Product: Cytochrome C Antibody
Catalog: AF0146
Source: Rabbit
Application: WB, IHC, IF/ICC, ELISA(peptide)
Reactivity: Human, Mouse, Rat, Monkey
Prediction: Pig, Zebrafish, Bovine, Horse, Sheep, Rabbit, Dog, Xenopus
Mol.Wt.: 15kD; 12kD(Calculated).
Uniprot: P99999
RRID: AB_2833328

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Product Info

Source:
Rabbit
Application:
WB 1:500-1:3000, IHC 1:50-1:200, IF/ICC 1:100-1:500, ELISA(peptide) 1:20000-1:40000
*The optimal dilutions should be determined by the end user.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human,Mouse,Rat,Monkey
Prediction:
Pig(100%), Zebrafish(88%), Bovine(100%), Horse(100%), Sheep(100%), Rabbit(100%), Dog(100%), Xenopus(100%)
Clonality:
Polyclonal
Specificity:
Cytochrome C Antibody detects endogenous levels of total Cytochrome C.
RRID:
AB_2833328
Cite Format: Affinity Biosciences Cat# AF0146, RRID:AB_2833328.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
Alias:

Fold/Unfold

CYC; CYC_HUMAN; CYCS; Cytochrome c; Cytochrome c somatic; HCS; THC4;

Immunogens

Immunogen:
Uniprot:
Gene(ID):
Description:
CYCS Electron carrier protein. The oxidized form of the cytochrome c heme group can accept an electron from the heme group of the cytochrome c1 subunit of cytochrome reductase. Cytochrome c then transfers this electron to the cytochrome oxidase complex, the final protein carrier in the mitochondrial electron-transport chain. Belongs to the cytochrome c family.
Sequence:
MGDVEKGKKIFIMKCSQCHTVEKGGKHKTGPNLHGLFGRKTGQAPGYSYTAANKNKGIIWGEDTLMEYLENPKKYIPGTKMIFVGIKKKEERADLIAYLKKATNE

Predictions

Predictions:

Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Species
Results
Score
Pig
100
Horse
100
Bovine
100
Sheep
100
Dog
100
Xenopus
100
Rabbit
100
Zebrafish
88
Chicken
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - P99999 As Substrate

Site PTM Type Enzyme
G2 Acetylation
K9 Acetylation
K28 Sumoylation
K28 Ubiquitination
T29 Phosphorylation
K40 Ubiquitination
T41 Phosphorylation
Y47 Phosphorylation
S48 Phosphorylation
Y49 Phosphorylation
T50 Phosphorylation
K54 Ubiquitination
Y68 Phosphorylation
K73 Acetylation
K73 Ubiquitination
K74 Acetylation
K74 Ubiquitination
Y75 Phosphorylation
T79 Phosphorylation
K80 Ubiquitination
K87 Acetylation
K87 Ubiquitination
K88 Acetylation
K89 Acetylation
Y98 Phosphorylation
K100 Acetylation
K100 Methylation
K100 Ubiquitination
K101 Methylation

Research Backgrounds

Function:

Electron carrier protein. The oxidized form of the cytochrome c heme group can accept an electron from the heme group of the cytochrome c1 subunit of cytochrome reductase. Cytochrome c then transfers this electron to the cytochrome oxidase complex, the final protein carrier in the mitochondrial electron-transport chain.

Plays a role in apoptosis. Suppression of the anti-apoptotic members or activation of the pro-apoptotic members of the Bcl-2 family leads to altered mitochondrial membrane permeability resulting in release of cytochrome c into the cytosol. Binding of cytochrome c to Apaf-1 triggers the activation of caspase-9, which then accelerates apoptosis by activating other caspases.

PTMs:

Binds 1 heme group per subunit.

Phosphorylation at Tyr-49 and Tyr-98 both reduce by half the turnover in the reaction with cytochrome c oxidase, down-regulating mitochondrial respiration.

Subcellular Location:

Mitochondrion intermembrane space.
Note: Loosely associated with the inner membrane.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Family&Domains:

Belongs to the cytochrome c family.

Research Fields

· Cellular Processes > Cell growth and death > p53 signaling pathway.   (View pathway)

· Cellular Processes > Cell growth and death > Apoptosis.   (View pathway)

· Cellular Processes > Cell growth and death > Apoptosis - multiple species.   (View pathway)

· Human Diseases > Drug resistance: Antineoplastic > Platinum drug resistance.

