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human female bone marrow epithelial sh sy5y cell lines  (ATCC)


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    ATCC human female bone marrow epithelial sh sy5y cell lines
    Ub-PINK1 interacts with VCP. A, Endogenous PINK1 interacting proteins revealed by Coomassie blue-stained SDS-PAGE gel. Endogenous PINK1 and its associated complexes were enriched by IP with anti-PINK1 antibody in HeLa cells. Anti-HA antibody and preimmune IgG (Ctr IgG) were used as controls. Bands labeled 1, 2, and 3 were identified as Ufd2A, VCP, and Npl4, respectively. Individual LC-MS/MS data can be found in Figure 1-1. B, PINK1 and VCP interaction in HEK293T cells cotransfected with WT PINK1 and VCP evidenced by co-IP using either an anti-PINK1 or anti-VCP antibody. *Denotes IgG heavy chain. C, Endogenous PINK1 and VCP interaction in <t>SH-SY5Y</t> cells evidenced by co-IP using anti-VCP-antibody. D, As in B, except that cells were transfected either with WT PINK1 or mutant PINK1K137R. *Denotes IgG heavy chain. E, PINK1 and Ufd2A interaction in HEK293T cells stably-expressing WT PINK1 and transfected with Ufd2A-flag evidenced by IP using an anti-PINK1 antibody. F, Ub-PINK1 IB in WT PINK1 stably-transfected HEK293T cells. Endogenous VCP was efficiently knocked down by VCP shRNAs. G, Ub-PINK1 IB in WT PINK1 stably-transfected HEK293T cells. Endogenous Ufd2A was efficiently knocked down by Ufd2A shRNAs. H, Ub-PINK1 IB in PINK1 stably-transfected HEK293T cells. Endogenous Ufd1 was efficiently knocked down by Ufd1 shRNAs. Data are representative of three independent experiments performed under identical conditions.
    Human Female Bone Marrow Epithelial Sh Sy5y Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 9187 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+female+bone+marrow+epithelial+sh+sy5y+cell+lines/pmc06733537-139-18-28?v=ATCC
    Average 99 stars, based on 9187 article reviews
    human female bone marrow epithelial sh sy5y cell lines - by Bioz Stars, 2026-08
    99/100 stars

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    1) Product Images from "PINK1 Content in Mitochondria is Regulated by ER-Associated Degradation"

    Article Title: PINK1 Content in Mitochondria is Regulated by ER-Associated Degradation

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.1691-18.2019

    Ub-PINK1 interacts with VCP. A, Endogenous PINK1 interacting proteins revealed by Coomassie blue-stained SDS-PAGE gel. Endogenous PINK1 and its associated complexes were enriched by IP with anti-PINK1 antibody in HeLa cells. Anti-HA antibody and preimmune IgG (Ctr IgG) were used as controls. Bands labeled 1, 2, and 3 were identified as Ufd2A, VCP, and Npl4, respectively. Individual LC-MS/MS data can be found in Figure 1-1. B, PINK1 and VCP interaction in HEK293T cells cotransfected with WT PINK1 and VCP evidenced by co-IP using either an anti-PINK1 or anti-VCP antibody. *Denotes IgG heavy chain. C, Endogenous PINK1 and VCP interaction in SH-SY5Y cells evidenced by co-IP using anti-VCP-antibody. D, As in B, except that cells were transfected either with WT PINK1 or mutant PINK1K137R. *Denotes IgG heavy chain. E, PINK1 and Ufd2A interaction in HEK293T cells stably-expressing WT PINK1 and transfected with Ufd2A-flag evidenced by IP using an anti-PINK1 antibody. F, Ub-PINK1 IB in WT PINK1 stably-transfected HEK293T cells. Endogenous VCP was efficiently knocked down by VCP shRNAs. G, Ub-PINK1 IB in WT PINK1 stably-transfected HEK293T cells. Endogenous Ufd2A was efficiently knocked down by Ufd2A shRNAs. H, Ub-PINK1 IB in PINK1 stably-transfected HEK293T cells. Endogenous Ufd1 was efficiently knocked down by Ufd1 shRNAs. Data are representative of three independent experiments performed under identical conditions.
    Figure Legend Snippet: Ub-PINK1 interacts with VCP. A, Endogenous PINK1 interacting proteins revealed by Coomassie blue-stained SDS-PAGE gel. Endogenous PINK1 and its associated complexes were enriched by IP with anti-PINK1 antibody in HeLa cells. Anti-HA antibody and preimmune IgG (Ctr IgG) were used as controls. Bands labeled 1, 2, and 3 were identified as Ufd2A, VCP, and Npl4, respectively. Individual LC-MS/MS data can be found in Figure 1-1. B, PINK1 and VCP interaction in HEK293T cells cotransfected with WT PINK1 and VCP evidenced by co-IP using either an anti-PINK1 or anti-VCP antibody. *Denotes IgG heavy chain. C, Endogenous PINK1 and VCP interaction in SH-SY5Y cells evidenced by co-IP using anti-VCP-antibody. D, As in B, except that cells were transfected either with WT PINK1 or mutant PINK1K137R. *Denotes IgG heavy chain. E, PINK1 and Ufd2A interaction in HEK293T cells stably-expressing WT PINK1 and transfected with Ufd2A-flag evidenced by IP using an anti-PINK1 antibody. F, Ub-PINK1 IB in WT PINK1 stably-transfected HEK293T cells. Endogenous VCP was efficiently knocked down by VCP shRNAs. G, Ub-PINK1 IB in WT PINK1 stably-transfected HEK293T cells. Endogenous Ufd2A was efficiently knocked down by Ufd2A shRNAs. H, Ub-PINK1 IB in PINK1 stably-transfected HEK293T cells. Endogenous Ufd1 was efficiently knocked down by Ufd1 shRNAs. Data are representative of three independent experiments performed under identical conditions.

