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sh sy5y cells  (Elabscience Biotechnology)


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    Elabscience Biotechnology sh sy5y cells
    A Sanger sequencing electropherograms showing predicted CRISPR-Cas9 cut site in wild type HPDL sequence (from <t>E.V.</t> <t>SH-SY5Y</t> cells) and c.318delC mutation in after cutting (in KO cells). B WB analysis shows the presence of full length HPDL protein in WT and E.V. SH-SY5Y cell lines and absence in HPDL KO SH-SY5Y cells. C BN-PAGE blots exhibiting the decrease in the levels of RCSs, individual complexes IV (CIV), and dimeric complex V, while no changes are found in complex II (CII). Bar plots indicate the significant decrease of RCS(CI), RCS(CIII 2 ), and RCS(CIII 2 )/CIII 2 and the proportional increase of CIII 2 in HPDL KO SH-SY5Y cells compared to E.V. ones. All data in bar plots are represented as mean ± SD ( N = 3 for each line). (*), aspecific band. All gels are cropped from the original one. D Gel images of loading control and corresponding bar plots show the significant reduction of NDUFB8 and COXII, while no changes were detected in the levels of SDHA, UQCRC2, and ATP5A. All data in bar plots are normalized to the mitochondrial protein VDAC1 and represented as mean ± SD ( N = 3 for each line). E Bar plots show comparison of ROS species in basal and oxidative (OX) stress conditions, demonstrating an increase in OX stress conditions in HPDL KO compared to E.V. lines. All data in bar plots are represented as mean ± SD ( N = 12 for each line). F Volcano plot showing dysregulated expression of genes in HPDL KO compared to E.V. cells. In evidence (purple), genes involved in oxidative metabolism, such as response to oxygen levels, reactive oxygen species biosynthetic process, and NAD metabolic processes.
    Sh Sy5y Cells, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 99/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/shsy+5y+cell+line/pmc12948981-227-12-24?v=Elabscience+Biotechnology
    Average 99 stars, based on 5 article reviews
    sh sy5y cells - by Bioz Stars, 2026-08
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    Images

    1) Product Images from "Loss of function variants in HPDL impair human cortical development via alterations of mitochondrial function"

    Article Title: Loss of function variants in HPDL impair human cortical development via alterations of mitochondrial function

