- PA5-26688 - Invitrogen Antibodies MT-CO1 antibody

Submitted references Mitochondrial RNA modifications shape metabolic plasticity in metastasis.

Delaunay S, Pascual G, Feng B, Klann K, Behm M, Hotz-Wagenblatt A, Richter K, Zaoui K, Herpel E, Münch C, Dietmann S, Hess J, Benitah SA, Frye M
Nature 2022 Jul;607(7919):593-603

Augmented Liver Uptake of the Membrane Voltage Sensor Tetraphenylphosphonium Distinguishes Early Fibrosis in a Mouse Model.

Pandita H, Mezey E, Ganapathy-Kanniappan S
Frontiers in physiology 2021;12:676722

Dual-Specificity Phosphatase 1 (DUSP1) Has a Central Role in Redox Homeostasis and Inflammation in the Mouse Cochlea.

Bermúdez-Muñoz JM, Celaya AM, García-Mato Á, Muñoz-Espín D, Rodríguez-de la Rosa L, Serrano M, Varela-Nieto I
Antioxidants (Basel, Switzerland) 2021 Aug 25;10(9)

Evidence of Oxidative Phosphorylation in Zebrafish Photoreceptor Outer Segments at Different Larval Stages.

Calzia D, Garbarino G, Caicci F, Pestarino M, Manni L, Traverso CE, Panfoli I, Candiani S
The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society 2018 Jul;66(7):497-509

Deletion of the Mitochondrial Complex-IV Cofactor Heme A:Farnesyltransferase Causes Focal Segmental Glomerulosclerosis and Interferon Response.

Baek JH, Gomez IG, Wada Y, Roach A, Mahad D, Duffield JS
The American journal of pathology 2018 Dec;188(12):2745-2762

RB1 deficiency in triple-negative breast cancer induces mitochondrial protein translation.

Jones RA, Robinson TJ, Liu JC, Shrestha M, Voisin V, Ju Y, Chung PE, Pellecchia G, Fell VL, Bae S, Muthuswamy L, Datti A, Egan SE, Jiang Z, Leone G, Bader GD, Schimmer A, Zacksenhaus E
The Journal of clinical investigation 2016 Oct 3;126(10):3739-3757

Heme Oxygenase-1/Carbon Monoxide System and Embryonic Stem Cell Differentiation and Maturation into Cardiomyocytes.

Suliman HB, Zobi F, Piantadosi CA
Antioxidants & redox signaling 2016 Mar 1;24(7):345-60

Depletion of TDP-43 decreases fibril and plaque β-amyloid and exacerbates neurodegeneration in an Alzheimer's mouse model.

LaClair KD, Donde A, Ling JP, Jeong YH, Chhabra R, Martin LJ, Wong PC
Acta neuropathologica 2016 Dec;132(6):859-873

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Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Western blot analysis using a Cytochrome C Oxidase Subunit 1 polyclonal antibody (Product # PA5-26688) in HL-60 cell lysates (35 µg per lane).

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Western blot analysis in MCF-7 cell lysates using a Cytochrome C Oxidase Subunit 1 polyclonal antibody (Product # PA5-26688).

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Western blot analysis was performed on whole cell extracts (30 µg lysate) of MCF7 (Lane 1), HeLa (Lane 2), LNCaP (Lane 3), Neuro-2a (Lane 4), C2C12 (Lane 5) and HCT 116 (Lane 6). The blot was probed with Anti- MTCO1 Polyclonal Antibody (Product # PA5-26688, 1:1000 dilution) and detected by chemiluminescence using Goat anti-Rabbit IgG (H+L) Superclonal™ Secondary Antibody, HRP conjugate (Product # A27036, 0.25 µg/mL, 1:4000 dilution). A 56 kDa band corresponding to MTCO1 was detected across cell lines tested. Certain uncharacterized bands were observed around ~30 kDa.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Immunofluorescent analysis of MCF-7 cells using a Cytochrome C Oxidase Subunit 1 polyclonal antibody (Product # PA5-26688) at a dilution of 1:10-50, followed by a fluor-conjugated goat anti-rabbit secondary antibody (green). Nuclei were stained with DAPI (blue).

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 3 Mitochondrial (mito-) oxidative phosphorylation (OxPhos) upregulated in early fibrosis. (A) Schematic diagram showing the overview of the regulation of mito-membrane potential. In OxPhos, ETC complexes release protons (H + ) into the space between the inner (MIM) and outer membranes (MOM) of mitochondria. H + accumulation establishes an electrochemical gradient leading to a negative potential (-) in the matrix. Thus, a higher rate of OxPhos (e.g., ATP synthesis) results in increased negative potential in the mito-matrix. (B) Immunoblot of mito-proteins shows an increase in mito-translocation of STAT3, F 1 -F 0 ATP synthase, and MT-CO1. COX IV remained unaltered. Immunoblot was re-probed for different targets to maintain the loading control. Numerical values at the bottom of the immunoblots represent the densitometry quantification of respective signals. Ponceau staining of the membrane shown for overall protein profile. (C) Metabolic flux analysis showing the oxygen consumption rate (OCR) of mitochondria isolated from the control, and F1 and F3 livers. Mitochondria showing a net increase in the OCR in the F1 liver. Unlike the typical cell-based assay, in this study, we used the mitochondria isolated from the respective livers as referred in the ""Materials and methods"" section. Hence, the extracellular acidification rate (ECAR) which is pertinent in the cellular assay is inapplicable. Data represent mean +- SE ( n = 3), t -test (* p < 0.05).

PA5-26688

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