proteintech 11802 1 ap iab Search Results


96
Proteintech proteintech 11802 1 ap iab
Proteintech 11802 1 Ap Iab, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Santa Cruz Biotechnology tom20
TAX1BP1 ubiquitination does not direct the autophagy adaptor to proteasomal degradation. WT-Parkin HeLa cells were transfected with HIS-tagged TAX1BP1 and subjected to mitochondrial depolarization for the indicated time points, in the presence (+) or absence (-) of the proteasomal inhibitior MG132. Mitophagy was confirmed by probing for the immediate-early protasome substrate MFN1 and the later autophagy substrate <t>TOM20.</t> Vinculin served as loading control.
Tom20, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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90
ABclonal Biotechnology anti-sirt7
TAX1BP1 ubiquitination does not direct the autophagy adaptor to proteasomal degradation. WT-Parkin HeLa cells were transfected with HIS-tagged TAX1BP1 and subjected to mitochondrial depolarization for the indicated time points, in the presence (+) or absence (-) of the proteasomal inhibitior MG132. Mitophagy was confirmed by probing for the immediate-early protasome substrate MFN1 and the later autophagy substrate <t>TOM20.</t> Vinculin served as loading control.
Anti Sirt7, supplied by ABclonal Biotechnology, 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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Santa Cruz Biotechnology antibody anti-sox2
TAX1BP1 ubiquitination does not direct the autophagy adaptor to proteasomal degradation. WT-Parkin HeLa cells were transfected with HIS-tagged TAX1BP1 and subjected to mitochondrial depolarization for the indicated time points, in the presence (+) or absence (-) of the proteasomal inhibitior MG132. Mitophagy was confirmed by probing for the immediate-early protasome substrate MFN1 and the later autophagy substrate <t>TOM20.</t> Vinculin served as loading control.
Antibody Anti Sox2, supplied by Santa Cruz Biotechnology, 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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90
Proteintech antibody anti-ho-1
TAX1BP1 ubiquitination does not direct the autophagy adaptor to proteasomal degradation. WT-Parkin HeLa cells were transfected with HIS-tagged TAX1BP1 and subjected to mitochondrial depolarization for the indicated time points, in the presence (+) or absence (-) of the proteasomal inhibitior MG132. Mitophagy was confirmed by probing for the immediate-early protasome substrate MFN1 and the later autophagy substrate <t>TOM20.</t> Vinculin served as loading control.
Antibody Anti Ho 1, supplied by Proteintech, 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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Cell Signaling Technology Inc anti mouse igg
TAX1BP1 ubiquitination does not direct the autophagy adaptor to proteasomal degradation. WT-Parkin HeLa cells were transfected with HIS-tagged TAX1BP1 and subjected to mitochondrial depolarization for the indicated time points, in the presence (+) or absence (-) of the proteasomal inhibitior MG132. Mitophagy was confirmed by probing for the immediate-early protasome substrate MFN1 and the later autophagy substrate <t>TOM20.</t> Vinculin served as loading control.
Anti Mouse Igg, supplied by Cell Signaling Technology Inc, 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/result/anti mouse igg/product/Cell Signaling Technology Inc
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90
Proteintech tom20 11802-1-ap antibody
TAX1BP1 ubiquitination does not direct the autophagy adaptor to proteasomal degradation. WT-Parkin HeLa cells were transfected with HIS-tagged TAX1BP1 and subjected to mitochondrial depolarization for the indicated time points, in the presence (+) or absence (-) of the proteasomal inhibitior MG132. Mitophagy was confirmed by probing for the immediate-early protasome substrate MFN1 and the later autophagy substrate <t>TOM20.</t> Vinculin served as loading control.
Tom20 11802 1 Ap Antibody, supplied by Proteintech, 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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96
Proteintech antitom20
TAX1BP1 ubiquitination does not direct the autophagy adaptor to proteasomal degradation. WT-Parkin HeLa cells were transfected with HIS-tagged TAX1BP1 and subjected to mitochondrial depolarization for the indicated time points, in the presence (+) or absence (-) of the proteasomal inhibitior MG132. Mitophagy was confirmed by probing for the immediate-early protasome substrate MFN1 and the later autophagy substrate <t>TOM20.</t> Vinculin served as loading control.
Antitom20, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Proteintech tim23
TAX1BP1 ubiquitination does not direct the autophagy adaptor to proteasomal degradation. WT-Parkin HeLa cells were transfected with HIS-tagged TAX1BP1 and subjected to mitochondrial depolarization for the indicated time points, in the presence (+) or absence (-) of the proteasomal inhibitior MG132. Mitophagy was confirmed by probing for the immediate-early protasome substrate MFN1 and the later autophagy substrate <t>TOM20.</t> Vinculin served as loading control.
Tim23, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Proteintech antitomm20
TAX1BP1 ubiquitination does not direct the autophagy adaptor to proteasomal degradation. WT-Parkin HeLa cells were transfected with HIS-tagged TAX1BP1 and subjected to mitochondrial depolarization for the indicated time points, in the presence (+) or absence (-) of the proteasomal inhibitior MG132. Mitophagy was confirmed by probing for the immediate-early protasome substrate MFN1 and the later autophagy substrate <t>TOM20.</t> Vinculin served as loading control.
Antitomm20, supplied by Proteintech, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Proteintech tom20 polyclonal antibody 11802-1
TAX1BP1 ubiquitination does not direct the autophagy adaptor to proteasomal degradation. WT-Parkin HeLa cells were transfected with HIS-tagged TAX1BP1 and subjected to mitochondrial depolarization for the indicated time points, in the presence (+) or absence (-) of the proteasomal inhibitior MG132. Mitophagy was confirmed by probing for the immediate-early protasome substrate MFN1 and the later autophagy substrate <t>TOM20.</t> Vinculin served as loading control.
Tom20 Polyclonal Antibody 11802 1, supplied by Proteintech, 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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96
Proteintech membrane 20
TAX1BP1 ubiquitination does not direct the autophagy adaptor to proteasomal degradation. WT-Parkin HeLa cells were transfected with HIS-tagged TAX1BP1 and subjected to mitochondrial depolarization for the indicated time points, in the presence (+) or absence (-) of the proteasomal inhibitior MG132. Mitophagy was confirmed by probing for the immediate-early protasome substrate MFN1 and the later autophagy substrate <t>TOM20.</t> Vinculin served as loading control.
Membrane 20, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