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-026-08476-9

    A Sanger sequencing electropherograms showing predicted CRISPR-Cas9 cut site in wild type HPDL sequence (from E.V. SH-SY5Y cells) and c.318delC mutation in after cutting (in KO cells). B WB analysis shows the presence of full length HPDL protein in WT and E.V. SH-SY5Y cell lines and absence in HPDL KO SH-SY5Y cells. C BN-PAGE blots exhibiting the decrease in the levels of RCSs, individual complexes IV (CIV), and dimeric complex V, while no changes are found in complex II (CII). Bar plots indicate the significant decrease of RCS(CI), RCS(CIII 2 ), and RCS(CIII 2 )/CIII 2 and the proportional increase of CIII 2 in HPDL KO SH-SY5Y cells compared to E.V. ones. All data in bar plots are represented as mean ± SD ( N = 3 for each line). (*), aspecific band. All gels are cropped from the original one. D Gel images of loading control and corresponding bar plots show the significant reduction of NDUFB8 and COXII, while no changes were detected in the levels of SDHA, UQCRC2, and ATP5A. All data in bar plots are normalized to the mitochondrial protein VDAC1 and represented as mean ± SD ( N = 3 for each line). E Bar plots show comparison of ROS species in basal and oxidative (OX) stress conditions, demonstrating an increase in OX stress conditions in HPDL KO compared to E.V. lines. All data in bar plots are represented as mean ± SD ( N = 12 for each line). F Volcano plot showing dysregulated expression of genes in HPDL KO compared to E.V. cells. In evidence (purple), genes involved in oxidative metabolism, such as response to oxygen levels, reactive oxygen species biosynthetic process, and NAD metabolic processes.
    Figure Legend Snippet: A Sanger sequencing electropherograms showing predicted CRISPR-Cas9 cut site in wild type HPDL sequence (from E.V. SH-SY5Y cells) and c.318delC mutation in after cutting (in KO cells). B WB analysis shows the presence of full length HPDL protein in WT and E.V. SH-SY5Y cell lines and absence in HPDL KO SH-SY5Y cells. C BN-PAGE blots exhibiting the decrease in the levels of RCSs, individual complexes IV (CIV), and dimeric complex V, while no changes are found in complex II (CII). Bar plots indicate the significant decrease of RCS(CI), RCS(CIII 2 ), and RCS(CIII 2 )/CIII 2 and the proportional increase of CIII 2 in HPDL KO SH-SY5Y cells compared to E.V. ones. All data in bar plots are represented as mean ± SD ( N = 3 for each line). (*), aspecific band. All gels are cropped from the original one. D Gel images of loading control and corresponding bar plots show the significant reduction of NDUFB8 and COXII, while no changes were detected in the levels of SDHA, UQCRC2, and ATP5A. All data in bar plots are normalized to the mitochondrial protein VDAC1 and represented as mean ± SD ( N = 3 for each line). E Bar plots show comparison of ROS species in basal and oxidative (OX) stress conditions, demonstrating an increase in OX stress conditions in HPDL KO compared to E.V. lines. All data in bar plots are represented as mean ± SD ( N = 12 for each line). F Volcano plot showing dysregulated expression of genes in HPDL KO compared to E.V. cells. In evidence (purple), genes involved in oxidative metabolism, such as response to oxygen levels, reactive oxygen species biosynthetic process, and NAD metabolic processes.

    Techniques Used: Sequencing, CRISPR, Mutagenesis, Control, Comparison, Expressing



