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mitochondrial heat shock protein 70  (Proteintech)


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    Structured Review

    Proteintech mitochondrial heat shock protein 70
    Mitochondrial Heat Shock Protein 70, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 81 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mitochondrial+heat+shock+protein+70/GRP75+Antibody/pm37020386-80-60-70
    Average 94 stars, based on 81 article reviews
    mitochondrial heat shock protein 70 - by Bioz Stars, 2026-09
    94/100 stars

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    Related Articles

    Blocking Assay:

    Article Title: TOM complex‐independent transport pathway of myoglobin into mitochondria in C2C12 myotubes
    Article Snippet: .. After blocking, the membranes were washed three times with TBS‐T for 10 min, and then incubated with mouse monoclonal antibodies against α‐tubulin (1:20,000; 66031‐1‐Ig; Proteintech), cytochrome c (Cyt c ; 1:5,000; 66264‐1‐Ig; Proteintech), oxidative phosphorylation complexes (1:1,000; ab110413; abcam), Mb (1:1,000; sc‐393020; Santa Cruz Biotechnology), Tom70 (1:5,000; 66593‐1‐Ig; Proteintech), and apoptosis‐inducing factor (AIF; 1:1,000; sc‐55519; Santa Cruz Biotechnology), and rabbit polyclonal antibodies against Tom20 (1:5,000; 11802‐1‐AP; Proteintech), voltage‐dependent anion channel (VDAC; 1:5,000; 55259‐1‐AP; Proteintech), Tom40 (1:5,000; 18409‐1‐AP; Proteintech), mitochondrial heat shock protein 70 (mtHSP70; 1:5,000; 14887‐1‐AP; Proteintech), COX‐IV (1:1,000; 11242‐1‐AP; Proteintech), and PTEN‐induced kinase 1 (PINK1; 1:1,000; 23274‐1‐AP; Proteintech) overnight at 4°C. ..

    Incubation:

    Article Title: TOM complex‐independent transport pathway of myoglobin into mitochondria in C2C12 myotubes
    Article Snippet: .. After blocking, the membranes were washed three times with TBS‐T for 10 min, and then incubated with mouse monoclonal antibodies against α‐tubulin (1:20,000; 66031‐1‐Ig; Proteintech), cytochrome c (Cyt c ; 1:5,000; 66264‐1‐Ig; Proteintech), oxidative phosphorylation complexes (1:1,000; ab110413; abcam), Mb (1:1,000; sc‐393020; Santa Cruz Biotechnology), Tom70 (1:5,000; 66593‐1‐Ig; Proteintech), and apoptosis‐inducing factor (AIF; 1:1,000; sc‐55519; Santa Cruz Biotechnology), and rabbit polyclonal antibodies against Tom20 (1:5,000; 11802‐1‐AP; Proteintech), voltage‐dependent anion channel (VDAC; 1:5,000; 55259‐1‐AP; Proteintech), Tom40 (1:5,000; 18409‐1‐AP; Proteintech), mitochondrial heat shock protein 70 (mtHSP70; 1:5,000; 14887‐1‐AP; Proteintech), COX‐IV (1:1,000; 11242‐1‐AP; Proteintech), and PTEN‐induced kinase 1 (PINK1; 1:1,000; 23274‐1‐AP; Proteintech) overnight at 4°C. ..

    Bioprocessing:

    Article Title: TOM complex‐independent transport pathway of myoglobin into mitochondria in C2C12 myotubes
    Article Snippet: .. After blocking, the membranes were washed three times with TBS‐T for 10 min, and then incubated with mouse monoclonal antibodies against α‐tubulin (1:20,000; 66031‐1‐Ig; Proteintech), cytochrome c (Cyt c ; 1:5,000; 66264‐1‐Ig; Proteintech), oxidative phosphorylation complexes (1:1,000; ab110413; abcam), Mb (1:1,000; sc‐393020; Santa Cruz Biotechnology), Tom70 (1:5,000; 66593‐1‐Ig; Proteintech), and apoptosis‐inducing factor (AIF; 1:1,000; sc‐55519; Santa Cruz Biotechnology), and rabbit polyclonal antibodies against Tom20 (1:5,000; 11802‐1‐AP; Proteintech), voltage‐dependent anion channel (VDAC; 1:5,000; 55259‐1‐AP; Proteintech), Tom40 (1:5,000; 18409‐1‐AP; Proteintech), mitochondrial heat shock protein 70 (mtHSP70; 1:5,000; 14887‐1‐AP; Proteintech), COX‐IV (1:1,000; 11242‐1‐AP; Proteintech), and PTEN‐induced kinase 1 (PINK1; 1:1,000; 23274‐1‐AP; Proteintech) overnight at 4°C. ..

