Product: Acetyl-SOD2/MnSOD (Lys68) Antibody
Catalog: AF3751
Description: Rabbit polyclonal antibody to Acetyl-SOD2/MnSOD (Lys68)
Application: WB IHC
Reactivity: Human, Mouse, Rat
Mol.Wt.: 25kD; 25kD(Calculated).
Uniprot: P04179
RRID: AB_2847065

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Product Info

Source:
Rabbit
Application:
IHC 1:50-1:200, WB 1:500-1:2000
*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
Clonality:
Polyclonal
Specificity:
Acetyl-SOD2 (Lys68) Antibody detects endogenous levels of SOD2 only when acetylated at Lys68.
RRID:
AB_2847065
Cite Format: Affinity Biosciences Cat# AF3751, RRID:AB_2847065.
Conjugate:
Unconjugated.
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

Indophenoloxidase B; IPO B; IPOB; Manganese containing superoxide dismutase; Manganese SOD; Manganese superoxide dismutase; Mangano superoxide dismutase; Mn SOD; Mn superoxide dismutase; MNSOD; MVCD6; SOD 2; SOD2; SODM_HUMAN; Superoxide dismutase [Mn] mitochondrial; Superoxide dismutase [Mn], mitochondrial; Superoxide dismutase 2 mitochondrial;

Immunogens

Immunogen:

A synthesized peptide derived from human SOD2 around the acetylation site of Lys68.

Uniprot:
Gene(ID):
Sequence:
MLSRAVCGTSRQLAPVLGYLGSRQKHSLPDLPYDYGALEPHINAQIMQLHHSKHHAAYVNNLNVTEEKYQEALAKGDVTAQIALQPALKFNGGGHINHSIFWTNLSPNGGGEPKGELLEAIKRDFGSFDKFKEKLTAASVGVQGSGWGWLGFNKERGHLQIAACPNQDPLQGTTGLIPLLGIDVWEHAYYLQYKNVRPDYLKAIWNVINWENVTERYMACKK

PTMs - P04179 As Substrate

Site PTM Type Enzyme
K53 Acetylation
Y58 Phosphorylation
K68 Acetylation
T79 Phosphorylation
S106 Phosphorylation P06493 (CDK1) , P11802 (CDK4)
K122 Acetylation
K122 Ubiquitination
S127 Phosphorylation
K130 Acetylation
K130 Methylation
K130 Ubiquitination
K132 Acetylation
K221 Acetylation

Research Backgrounds

Function:

Destroys superoxide anion radicals which are normally produced within the cells and which are toxic to biological systems.

PTMs:

Nitrated under oxidative stress. Nitration coupled with oxidation inhibits the catalytic activity.

Acetylation at Lys-122 decreases enzymatic activity. Deacetylated by SIRT3 upon exposure to ionizing radiations or after long fasting (By similarity).

Polyubiquitinated; leading to proteasomal degradation. Deubiquitinated by USP36 which increases protein stability.

Subcellular Location:

Mitochondrion matrix.

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

Homotetramer.

Family&Domains:

Belongs to the iron/manganese superoxide dismutase family.

Research Fields

· Cellular Processes > Transport and catabolism > Peroxisome.   (View pathway)

· Environmental Information Processing > Signal transduction > FoxO signaling pathway.   (View pathway)

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

· Organismal Systems > Aging > Longevity regulating pathway.   (View pathway)

· Organismal Systems > Aging > Longevity regulating pathway - multiple species.   (View pathway)

References

1). Nicotinamide reverses deficits in puberty-born neurons and cognitive function after maternal separation. Journal of Neuroinflammation, 2022 (PubMed: 36131290) [IF=9.3]