TAX1BP1 ubiquitination does not direct the autophagy adaptor to proteasomal degradation. WT-Parkin HeLa cells were transfected with HIS-tagged TAX1BP1 and subjected to mitochondrial depolarization for the indicated time points, in the presence (+) or absence (-) of the proteasomal inhibitior MG132. Mitophagy was confirmed by probing for the immediate-early protasome substrate MFN1 and the later autophagy substrate TOM20. Vinculin served as loading control.

Journal: bioRxiv

Article Title: Parkin-dependent ubiquitination of TAX1BP1 directs efficient autophagic removal of defective mitochondria

doi: 10.1101/2025.05.16.654474

Figure Lengend Snippet: TAX1BP1 ubiquitination does not direct the autophagy adaptor to proteasomal degradation. WT-Parkin HeLa cells were transfected with HIS-tagged TAX1BP1 and subjected to mitochondrial depolarization for the indicated time points, in the presence (+) or absence (-) of the proteasomal inhibitior MG132. Mitophagy was confirmed by probing for the immediate-early protasome substrate MFN1 and the later autophagy substrate TOM20. Vinculin served as loading control.

Article Snippet: The following primary antibodies were used: Actin (1:50000, Sigma Aldrich, A5441), Calnexin (1:10000, Enzo Life Sciences, ADI-SPA-860), CS (1:6000, GeneTex, GTX110624), Flag-tag (1:10000, Sigma-Aldrich, F1804), LAMP1 (1:10000, DSHB Hybridoma bank, Clone H4A3), LC3B (1:10000, GeneTex, GT3612), LC3B (1:10000, Cell signaling, 835065), MFN1 (1:10000, Abnova, H00055669-M04), NBR1 (1:10000, ProteinTech, 16004-1-AP), NDP52 (1:10000, ProteinTech, 12229-1-AP), OPTN (1:10000, Atlas antibodies, HPA003360), SQSTM1/p62 (1:10000, BD Biosciences, 610832), Parkin (1:50000, Cell signaling, 4211S), TAX1BP1 (1:1000, Novus Biologicals, NBP1-86662), TOM20 (1:30000, Santa Cruz, sc-17764), TOM20 (1:6000, Proteintech, 11802-1-AP), VDAC (1:10000, ProteinTech, 66345-1), VDAC (1:30000, Millipore, AB10527), Vinculin (1:50000, Sigma Aldrich, V9131).