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    Elabscience Biotechnology sh sy5y cells
    A Sanger sequencing electropherograms showing predicted CRISPR-Cas9 cut site in wild type HPDL sequence (from <t>E.V.</t> <t>SH-SY5Y</t> cells) and c.318delC mutation in after cutting (in KO cells). B WB analysis shows the presence of full length HPDL protein in WT and E.V. SH-SY5Y cell lines and absence in HPDL KO SH-SY5Y cells. C BN-PAGE blots exhibiting the decrease in the levels of RCSs, individual complexes IV (CIV), and dimeric complex V, while no changes are found in complex II (CII). Bar plots indicate the significant decrease of RCS(CI), RCS(CIII 2 ), and RCS(CIII 2 )/CIII 2 and the proportional increase of CIII 2 in HPDL KO SH-SY5Y cells compared to E.V. ones. All data in bar plots are represented as mean ± SD ( N = 3 for each line). (*), aspecific band. All gels are cropped from the original one. D Gel images of loading control and corresponding bar plots show the significant reduction of NDUFB8 and COXII, while no changes were detected in the levels of SDHA, UQCRC2, and ATP5A. All data in bar plots are normalized to the mitochondrial protein VDAC1 and represented as mean ± SD ( N = 3 for each line). E Bar plots show comparison of ROS species in basal and oxidative (OX) stress conditions, demonstrating an increase in OX stress conditions in HPDL KO compared to E.V. lines. All data in bar plots are represented as mean ± SD ( N = 12 for each line). F Volcano plot showing dysregulated expression of genes in HPDL KO compared to E.V. cells. In evidence (purple), genes involved in oxidative metabolism, such as response to oxygen levels, reactive oxygen species biosynthetic process, and NAD metabolic processes.
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    A Sanger sequencing electropherograms showing predicted CRISPR-Cas9 cut site in wild type HPDL sequence (from <t>E.V.</t> <t>SH-SY5Y</t> cells) and c.318delC mutation in after cutting (in KO cells). B WB analysis shows the presence of full length HPDL protein in WT and E.V. SH-SY5Y cell lines and absence in HPDL KO SH-SY5Y cells. C BN-PAGE blots exhibiting the decrease in the levels of RCSs, individual complexes IV (CIV), and dimeric complex V, while no changes are found in complex II (CII). Bar plots indicate the significant decrease of RCS(CI), RCS(CIII 2 ), and RCS(CIII 2 )/CIII 2 and the proportional increase of CIII 2 in HPDL KO SH-SY5Y cells compared to E.V. ones. All data in bar plots are represented as mean ± SD ( N = 3 for each line). (*), aspecific band. All gels are cropped from the original one. D Gel images of loading control and corresponding bar plots show the significant reduction of NDUFB8 and COXII, while no changes were detected in the levels of SDHA, UQCRC2, and ATP5A. All data in bar plots are normalized to the mitochondrial protein VDAC1 and represented as mean ± SD ( N = 3 for each line). E Bar plots show comparison of ROS species in basal and oxidative (OX) stress conditions, demonstrating an increase in OX stress conditions in HPDL KO compared to E.V. lines. All data in bar plots are represented as mean ± SD ( N = 12 for each line). F Volcano plot showing dysregulated expression of genes in HPDL KO compared to E.V. cells. In evidence (purple), genes involved in oxidative metabolism, such as response to oxygen levels, reactive oxygen species biosynthetic process, and NAD metabolic processes.
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    A Sanger sequencing electropherograms showing predicted CRISPR-Cas9 cut site in wild type HPDL sequence (from <t>E.V.</t> <t>SH-SY5Y</t> cells) and c.318delC mutation in after cutting (in KO cells). B WB analysis shows the presence of full length HPDL protein in WT and E.V. SH-SY5Y cell lines and absence in HPDL KO SH-SY5Y cells. C BN-PAGE blots exhibiting the decrease in the levels of RCSs, individual complexes IV (CIV), and dimeric complex V, while no changes are found in complex II (CII). Bar plots indicate the significant decrease of RCS(CI), RCS(CIII 2 ), and RCS(CIII 2 )/CIII 2 and the proportional increase of CIII 2 in HPDL KO SH-SY5Y cells compared to E.V. ones. All data in bar plots are represented as mean ± SD ( N = 3 for each line). (*), aspecific band. All gels are cropped from the original one. D Gel images of loading control and corresponding bar plots show the significant reduction of NDUFB8 and COXII, while no changes were detected in the levels of SDHA, UQCRC2, and ATP5A. All data in bar plots are normalized to the mitochondrial protein VDAC1 and represented as mean ± SD ( N = 3 for each line). E Bar plots show comparison of ROS species in basal and oxidative (OX) stress conditions, demonstrating an increase in OX stress conditions in HPDL KO compared to E.V. lines. All data in bar plots are represented as mean ± SD ( N = 12 for each line). F Volcano plot showing dysregulated expression of genes in HPDL KO compared to E.V. cells. In evidence (purple), genes involved in oxidative metabolism, such as response to oxygen levels, reactive oxygen species biosynthetic process, and NAD metabolic processes.
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    A Sanger sequencing electropherograms showing predicted CRISPR-Cas9 cut site in wild type HPDL sequence (from <t>E.V.</t> <t>SH-SY5Y</t> cells) and c.318delC mutation in after cutting (in KO cells). B WB analysis shows the presence of full length HPDL protein in WT and E.V. SH-SY5Y cell lines and absence in HPDL KO SH-SY5Y cells. C BN-PAGE blots exhibiting the decrease in the levels of RCSs, individual complexes IV (CIV), and dimeric complex V, while no changes are found in complex II (CII). Bar plots indicate the significant decrease of RCS(CI), RCS(CIII 2 ), and RCS(CIII 2 )/CIII 2 and the proportional increase of CIII 2 in HPDL KO SH-SY5Y cells compared to E.V. ones. All data in bar plots are represented as mean ± SD ( N = 3 for each line). (*), aspecific band. All gels are cropped from the original one. D Gel images of loading control and corresponding bar plots show the significant reduction of NDUFB8 and COXII, while no changes were detected in the levels of SDHA, UQCRC2, and ATP5A. All data in bar plots are normalized to the mitochondrial protein VDAC1 and represented as mean ± SD ( N = 3 for each line). E Bar plots show comparison of ROS species in basal and oxidative (OX) stress conditions, demonstrating an increase in OX stress conditions in HPDL KO compared to E.V. lines. All data in bar plots are represented as mean ± SD ( N = 12 for each line). F Volcano plot showing dysregulated expression of genes in HPDL KO compared to E.V. cells. In evidence (purple), genes involved in oxidative metabolism, such as response to oxygen levels, reactive oxygen species biosynthetic process, and NAD metabolic processes.