· Human Diseases > Endocrine and metabolic diseases > Non-alcoholic fatty liver disease (NAFLD).

· Human Diseases > Neurodegenerative diseases > Alzheimer's disease.

· Human Diseases > Neurodegenerative diseases > Parkinson's disease.

· Human Diseases > Neurodegenerative diseases > Amyotrophic lateral sclerosis (ALS).

· Human Diseases > Neurodegenerative diseases > Huntington's disease.

· Human Diseases > Infectious diseases: Bacterial > Legionellosis.

· Human Diseases > Infectious diseases: Parasitic > Toxoplasmosis.

· Human Diseases > Infectious diseases: Bacterial > Tuberculosis.

· Human Diseases > Infectious diseases: Viral > Hepatitis B.

· Human Diseases > Infectious diseases: Viral > Influenza A.

· Human Diseases > Infectious diseases: Viral > Herpes simplex infection.

· Human Diseases > Cancers: Overview > Pathways in cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Colorectal cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Small cell lung cancer.   (View pathway)

· Human Diseases > Cardiovascular diseases > Viral myocarditis.

· Metabolism > Energy metabolism > Sulfur metabolism.

· Metabolism > Global and overview maps > Metabolic pathways.

References

1). Wang Y et al. Inhibition of fatty acid catabolism augments the efficacy of oxaliplatin-based chemotherapy in gastrointestinal cancers. Cancer Lett 2020 Jan 2;473:74-89 (PubMed: 31904482) [IF=9.756]

2). Wang T et al. Proteus mirabilis Vesicles Induce Mitochondrial Apoptosis by Regulating miR96-5p/Abca1 to Inhibit Osteoclastogenesis and Bone Loss. Front Immunol 2022 Feb 15;13:833040. (PubMed: 35242136) [IF=8.786]

Application: WB    Species: mouse    Sample: Osteoclasts

FIGURE 4 | Effect of P.M OMVs on mitochondria-dependent osteoclast apoptosis.(J) Cyto c expression in the cytoplasm and mitochondria with or without P.M OMV treatment. Data were obtained from three independent experiments and represented as mean ± SD. ####p < 0.0001 compared to M-CSF. *p < 0.05; **p < 001; ***p < 0.001; ****p < 0.0001 compared to M-CSF + RANKL. ns, not significant.

Application: WB    Species: Mouse    Sample: osteoclasts

Figure 4 Effect of P.M OMVs on mitochondria-dependent osteoclast apoptosis. (A) Venn diagram showing the intersection of negatively correlated miRNA–mRNA pairs within miRNA and mRNA sequences. (B) KEGG enrichment analysis of upregulated genes is shown in the bubble chart. The top 15 genes significantly enriched in the KEGG pathway (p < 0.05) are presented. Changes in osteoclast (C, D) apoptosis, (E, F) intracellular ROS, and (G, H) mitochondrial membrane potential level after being cultured with or without 0.15 or 0.3 μg/ml of P.M OMVs for 5 days. (I) Western blot analysis of caspase-3, Bcl-2, and Bax. (J) Cyto c expression in the cytoplasm and mitochondria with or without P.M OMV treatment. Data were obtained from three independent experiments and represented as mean ± SD. ####p < 0.0001 compared to M-CSF. *p < 0.05; **p < 001; ***p < 0.001; ****p < 0.0001 compared to M-CSF + RANKL. ns, not significant.

3). Zhang L et al. Emodin targets mitochondrial cyclophilin D to induce apoptosis in HepG2 cells. Biomed Pharmacother 2017 Jun;90:222-228 (PubMed: 28363167) [IF=7.419]

Application: WB    Species: human    Sample:

Fig. 2. Effects of CsA on emodin-induced apoptosis. The cells were treated with emodin for 48 h in the presence or absence of CsA (5mM), then assays were performed. (A) Analysis of apoptosis by nuclear condensation. The Hoechst 33342 staining showed typical apoptotic morphology changes after emodin treatment. The images were acquired by inverted fluorescence microscopy. (B) Analysis of apoptosis by Annexin V/PI double-staining assay. (C) Determination of Cyto-C level in mitochondria and cytosol by western blots. b-actin and VDAC1 were used as internal control.