    Phospho-proteomics:

    Article Title: TOM complex‐independent transport pathway of myoglobin into mitochondria in C2C12 myotubes
    Article Snippet: .. After blocking, the membranes were washed three times with TBS‐T for 10 min, and then incubated with mouse monoclonal antibodies against α‐tubulin (1:20,000; 66031‐1‐Ig; Proteintech), cytochrome c (Cyt c ; 1:5,000; 66264‐1‐Ig; Proteintech), oxidative phosphorylation complexes (1:1,000; ab110413; abcam), Mb (1:1,000; sc‐393020; Santa Cruz Biotechnology), Tom70 (1:5,000; 66593‐1‐Ig; Proteintech), and apoptosis‐inducing factor (AIF; 1:1,000; sc‐55519; Santa Cruz Biotechnology), and rabbit polyclonal antibodies against Tom20 (1:5,000; 11802‐1‐AP; Proteintech), voltage‐dependent anion channel (VDAC; 1:5,000; 55259‐1‐AP; Proteintech), Tom40 (1:5,000; 18409‐1‐AP; Proteintech), mitochondrial heat shock protein 70 (mtHSP70; 1:5,000; 14887‐1‐AP; Proteintech), COX‐IV (1:1,000; 11242‐1‐AP; Proteintech), and PTEN‐induced kinase 1 (PINK1; 1:1,000; 23274‐1‐AP; Proteintech) overnight at 4°C. ..



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    The importance of mitochondrial dysfunction, α-syn aggregation, and the autophagy-endo-lysosomal system dysregulation in PD (Parkinson’s disease) pathogenesis. The clearance of damaged mitochondria and denatured α-synuclein (α-syn) are through autophagy-lysosome pathways. Minor mitochondrial damage is fixed via dynamic fission and fusion, complementing the damaged organelles and mitochondrial proteins. Medium amounts of damaged mitochondrial proteins and mitochondria parts are delivered to the lysosome via mitochondrial-derived vesicles (MDVs). The whole mitochondrion is trafficked to the lysosome for degradation via the mitophagy process (this figure depicts the most well-known PINK1/parkin dependent mitophagy pathway). Mitochondrial membrane potential dissipation leads to PINK1 kinase stabilization on the mitochondrial outer membrane (OM) and recruits cytosolic E3 ubiquitin ligase, parkin, to the mitochondria. Parkin subsequently ubiquitinates mitochondrial OM proteins, tagging them for autophagy receptors (such as p62) recognition. These autophagy receptors bind with LC3-II-positive phagophores and the double-membraned structure closes up around the mitochondrion to form autophagosomes. Autophagosomes eventually fuse with lysosomes to form autolysosomes where damaged mitochondrion is degraded. Upon initiation of the PINK1/parkin dependent pathway, the dynamic fusion and motility of the damaged mitochondrion is disabled by targeting Mitofusin (Mfn) and Miro for ubiquitin-proteasomal degradation. Native α-syn monomers are able to transition into toxic beta-sheet containing oligomers, which further converts into insoluble amyloid fibrils and are eventually deposited into Lewy bodies. α-syn monomers are degraded via the chaperone mediated autophagy (CMA) under physiological conditions. In this process, the heat shock cognate 71 <t>kDa</t> protein (Hsc70) chaperone recognizes the KFERQ domain of α-syn and targets the protein for the lysosome. At the lysosome membrane, the lysosome-associated membrane protein type 2A (LAMP2A) receptor assists in α-syn docking and internalization into the lysosome, where α-syn is degraded by hydrolases. Toxic α-syn oligomers and non-toxic monomers can both be degraded via the macroautophagy process.
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    The importance of mitochondrial dysfunction, α-syn aggregation, and the autophagy-endo-lysosomal system dysregulation in PD (Parkinson’s disease) pathogenesis. The clearance of damaged mitochondria and denatured α-synuclein (α-syn) are through autophagy-lysosome pathways. Minor mitochondrial damage is fixed via dynamic fission and fusion, complementing the damaged organelles and mitochondrial proteins. Medium amounts of damaged mitochondrial proteins and mitochondria parts are delivered to the lysosome via mitochondrial-derived vesicles (MDVs). The whole mitochondrion is trafficked to the lysosome for degradation via the mitophagy process (this figure depicts the most well-known PINK1/parkin dependent mitophagy pathway). Mitochondrial membrane potential dissipation leads to PINK1 kinase stabilization on the mitochondrial outer membrane (OM) and recruits cytosolic E3 ubiquitin ligase, parkin, to the mitochondria. Parkin subsequently ubiquitinates mitochondrial OM proteins, tagging them for autophagy receptors (such as p62) recognition. These autophagy receptors bind with LC3-II-positive phagophores and the double-membraned structure closes up around the mitochondrion to form autophagosomes. Autophagosomes eventually fuse with lysosomes to form autolysosomes where damaged mitochondrion is degraded. Upon initiation of the PINK1/parkin dependent pathway, the dynamic fusion and motility of the damaged mitochondrion is disabled by targeting Mitofusin (Mfn) and Miro for ubiquitin-proteasomal degradation. Native α-syn monomers are able to transition into toxic beta-sheet containing oligomers, which further converts into insoluble amyloid fibrils and are eventually deposited into Lewy bodies. α-syn monomers are degraded via the chaperone mediated autophagy (CMA) under physiological conditions. In this process, the heat shock cognate 71 kDa protein (Hsc70) chaperone recognizes the KFERQ domain of α-syn and targets the protein for the lysosome. At the lysosome membrane, the lysosome-associated membrane protein type 2A (LAMP2A) receptor assists in α-syn docking and internalization into the lysosome, where α-syn is degraded by hydrolases. Toxic α-syn oligomers and non-toxic monomers can both be degraded via the macroautophagy process.