    Techniques Used: Staining, SDS Page, Labeling, Liquid Chromatography with Mass Spectroscopy, Co-Immunoprecipitation Assay, Transfection, Mutagenesis, Stable Transfection, Expressing

    52 kDa PINK1 interacts with the ERAD machinery. A, PINK1 and Sec61β interaction in WT PINK1 stably-expressing HEK293T cells transfected with Sec61β evidenced by IP using either an anti-PINK1 or anti-Sec61β antibody. *Denotes IgG heavy chain. B, Endogenous PINK1 and Sec61β interaction in SH-SY5Y cells evidenced by IP using an anti-Sec61β antibody. C, WT PINK1 and endogenous gp78 interaction in stably PINK1 expressing HEK293T cells evidenced by co-IP using either an anti-PINK1 or anti-gp78 antibody. D, Ub-PINK1 IB in PINK1 stably-transfected HEK293T cells. Endogenous Sec61β was efficiently knocked down by Sec61β shRNAs. E, Ub-PINK1 IB in PINK1 stably-transfected HEK293T cells. Endogenous gp78 was efficiently knocked down by gp78 shRNA validated by IB. F, Ub-PINK1 IB in Hrd1 deficient HEK293T cells generated by CRISPR that were transfected with WT PINK1. Experiment shown in F was repeated once independently with similar results while those shown in A–E are representative of 3–4 independent experiments performed under identical conditions.
    Figure Legend Snippet: 52 kDa PINK1 interacts with the ERAD machinery. A, PINK1 and Sec61β interaction in WT PINK1 stably-expressing HEK293T cells transfected with Sec61β evidenced by IP using either an anti-PINK1 or anti-Sec61β antibody. *Denotes IgG heavy chain. B, Endogenous PINK1 and Sec61β interaction in SH-SY5Y cells evidenced by IP using an anti-Sec61β antibody. C, WT PINK1 and endogenous gp78 interaction in stably PINK1 expressing HEK293T cells evidenced by co-IP using either an anti-PINK1 or anti-gp78 antibody. D, Ub-PINK1 IB in PINK1 stably-transfected HEK293T cells. Endogenous Sec61β was efficiently knocked down by Sec61β shRNAs. E, Ub-PINK1 IB in PINK1 stably-transfected HEK293T cells. Endogenous gp78 was efficiently knocked down by gp78 shRNA validated by IB. F, Ub-PINK1 IB in Hrd1 deficient HEK293T cells generated by CRISPR that were transfected with WT PINK1. Experiment shown in F was repeated once independently with similar results while those shown in A–E are representative of 3–4 independent experiments performed under identical conditions.

