpression. B . Representative images of colonies are shown. The same magnification (4x) was applied for all the images.

    Journal: American journal of human genetics

    Article Title: Functional characterization of the 9q34.13 locus identifies RAPGEF1 as a candidate gene modulating risk for melanoma and nevi via RAS activation

    doi: 10.1016/j.ajhg.2026.08.014

    Figure Lengend Snippet: A . Immortalized melanocytes (p’mel cells) expressing constitutively active BRAF p.Val600Glu were infected with empty pLX304 vector or constructs expressing different proteins and seeded in soft-agar plates after blasticidin selection. Images were taken between week 4-5 after plating, and colonies were counted from two sets of triplicates ( n = 6), with counts from each individual replicate shown as a dot. Whiskers show mean with SEM. P -values were calculated using two-tailed, unpaired Student’s t-test. Significance is shown only for comparisons with the empty vector control and RAPGEF1 overexpression. B . Representative images of colonies are shown. The same magnification (4x) was applied for all the images.

    Article Snippet: Melanocytes were grown in Dermal Cell Basal Medium (American Type Culture Collection/ATCC PCS-200-030) supplemented with Melanocyte Growth Kit (ATCC PCS-200-041) and 1% amphotericin B/penicillin/streptomycin (120-096-711, Quality Biological) at 37°C with 5% CO 2 .

    Techniques: Colony Assay, Stable Transfection, Expressing, Infection, Plasmid Preparation, Construct, Selection, Two Tailed Test, Control, Over Expression

    C283T immortalized melanocytes with doxycycline-inducible expression of RAPGEF1 were grown in supplement-free medium for 24hrs and subsequently treated with human EGF (hEGF) protein for the indicated time. A . Active GTP-bound RAP1 was pulled down by RalGDS-RBD beads from whole-cell extract. Pull-down and whole-cell (total RAP) fractions were compared by Western blotting with an antibody against RAP1. B . Active GTP-bound RAS was pulled down by Raf-RBD beads, with the pull-down and whole-cell (total RAS) fractions compared by Western blotting with an antibody against RAS. Active and total AKT and ERK were compared via Western blotting. The intensity of the phospho- versus total-AKT and ERK was determined by the ratio of the band intensity. Figures are representative experiments from three biological replicates.

    Journal: American journal of human genetics

    Article Title: Functional characterization of the 9q34.13 locus identifies RAPGEF1 as a candidate gene modulating risk for melanoma and nevi via RAS activation

    doi: 10.1016/j.ajhg.2026.08.014

    Figure Lengend Snippet: C283T immortalized melanocytes with doxycycline-inducible expression of RAPGEF1 were grown in supplement-free medium for 24hrs and subsequently treated with human EGF (hEGF) protein for the indicated time. A . Active GTP-bound RAP1 was pulled down by RalGDS-RBD beads from whole-cell extract. Pull-down and whole-cell (total RAP) fractions were compared by Western blotting with an antibody against RAP1. B . Active GTP-bound RAS was pulled down by Raf-RBD beads, with the pull-down and whole-cell (total RAS) fractions compared by Western blotting with an antibody against RAS. Active and total AKT and ERK were compared via Western blotting. The intensity of the phospho- versus total-AKT and ERK was determined by the ratio of the band intensity. Figures are representative experiments from three biological replicates.

    Article Snippet: Melanocytes were grown in Dermal Cell Basal Medium (American Type Culture Collection/ATCC PCS-200-030) supplemented with Melanocyte Growth Kit (ATCC PCS-200-041) and 1% amphotericin B/penicillin/streptomycin (120-096-711, Quality Biological) at 37°C with 5% CO 2 .

    Techniques: Activation Assay, Expressing, Pull Down Assay, Western Blot