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    A Sanger sequencing electropherograms showing predicted CRISPR-Cas9 cut site in wild type HPDL sequence (from <t>E.V.</t> <t>SH-SY5Y</t> cells) and c.318delC mutation in after cutting (in KO cells). B WB analysis shows the presence of full length HPDL protein in WT and E.V. SH-SY5Y cell lines and absence in HPDL KO SH-SY5Y cells. C BN-PAGE blots exhibiting the decrease in the levels of RCSs, individual complexes IV (CIV), and dimeric complex V, while no changes are found in complex II (CII). Bar plots indicate the significant decrease of RCS(CI), RCS(CIII 2 ), and RCS(CIII 2 )/CIII 2 and the proportional increase of CIII 2 in HPDL KO SH-SY5Y cells compared to E.V. ones. All data in bar plots are represented as mean ± SD ( N = 3 for each line). (*), aspecific band. All gels are cropped from the original one. D Gel images of loading control and corresponding bar plots show the significant reduction of NDUFB8 and COXII, while no changes were detected in the levels of SDHA, UQCRC2, and ATP5A. All data in bar plots are normalized to the mitochondrial protein VDAC1 and represented as mean ± SD ( N = 3 for each line). E Bar plots show comparison of ROS species in basal and oxidative (OX) stress conditions, demonstrating an increase in OX stress conditions in HPDL KO compared to E.V. lines. All data in bar plots are represented as mean ± SD ( N = 12 for each line). F Volcano plot showing dysregulated expression of genes in HPDL KO compared to E.V. cells. In evidence (purple), genes involved in oxidative metabolism, such as response to oxygen levels, reactive oxygen species biosynthetic process, and NAD metabolic processes.
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    A Sanger sequencing electropherograms showing predicted CRISPR-Cas9 cut site in wild type HPDL sequence (from <t>E.V.</t> <t>SH-SY5Y</t> cells) and c.318delC mutation in after cutting (in KO cells). B WB analysis shows the presence of full length HPDL protein in WT and E.V. SH-SY5Y cell lines and absence in HPDL KO SH-SY5Y cells. C BN-PAGE blots exhibiting the decrease in the levels of RCSs, individual complexes IV (CIV), and dimeric complex V, while no changes are found in complex II (CII). Bar plots indicate the significant decrease of RCS(CI), RCS(CIII 2 ), and RCS(CIII 2 )/CIII 2 and the proportional increase of CIII 2 in HPDL KO SH-SY5Y cells compared to E.V. ones. All data in bar plots are represented as mean ± SD ( N = 3 for each line). (*), aspecific band. All gels are cropped from the original one. D Gel images of loading control and corresponding bar plots show the significant reduction of NDUFB8 and COXII, while no changes were detected in the levels of SDHA, UQCRC2, and ATP5A. All data in bar plots are normalized to the mitochondrial protein VDAC1 and represented as mean ± SD ( N = 3 for each line). E Bar plots show comparison of ROS species in basal and oxidative (OX) stress conditions, demonstrating an increase in OX stress conditions in HPDL KO compared to E.V. lines. All data in bar plots are represented as mean ± SD ( N = 12 for each line). F Volcano plot showing dysregulated expression of genes in HPDL KO compared to E.V. cells. In evidence (purple), genes involved in oxidative metabolism, such as response to oxygen levels, reactive oxygen species biosynthetic process, and NAD metabolic processes.
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    A Sanger sequencing electropherograms showing predicted CRISPR-Cas9 cut site in wild type HPDL sequence (from <t>E.V.</t> <t>SH-SY5Y</t> cells) and c.318delC mutation in after cutting (in KO cells). B WB analysis shows the presence of full length HPDL protein in WT and E.V. SH-SY5Y cell lines and absence in HPDL KO SH-SY5Y cells. C BN-PAGE blots exhibiting the decrease in the levels of RCSs, individual complexes IV (CIV), and dimeric complex V, while no changes are found in complex II (CII). Bar plots indicate the significant decrease of RCS(CI), RCS(CIII 2 ), and RCS(CIII 2 )/CIII 2 and the proportional increase of CIII 2 in HPDL KO SH-SY5Y cells compared to E.V. ones. All data in bar plots are represented as mean ± SD ( N = 3 for each line). (*), aspecific band. All gels are cropped from the original one. D Gel images of loading control and corresponding bar plots show the significant reduction of NDUFB8 and COXII, while no changes were detected in the levels of SDHA, UQCRC2, and ATP5A. All data in bar plots are normalized to the mitochondrial protein VDAC1 and represented as mean ± SD ( N = 3 for each line). E Bar plots show comparison of ROS species in basal and oxidative (OX) stress conditions, demonstrating an increase in OX stress conditions in HPDL KO compared to E.V. lines. All data in bar plots are represented as mean ± SD ( N = 12 for each line). F Volcano plot showing dysregulated expression of genes in HPDL KO compared to E.V. cells. In evidence (purple), genes involved in oxidative metabolism, such as response to oxygen levels, reactive oxygen species biosynthetic process, and NAD metabolic processes.
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    shsy 5y cell lines  (ATCC)
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    ATCC shsy 5y cell lines
    A Sanger sequencing electropherograms showing predicted CRISPR-Cas9 cut site in wild type HPDL sequence (from <t>E.V.</t> <t>SH-SY5Y</t> cells) and c.318delC mutation in after cutting (in KO cells). B WB analysis shows the presence of full length HPDL protein in WT and E.V. SH-SY5Y cell lines and absence in HPDL KO SH-SY5Y cells. C BN-PAGE blots exhibiting the decrease in the levels of RCSs, individual complexes IV (CIV), and dimeric complex V, while no changes are found in complex II (CII). Bar plots indicate the significant decrease of RCS(CI), RCS(CIII 2 ), and RCS(CIII 2 )/CIII 2 and the proportional increase of CIII 2 in HPDL KO SH-SY5Y cells compared to E.V. ones. All data in bar plots are represented as mean ± SD ( N = 3 for each line). (*), aspecific band. All gels are cropped from the original one. D Gel images of loading control and corresponding bar plots show the significant reduction of NDUFB8 and COXII, while no changes were detected in the levels of SDHA, UQCRC2, and ATP5A. All data in bar plots are normalized to the mitochondrial protein VDAC1 and represented as mean ± SD ( N = 3 for each line). E Bar plots show comparison of ROS species in basal and oxidative (OX) stress conditions, demonstrating an increase in OX stress conditions in HPDL KO compared to E.V. lines. All data in bar plots are represented as mean ± SD ( N = 12 for each line). F Volcano plot showing dysregulated expression of genes in HPDL KO compared to E.V. cells. In evidence (purple), genes involved in oxidative metabolism, such as response to oxygen levels, reactive oxygen species biosynthetic process, and NAD metabolic processes.
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    Image Search Results