Application: WB    Species: Rat    Sample: hippocampus

Fig. 4 The expression of NAD+, Sirt3, and acetylated SOD2 and microglial inflammation. A NAD+ levels in the hippocampus at PND40 (CON, n = 8; MS, n = 8). B–D Immunoblots and quantification of Sirt3, acetylated SOD2, and total SOD2 in the hippocampus at PND40 (CON, n = 4; MS, n = 4). (E) NAD+ levels in the hippocampus at PND65 (CON, n = 8; MS, n = 8). F–H Immunoblots and quantification of Sirt3, acetylated SOD2, and total SOD2 in the hippocampus at PND65 (CON, n = 6; MS, n = 6). I Representative immunofluorescence images show the expression of Iba1 (green pixels) and Sirt3 (red pixels) in the DG at PND40 (n = 4 per group). J Quantitative analyses of the percentage of Sirt3 expression. (K) Quantitative analyses of the percentage of Iba1 and Sirt3 co-labeling. L Quantitative analyses of Iba1+ immunostained cells. M Representative immunofluorescence images showing the expression of Iba1 (green pixels) and Sirt3 (red pixels) in the DG at PND65 (n = 4 per group). N Quantitative analyses of the percentage of Sirt3 expression. O Quantitative analyses of the percentage of Iba1 and Sirt3 co-labeling. (P) Quantitative analyses of Iba1+ immunostained cells. Q Real-time qPCR analysis of TNF-α, IL-1β, and IL-6 in the hippocampus at PND40 (CON, n = 4; MS, n = 4). R Real-time qPCR analysis of TNF-α, IL-1β, and IL-6 in the hippocampus at PND65 (CON, n = 6; MS, n = 6). Data are presented as mean ± SEM for each group. n.s. not significant;

2). PGC-1α activation ameliorates cancer-induced bone pain via inhibiting apoptosis of GABAergic interneurons. Biochemical pharmacology, 2024 (PubMed: 38354958) [IF=5.8]

3). The role of SIRT3 in mediating the cognitive deficits and neuroinflammatory changes associated with a developmental animal model of schizophrenia. Progress in neuro-psychopharmacology & biological psychiatry, 2024 (PubMed: 38122862) [IF=5.6]

4). Nicotinamide ameliorates mitochondria-related neuronal apoptosis and cognitive impairment via the NAD+/SIRT3 pathway. Schizophrenia, 2023 (PubMed: 37210391)

Application: WB    Species: Mouse    Sample: HT22 cells

Fig. 5 SIRT3 inhibition causes mitochondrial damage and increases apoptosis in HT22 cells. A–C Immunoblots and quantification analysis of the level of acetylated SOD2 in HT22 cells (n = 3, per group). Data were normalized to controls. D Representative images of ROS (green) levels in HT22 cells. E Quantitative analyses of the percentage ROS area the HT22 cells (n = 6, per group). F Representative images of the mitochondrial membrane potential in HT22 cells. G Bar graph presenting the green/red fluorescence ratio, which reflects changes in the mitochondrial membrane potential. H Neuronal apoptosis was assessed by TUNEL staining in HT22 cells. TUNEL positive cells (red), DAPI (blue) labeling. I Quantification of TUNEL‐positive cells in HT22 cells (n = 4 per group). J Apoptotic HT22 cells were detected by flow cytometry. K The percentage of apoptotic cells was determined (n = 4, per group). L, M Immunoblots and quantification analysis of cleaved caspase 3 levels in HT22 cells (n = 4, per group). Data were normalized to controls. The data are presented as mean ± SEM for each group. n.s. was not significant;

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Affinity Biosciences tests all products strictly. Citations are provided as a resource for additional applications that have not been validated by Affinity Biosciences. Please choose the appropriate format for each application and consult Materials and Methods sections for additional details about the use of any product in these publications.

For Research Use Only.
Not for use in diagnostic or therapeutic procedures. Not for resale. Not for distribution without written consent. Affinity Biosciences will not be held responsible for patent infringement or other violations that may occur with the use of our products. Affinity Biosciences, Affinity Biosciences Logo and all other trademarks are the property of Affinity Biosciences LTD.