4). Yarong Du et al. The Reduced Oligomerization of MAVS Mediated by ROS Enhances the Cellular Radioresistance. OXID MED CELL LONGEV 2020 Mar 4;Article ID 2167129 [IF=7.310]

5). Li Q et al. Inhibition of microRNA-327 ameliorates ischemia/reperfusion injury-induced cardiomyocytes apoptosis through targeting apoptosis repressor with caspase recruitment domain. J Cell Physiol 2019 Oct 6 (PubMed: 31587299) [IF=6.513]

Application: WB    Species: rat    Sample: heart

FIGURE 7| Inhibition of miR‐327 suppressed I/R‐induced extrinsic and intrinsic apoptosis‐associated molecules expression. Caspase‐8, Fas and FasL protein expression was detected in heart tissues of MI/RI rats by western blot (a). Quantitative analysis of Caspase‐8 (b), Fas (c), and FasL(d) expression was shown in Bar graphs.Caspase‐9, Bax, Bcl‐2, and Cyt‐c proteinexpression was detected in heart tissues of MI/RI rats by Western blot (e).

6). Huang L et al. Lactoferrin ameliorates pathological cardiac hypertrophy related to mitochondrial quality control in aged mice. Food Funct 2021 Aug 21;12(16):7514-7526. (PubMed: 34223567) [IF=6.317]

Application: WB    Species: Mice    Sample:

Fig. 2 LF inhibited mitochondria-dependent apoptosis of myocardium in aged mice. (A) Representative images of the TUNEL assay. (B) Quantification of TUNEL-positive nuclei. (C) Representative immunoblotting images of relative protein expression. (D)–(I) Quantification of relative protein expression involved in mitochondria-dependent apoptosis; *P < 0.05 and **P < 0.01 vs. 2-month group; #P < 0.05 and ##P < 0.01 vs. 16-month group.

7). Xie SY et al. SHMT2 promotes tumor growth through VEGF and MAPK signaling pathway in breast cancer. Am J Cancer Res 2022 Jul 15;12(7):3405-3421. (PubMed: 35968337) [IF=5.942]

8). Wang Y et al. SLC25A21 Suppresses Cell Growth in Bladder Cancer via an Oxidative Stress-Mediated Mechanism. Front Oncol 2021 Sep 9;11:682710. (PubMed: 34568013) [IF=5.738]

Application: WB    Species: Mouse    Sample: BCa cells

Figure 5 SLC25A21 overexpression induces cell apoptosis by the α-KG-mediated ROS pathway in BCa. (A) SLC25A21 promoted the efflux of α-KG from the mitochondria to the cytosol. (B) The levels of α-KG in the mitochondria affected succinate production. (C) The upregulation of SLC25A21 promoted ROS accumulation in BCa cells. (D) The upregulation of SLC25A21 decreased Δψm in both BCa cell lines. (E) Western blot assays showed that SLC25A21 induced cyto C transfer from the mitochondria to the cytosol and increased the activation of caspase-9 and caspase-3 in BCa cells. (F) Immunohistochemistry showed that SLC25A21 increased the activation of caspase-9 and caspase-3 in BCa xenograft tissues. (G) Schematic diagram showing the mechanism of action of SLC25A21 on cell apoptosis in BCa. The results were reproducible in three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001 and ****P < 0.0001.

9). Wang CH et al. POH1 Knockdown Induces Cancer Cell Apoptosis via p53 and Bim. Neoplasia 2018 May;20(5):411-424 (PubMed: 29573636) [IF=5.715]

10). Liu Y et al. Oligo-Porphyran Ameliorates Neurobehavioral Deficits in Parkinsonian Mice by Regulating the PI3K/Akt/Bcl-2 Pathway. Mar Drugs 2018 Mar 6;16(3) (PubMed: 29509717) [IF=5.118]

Application: WB    Species: mouse    Sample:

Figure 5. | Effects on apoptosis-related protein expression, poly ADP ribose polymerase (PARP), and caspase-3 activity in vivo. After pretreated with MPTP for seven days, the C57BL/6 mice were administrated with MA or different concentrations of OP for the followed 7 days. (A): Original bands of cytochrome c (CytC), cleaved caspased-3, B-cell lymphoma 2 (Bcl-2), BCL2 associated X (Bax), PARP, and β-actin.

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