    A Sanger sequencing electropherograms showing predicted CRISPR-Cas9 cut site in wild type HPDL sequence (from E.V. SH-SY5Y cells) and c.318delC mutation in after cutting (in KO cells). B WB analysis shows the presence of full length HPDL protein in WT and E.V. SH-SY5Y cell lines and absence in HPDL KO SH-SY5Y cells. C BN-PAGE blots exhibiting the decrease in the levels of RCSs, individual complexes IV (CIV), and dimeric complex V, while no changes are found in complex II (CII). Bar plots indicate the significant decrease of RCS(CI), RCS(CIII 2 ), and RCS(CIII 2 )/CIII 2 and the proportional increase of CIII 2 in HPDL KO SH-SY5Y cells compared to E.V. ones. All data in bar plots are represented as mean ± SD ( N = 3 for each line). (*), aspecific band. All gels are cropped from the original one. D Gel images of loading control and corresponding bar plots show the significant reduction of NDUFB8 and COXII, while no changes were detected in the levels of SDHA, UQCRC2, and ATP5A. All data in bar plots are normalized to the mitochondrial protein VDAC1 and represented as mean ± SD ( N = 3 for each line). E Bar plots show comparison of ROS species in basal and oxidative (OX) stress conditions, demonstrating an increase in OX stress conditions in HPDL KO compared to E.V. lines. All data in bar plots are represented as mean ± SD ( N = 12 for each line). F Volcano plot showing dysregulated expression of genes in HPDL KO compared to E.V. cells. In evidence (purple), genes involved in oxidative metabolism, such as response to oxygen levels, reactive oxygen species biosynthetic process, and NAD metabolic processes.