    Techniques Used: Stable Transfection, Expressing, Transfection, Co-Immunoprecipitation Assay, shRNA, Generated, CRISPR



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    human female bone marrow epithelial sh sy5y cell lines  (ATCC)
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    ATCC human female bone marrow epithelial sh sy5y cell lines
    Ub-PINK1 interacts with VCP. A, Endogenous PINK1 interacting proteins revealed by Coomassie blue-stained SDS-PAGE gel. Endogenous PINK1 and its associated complexes were enriched by IP with anti-PINK1 antibody in HeLa cells. Anti-HA antibody and preimmune IgG (Ctr IgG) were used as controls. Bands labeled 1, 2, and 3 were identified as Ufd2A, VCP, and Npl4, respectively. Individual LC-MS/MS data can be found in Figure 1-1. B, PINK1 and VCP interaction in HEK293T cells cotransfected with WT PINK1 and VCP evidenced by co-IP using either an anti-PINK1 or anti-VCP antibody. *Denotes IgG heavy chain. C, Endogenous PINK1 and VCP interaction in <t>SH-SY5Y</t> cells evidenced by co-IP using anti-VCP-antibody. D, As in B, except that cells were transfected either with WT PINK1 or mutant PINK1K137R. *Denotes IgG heavy chain. E, PINK1 and Ufd2A interaction in HEK293T cells stably-expressing WT PINK1 and transfected with Ufd2A-flag evidenced by IP using an anti-PINK1 antibody. F, Ub-PINK1 IB in WT PINK1 stably-transfected HEK293T cells. Endogenous VCP was efficiently knocked down by VCP shRNAs. G, Ub-PINK1 IB in WT PINK1 stably-transfected HEK293T cells. Endogenous Ufd2A was efficiently knocked down by Ufd2A shRNAs. H, Ub-PINK1 IB in PINK1 stably-transfected HEK293T cells. Endogenous Ufd1 was efficiently knocked down by Ufd1 shRNAs. Data are representative of three independent experiments performed under identical conditions.
    Human Female Bone Marrow Epithelial Sh Sy5y Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+female+bone+marrow+epithelial+sh+sy5y+cell+lines/pmc06733537-139-18-28?v=ATCC
    Average 99 stars, based on 1 article reviews
    human female bone marrow epithelial sh sy5y cell lines - by Bioz Stars, 2026-08
    99/100 stars
    		  Buy from Supplier

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    Ub-PINK1 interacts with VCP. A, Endogenous PINK1 interacting proteins revealed by Coomassie blue-stained SDS-PAGE gel. Endogenous PINK1 and its associated complexes were enriched by IP with anti-PINK1 antibody in HeLa cells. Anti-HA antibody and preimmune IgG (Ctr IgG) were used as controls. Bands labeled 1, 2, and 3 were identified as Ufd2A, VCP, and Npl4, respectively. Individual LC-MS/MS data can be found in Figure 1-1. B, PINK1 and VCP interaction in HEK293T cells cotransfected with WT PINK1 and VCP evidenced by co-IP using either an anti-PINK1 or anti-VCP antibody. *Denotes IgG heavy chain. C, Endogenous PINK1 and VCP interaction in SH-SY5Y cells evidenced by co-IP using anti-VCP-antibody. D, As in B, except that cells were transfected either with WT PINK1 or mutant PINK1K137R. *Denotes IgG heavy chain. E, PINK1 and Ufd2A interaction in HEK293T cells stably-expressing WT PINK1 and transfected with Ufd2A-flag evidenced by IP using an anti-PINK1 antibody. F, Ub-PINK1 IB in WT PINK1 stably-transfected HEK293T cells. Endogenous VCP was efficiently knocked down by VCP shRNAs. G, Ub-PINK1 IB in WT PINK1 stably-transfected HEK293T cells. Endogenous Ufd2A was efficiently knocked down by Ufd2A shRNAs. H, Ub-PINK1 IB in PINK1 stably-transfected HEK293T cells. Endogenous Ufd1 was efficiently knocked down by Ufd1 shRNAs. Data are representative of three independent experiments performed under identical conditions.

    Journal: The Journal of Neuroscience

    Article Title: PINK1 Content in Mitochondria is Regulated by ER-Associated Degradation