Techniques: Ubiquitin Proteomics, Transfection, Control

( A ) TAX1BP1 siRNA mediated knockdown in WT-Parkin HeLa cells does not impair VDAC and TOM20 degradation upon acute mitochondria depolarization. WT-Parkin HeLa cells were transfected with siRNA against TAX1BP1 for three consecutive days. After the third day, mitochondria were depolarized with CCCP for the indicated time points and protein quantification was performed. ( B ) WT-Parkin HeLa cells were transfected with His-tagged TAX1BP1 for 24h. Further, mitochondria were depolarized with 10 µm CCCP for the indicated time points. Left panel: Representative immunofluorescence images showing SSBP1 (cyan) and TAX1BP1 (yellow) upon mock or HIS-TAX1BP1 transfection after CCCP-mediated depolarization at the indicated time points. Right panel: Reduction of SSBP1 area after TAX1BP1 transfection after short (4h) or extended (14h) CCCP treatment. Scale bars: 5 µm. ( C ) Changes in ubiquitination pattern of His-tagged TAX1BP1 after 4h CCCP in 5KO-PARK HeLa cells.

Journal: bioRxiv

Article Title: Parkin-dependent ubiquitination of TAX1BP1 directs efficient autophagic removal of defective mitochondria

doi: 10.1101/2025.05.16.654474

Figure Lengend Snippet: ( A ) TAX1BP1 siRNA mediated knockdown in WT-Parkin HeLa cells does not impair VDAC and TOM20 degradation upon acute mitochondria depolarization. WT-Parkin HeLa cells were transfected with siRNA against TAX1BP1 for three consecutive days. After the third day, mitochondria were depolarized with CCCP for the indicated time points and protein quantification was performed. ( B ) WT-Parkin HeLa cells were transfected with His-tagged TAX1BP1 for 24h. Further, mitochondria were depolarized with 10 µm CCCP for the indicated time points. Left panel: Representative immunofluorescence images showing SSBP1 (cyan) and TAX1BP1 (yellow) upon mock or HIS-TAX1BP1 transfection after CCCP-mediated depolarization at the indicated time points. Right panel: Reduction of SSBP1 area after TAX1BP1 transfection after short (4h) or extended (14h) CCCP treatment. Scale bars: 5 µm. ( C ) Changes in ubiquitination pattern of His-tagged TAX1BP1 after 4h CCCP in 5KO-PARK HeLa cells.

Article Snippet: The following primary antibodies were used: Actin (1:50000, Sigma Aldrich, A5441), Calnexin (1:10000, Enzo Life Sciences, ADI-SPA-860), CS (1:6000, GeneTex, GTX110624), Flag-tag (1:10000, Sigma-Aldrich, F1804), LAMP1 (1:10000, DSHB Hybridoma bank, Clone H4A3), LC3B (1:10000, GeneTex, GT3612), LC3B (1:10000, Cell signaling, 835065), MFN1 (1:10000, Abnova, H00055669-M04), NBR1 (1:10000, ProteinTech, 16004-1-AP), NDP52 (1:10000, ProteinTech, 12229-1-AP), OPTN (1:10000, Atlas antibodies, HPA003360), SQSTM1/p62 (1:10000, BD Biosciences, 610832), Parkin (1:50000, Cell signaling, 4211S), TAX1BP1 (1:1000, Novus Biologicals, NBP1-86662), TOM20 (1:30000, Santa Cruz, sc-17764), TOM20 (1:6000, Proteintech, 11802-1-AP), VDAC (1:10000, ProteinTech, 66345-1), VDAC (1:30000, Millipore, AB10527), Vinculin (1:50000, Sigma Aldrich, V9131).

Techniques: Knockdown, Transfection, Immunofluorescence, Ubiquitin Proteomics

TAX1BP1 ubiquitination does not direct the autophagy adaptor to proteasomal degradation. WT-Parkin HeLa cells were transfected with HIS-tagged TAX1BP1 and subjected to mitochondrial depolarization for the indicated time points, in the presence (+) or absence (-) of the proteasomal inhibitior MG132. Mitophagy was confirmed by probing for the immediate-early protasome substrate MFN1 and the later autophagy substrate TOM20. Vinculin served as loading control.

Journal: bioRxiv

Article Title: Parkin-dependent ubiquitination of TAX1BP1 directs efficient autophagic removal of defective mitochondria

doi: 10.1101/2025.05.16.654474

Figure Lengend Snippet: TAX1BP1 ubiquitination does not direct the autophagy adaptor to proteasomal degradation. WT-Parkin HeLa cells were transfected with HIS-tagged TAX1BP1 and subjected to mitochondrial depolarization for the indicated time points, in the presence (+) or absence (-) of the proteasomal inhibitior MG132. Mitophagy was confirmed by probing for the immediate-early protasome substrate MFN1 and the later autophagy substrate TOM20. Vinculin served as loading control.