    Journal: Cell Death & Disease

    Article Title: Loss of function variants in HPDL impair human cortical development via alterations of mitochondrial function

    doi: 10.1038/s41419-026-08476-9

    Figure Lengend Snippet: A Sanger sequencing electropherograms showing predicted CRISPR-Cas9 cut site in wild type HPDL sequence (from E.V. SH-SY5Y cells) and c.318delC mutation in after cutting (in KO cells). B WB analysis shows the presence of full length HPDL protein in WT and E.V. SH-SY5Y cell lines and absence in HPDL KO SH-SY5Y cells. C BN-PAGE blots exhibiting the decrease in the levels of RCSs, individual complexes IV (CIV), and dimeric complex V, while no changes are found in complex II (CII). Bar plots indicate the significant decrease of RCS(CI), RCS(CIII 2 ), and RCS(CIII 2 )/CIII 2 and the proportional increase of CIII 2 in HPDL KO SH-SY5Y cells compared to E.V. ones. All data in bar plots are represented as mean ± SD ( N = 3 for each line). (*), aspecific band. All gels are cropped from the original one. D Gel images of loading control and corresponding bar plots show the significant reduction of NDUFB8 and COXII, while no changes were detected in the levels of SDHA, UQCRC2, and ATP5A. All data in bar plots are normalized to the mitochondrial protein VDAC1 and represented as mean ± SD ( N = 3 for each line). E Bar plots show comparison of ROS species in basal and oxidative (OX) stress conditions, demonstrating an increase in OX stress conditions in HPDL KO compared to E.V. lines. All data in bar plots are represented as mean ± SD ( N = 12 for each line). F Volcano plot showing dysregulated expression of genes in HPDL KO compared to E.V. cells. In evidence (purple), genes involved in oxidative metabolism, such as response to oxygen levels, reactive oxygen species biosynthetic process, and NAD metabolic processes.

    Article Snippet: To prompt metabolic switching from glycolysis to respiration without affecting cell viability, SH-SY5Y cells were grown for 48 h in DMEM/F12 no glucose (PM150322, Elabscience), supplemented with 2 mM D-Glucose (16325, Riedel-de Haen), 15% FBS, 2mM L-glutamine (25030081, Thermo Fisher Scientific) and 100 μg/ml Pen/Strep (OxPhos medium).

    Techniques: Sequencing, CRISPR, Mutagenesis, Control, Comparison, Expressing