    doi: 10.1523/JNEUROSCI.1691-18.2019

    Figure Lengend Snippet: Ub-PINK1 interacts with VCP. A, Endogenous PINK1 interacting proteins revealed by Coomassie blue-stained SDS-PAGE gel. Endogenous PINK1 and its associated complexes were enriched by IP with anti-PINK1 antibody in HeLa cells. Anti-HA antibody and preimmune IgG (Ctr IgG) were used as controls. Bands labeled 1, 2, and 3 were identified as Ufd2A, VCP, and Npl4, respectively. Individual LC-MS/MS data can be found in Figure 1-1. B, PINK1 and VCP interaction in HEK293T cells cotransfected with WT PINK1 and VCP evidenced by co-IP using either an anti-PINK1 or anti-VCP antibody. *Denotes IgG heavy chain. C, Endogenous PINK1 and VCP interaction in SH-SY5Y cells evidenced by co-IP using anti-VCP-antibody. D, As in B, except that cells were transfected either with WT PINK1 or mutant PINK1K137R. *Denotes IgG heavy chain. E, PINK1 and Ufd2A interaction in HEK293T cells stably-expressing WT PINK1 and transfected with Ufd2A-flag evidenced by IP using an anti-PINK1 antibody. F, Ub-PINK1 IB in WT PINK1 stably-transfected HEK293T cells. Endogenous VCP was efficiently knocked down by VCP shRNAs. G, Ub-PINK1 IB in WT PINK1 stably-transfected HEK293T cells. Endogenous Ufd2A was efficiently knocked down by Ufd2A shRNAs. H, Ub-PINK1 IB in PINK1 stably-transfected HEK293T cells. Endogenous Ufd1 was efficiently knocked down by Ufd1 shRNAs. Data are representative of three independent experiments performed under identical conditions.

    Article Snippet: Human female embryonic kidney epithelial HEK293T, human female cervical epithelial HeLa, monkey kidney fibroblast COS-7 (unknown sex), and human female bone marrow epithelial SH-SY5Y cell lines were from ATCC and maintained in medium suggested by the provider.

    Techniques: Staining, SDS Page, Labeling, Liquid Chromatography with Mass Spectroscopy, Co-Immunoprecipitation Assay, Transfection, Mutagenesis, Stable Transfection, Expressing

    52 kDa PINK1 interacts with the ERAD machinery. A, PINK1 and Sec61β interaction in WT PINK1 stably-expressing HEK293T cells transfected with Sec61β evidenced by IP using either an anti-PINK1 or anti-Sec61β antibody. *Denotes IgG heavy chain. B, Endogenous PINK1 and Sec61β interaction in SH-SY5Y cells evidenced by IP using an anti-Sec61β antibody. C, WT PINK1 and endogenous gp78 interaction in stably PINK1 expressing HEK293T cells evidenced by co-IP using either an anti-PINK1 or anti-gp78 antibody. D, Ub-PINK1 IB in PINK1 stably-transfected HEK293T cells. Endogenous Sec61β was efficiently knocked down by Sec61β shRNAs. E, Ub-PINK1 IB in PINK1 stably-transfected HEK293T cells. Endogenous gp78 was efficiently knocked down by gp78 shRNA validated by IB. F, Ub-PINK1 IB in Hrd1 deficient HEK293T cells generated by CRISPR that were transfected with WT PINK1. Experiment shown in F was repeated once independently with similar results while those shown in A–E are representative of 3–4 independent experiments performed under identical conditions.

    Journal: The Journal of Neuroscience

    Article Title: PINK1 Content in Mitochondria is Regulated by ER-Associated Degradation

    doi: 10.1523/JNEUROSCI.1691-18.2019

    Figure Lengend Snippet: 52 kDa PINK1 interacts with the ERAD machinery. A, PINK1 and Sec61β interaction in WT PINK1 stably-expressing HEK293T cells transfected with Sec61β evidenced by IP using either an anti-PINK1 or anti-Sec61β antibody. *Denotes IgG heavy chain. B, Endogenous PINK1 and Sec61β interaction in SH-SY5Y cells evidenced by IP using an anti-Sec61β antibody. C, WT PINK1 and endogenous gp78 interaction in stably PINK1 expressing HEK293T cells evidenced by co-IP using either an anti-PINK1 or anti-gp78 antibody. D, Ub-PINK1 IB in PINK1 stably-transfected HEK293T cells. Endogenous Sec61β was efficiently knocked down by Sec61β shRNAs. E, Ub-PINK1 IB in PINK1 stably-transfected HEK293T cells. Endogenous gp78 was efficiently knocked down by gp78 shRNA validated by IB. F, Ub-PINK1 IB in Hrd1 deficient HEK293T cells generated by CRISPR that were transfected with WT PINK1. Experiment shown in F was repeated once independently with similar results while those shown in A–E are representative of 3–4 independent experiments performed under identical conditions.

    Article Snippet: Human female embryonic kidney epithelial HEK293T, human female cervical epithelial HeLa, monkey kidney fibroblast COS-7 (unknown sex), and human female bone marrow epithelial SH-SY5Y cell lines were from ATCC and maintained in medium suggested by the provider.

    Techniques: Stable Transfection, Expressing, Transfection, Co-Immunoprecipitation Assay, shRNA, Generated, CRISPR