Article Snippet: The following primary antibodies were used: Actin (1:50000, Sigma Aldrich, A5441), Calnexin (1:10000, Enzo Life Sciences, ADI-SPA-860), CS (1:6000, GeneTex, GTX110624), Flag-tag (1:10000, Sigma-Aldrich, F1804), LAMP1 (1:10000, DSHB Hybridoma bank, Clone H4A3), LC3B (1:10000, GeneTex, GT3612), LC3B (1:10000, Cell signaling, 835065), MFN1 (1:10000, Abnova, H00055669-M04), NBR1 (1:10000, ProteinTech, 16004-1-AP), NDP52 (1:10000, ProteinTech, 12229-1-AP), OPTN (1:10000, Atlas antibodies, HPA003360), SQSTM1/p62 (1:10000, BD Biosciences, 610832), Parkin (1:50000, Cell signaling, 4211S), TAX1BP1 (1:1000, Novus Biologicals, NBP1-86662), TOM20 (1:30000, Santa Cruz, sc-17764), TOM20 (1:6000, Proteintech, 11802-1-AP), VDAC (1:10000, ProteinTech, 66345-1), VDAC (1:30000, Millipore, AB10527), Vinculin (1:50000, Sigma Aldrich, V9131).

Techniques: Ubiquitin Proteomics, Transfection, Control

( A ) TAX1BP1 siRNA mediated knockdown in WT-Parkin HeLa cells does not impair VDAC and TOM20 degradation upon acute mitochondria depolarization. WT-Parkin HeLa cells were transfected with siRNA against TAX1BP1 for three consecutive days. After the third day, mitochondria were depolarized with CCCP for the indicated time points and protein quantification was performed. ( B ) WT-Parkin HeLa cells were transfected with His-tagged TAX1BP1 for 24h. Further, mitochondria were depolarized with 10 µm CCCP for the indicated time points. Left panel: Representative immunofluorescence images showing SSBP1 (cyan) and TAX1BP1 (yellow) upon mock or HIS-TAX1BP1 transfection after CCCP-mediated depolarization at the indicated time points. Right panel: Reduction of SSBP1 area after TAX1BP1 transfection after short (4h) or extended (14h) CCCP treatment. Scale bars: 5 µm. ( C ) Changes in ubiquitination pattern of His-tagged TAX1BP1 after 4h CCCP in 5KO-PARK HeLa cells.

Journal: bioRxiv

Article Title: Parkin-dependent ubiquitination of TAX1BP1 directs efficient autophagic removal of defective mitochondria

doi: 10.1101/2025.05.16.654474

Figure Lengend Snippet: ( A ) TAX1BP1 siRNA mediated knockdown in WT-Parkin HeLa cells does not impair VDAC and TOM20 degradation upon acute mitochondria depolarization. WT-Parkin HeLa cells were transfected with siRNA against TAX1BP1 for three consecutive days. After the third day, mitochondria were depolarized with CCCP for the indicated time points and protein quantification was performed. ( B ) WT-Parkin HeLa cells were transfected with His-tagged TAX1BP1 for 24h. Further, mitochondria were depolarized with 10 µm CCCP for the indicated time points. Left panel: Representative immunofluorescence images showing SSBP1 (cyan) and TAX1BP1 (yellow) upon mock or HIS-TAX1BP1 transfection after CCCP-mediated depolarization at the indicated time points. Right panel: Reduction of SSBP1 area after TAX1BP1 transfection after short (4h) or extended (14h) CCCP treatment. Scale bars: 5 µm. ( C ) Changes in ubiquitination pattern of His-tagged TAX1BP1 after 4h CCCP in 5KO-PARK HeLa cells.

Article Snippet: The following primary antibodies were used: Actin (1:50000, Sigma Aldrich, A5441), Calnexin (1:10000, Enzo Life Sciences, ADI-SPA-860), CS (1:6000, GeneTex, GTX110624), Flag-tag (1:10000, Sigma-Aldrich, F1804), LAMP1 (1:10000, DSHB Hybridoma bank, Clone H4A3), LC3B (1:10000, GeneTex, GT3612), LC3B (1:10000, Cell signaling, 835065), MFN1 (1:10000, Abnova, H00055669-M04), NBR1 (1:10000, ProteinTech, 16004-1-AP), NDP52 (1:10000, ProteinTech, 12229-1-AP), OPTN (1:10000, Atlas antibodies, HPA003360), SQSTM1/p62 (1:10000, BD Biosciences, 610832), Parkin (1:50000, Cell signaling, 4211S), TAX1BP1 (1:1000, Novus Biologicals, NBP1-86662), TOM20 (1:30000, Santa Cruz, sc-17764), TOM20 (1:6000, Proteintech, 11802-1-AP), VDAC (1:10000, ProteinTech, 66345-1), VDAC (1:30000, Millipore, AB10527), Vinculin (1:50000, Sigma Aldrich, V9131).

Techniques: Knockdown, Transfection, Immunofluorescence, Ubiquitin Proteomics