    Journal: International Journal of Molecular Sciences

    Article Title: The Overcrowded Crossroads: Mitochondria, Alpha-Synuclein, and the Endo-Lysosomal System Interaction in Parkinson’s Disease

    doi: 10.3390/ijms20215312

    Figure Lengend Snippet: The importance of mitochondrial dysfunction, α-syn aggregation, and the autophagy-endo-lysosomal system dysregulation in PD (Parkinson’s disease) pathogenesis. The clearance of damaged mitochondria and denatured α-synuclein (α-syn) are through autophagy-lysosome pathways. Minor mitochondrial damage is fixed via dynamic fission and fusion, complementing the damaged organelles and mitochondrial proteins. Medium amounts of damaged mitochondrial proteins and mitochondria parts are delivered to the lysosome via mitochondrial-derived vesicles (MDVs). The whole mitochondrion is trafficked to the lysosome for degradation via the mitophagy process (this figure depicts the most well-known PINK1/parkin dependent mitophagy pathway). Mitochondrial membrane potential dissipation leads to PINK1 kinase stabilization on the mitochondrial outer membrane (OM) and recruits cytosolic E3 ubiquitin ligase, parkin, to the mitochondria. Parkin subsequently ubiquitinates mitochondrial OM proteins, tagging them for autophagy receptors (such as p62) recognition. These autophagy receptors bind with LC3-II-positive phagophores and the double-membraned structure closes up around the mitochondrion to form autophagosomes. Autophagosomes eventually fuse with lysosomes to form autolysosomes where damaged mitochondrion is degraded. Upon initiation of the PINK1/parkin dependent pathway, the dynamic fusion and motility of the damaged mitochondrion is disabled by targeting Mitofusin (Mfn) and Miro for ubiquitin-proteasomal degradation. Native α-syn monomers are able to transition into toxic beta-sheet containing oligomers, which further converts into insoluble amyloid fibrils and are eventually deposited into Lewy bodies. α-syn monomers are degraded via the chaperone mediated autophagy (CMA) under physiological conditions. In this process, the heat shock cognate 71 kDa protein (Hsc70) chaperone recognizes the KFERQ domain of α-syn and targets the protein for the lysosome. At the lysosome membrane, the lysosome-associated membrane protein type 2A (LAMP2A) receptor assists in α-syn docking and internalization into the lysosome, where α-syn is degraded by hydrolases. Toxic α-syn oligomers and non-toxic monomers can both be degraded via the macroautophagy process.

    Article Snippet: The major players of mitochondrial protein homeostasis (proteostasis) include mitochondrial chaperones, such as mitochondrial 70 kilodalton heat shock proteins (mtHsp70), mitochondrial heat shock protein (Hsp60), tumor necrosis factor receptor-associated protein 1/Hsp90 (Trap1), and mortalin (HSPA9).

    Techniques: Derivative Assay, Membrane, Ubiquitin Proteomics