Rabbit MT-ATP6 Polyclonal Antibody | anti-MT-ATP6 antibody

MT-ATP6 Polyclonal Antibody

Cat. Num. AAA3006383

• Gene Names: MT-ATP6; ATPase6; MTATP6; ATP6
• Reactivity: Human, Mouse, Rat
• Applications: Western Blot
• Purity: The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen and the purity is >95% (by SDS-PAGE).
• Synonyms: MT-ATP6; Polyclonal Antibody; MT-ATP6 Polyclonal Antibody; ATP synthase subunit a; F-ATPase protein 6; ATP6; ATPASE6; MTATP6; anti-MT-ATP6 antibody

• Host: Rabbit
• Reactivity: Human, Mouse, Rat
• Clonality: Polyclonal
• Isotype: IgG
• Specificity: MT-ATP6 polyclonal antibody detects endogenous levels of MT-ATP6 protein.
• Purity/Purification: The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen and the purity is >95% (by SDS-PAGE).
• Form/Format: Rabbit IgG, 1mg/ml in PBS with 0.02% sodium azide, 50% glycerol, pH7.2
• Sequence Length: 226

• Applicable Applications for anti-MT-ATP6 antibody: Western Blot (WB)
• Application Notes: WB: 1:500-1:1000
• Immunogen: A synthetic peptide corresponding to residues in Human MT-ATP6.
• Preparation and Storage: Store at 4 degree C short term.; Aliquot and store at -20 degree C long term.; Avoid freeze-thaw cycles.

Western Blot (WB)

(Western Blot (WB) analysis of MT-ATP6 polyclonal antibody at 1:500 dilutionLane1:Hela whole cell lysateLane2:A549 whole cell lysateLane3:PC12 whole cell lysate)

Related Product Information for anti-MT-ATP6 antibody

The MT-ATP6 gene provides information for making a protein that is essential for normal mitochondrial function. Mitochondria are structures within cells that convert the energy from food into a form that cells can use. These cellular structures produce energy through a process called oxidative phosphorylation, which uses oxygen and simple sugars to create adenosine triphosphate (ATP), the cell's main energy source. The MT-ATP6 protein forms one part (subunit) of a large enzyme called ATP synthase. This enzyme, which is also known as complex V, is responsible for the final step of oxidative phosphorylation. Specifically, one segment of ATP synthase allows positively charged particles, called protons, to flow across a specialized membrane inside mitochondria. Another segment of the enzyme uses the energy created by this proton flow to convert a molecule called adenosine diphosphate (ADP) to ATP.

NCBI and Uniprot Product Information

• NCBI GI #: 251831112
• NCBI GeneID: 4508
• NCBI Accession #: YP_003024031.1
• NCBI GenBank Nucleotide #: YP_003024031.1
• UniProt Accession #: P00846
• Molecular Weight: ~ 27kDa
• NCBI Official Full Name: ATP synthase F0 subunit 6 (mitochondrion)
• NCBI Official Synonym Full Names: mitochondrially encoded ATP synthase 6
• NCBI Official Symbol: MT-ATP6
• NCBI Official Synonym Symbols: ATPase6; MTATP6; ATP6
• NCBI Protein Information: ATP synthase F0 subunit 6
• UniProt Protein Name: ATP synthase subunit a
• UniProt Gene Name: MT-ATP6
• UniProt Synonym Gene Names: ATP6; ATPASE6; MTATP6
• UniProt Entry Name: ATP6_HUMAN

Uniprot Description

ATP6: Mitochondrial membrane ATP synthase (F(1)F(0) ATP synthase or Complex V) produces ATP from ADP in the presence of a proton gradient across the membrane which is generated by electron transport complexes of the respiratory chain. F-type ATPases consist of two structural domains, F(1) - containing the extramembraneous catalytic core and F(0) - containing the membrane proton channel, linked together by a central stalk and a peripheral stalk. During catalysis, ATP synthesis in the catalytic domain of F(1) is coupled via a rotary mechanism of the central stalk subunits to proton translocation. Key component of the proton channel; it may play a direct role in the translocation of protons across the membrane. Defects in MT-ATP6 are the cause of neurogenic muscle weakness, ataxia, and retinitis pigmentosa (NARP). Defects in MT-ATP6 are a cause of Leber hereditary optic neuropathy (LHON). LHON is a maternally inherited disease resulting in acute or subacute loss of central vision, due to optic nerve dysfunction. Cardiac conduction defects and neurological defects have also been described in some patients. LHON results from primary mitochondrial DNA mutations affecting the respiratory chain complexes. Defects in MT-ATP6 are a cause of Leigh syndrome (LS). LS is a severe neurological disorder characterized by bilaterally symmetrical necrotic lesions in subcortical brain regions. Defects in MT-ATP6 are a cause of mitochondrial infantile bilateral striatal necrosis (MIBSN). Bilateral striatal necrosis is a neurological disorder resembling Leigh syndrome. Belongs to the ATPase A chain family.

Protein type: Transporter, ion channel; Membrane protein, multi-pass; Mitochondrial; Membrane protein, integral; Transporter

Chromosomal Location of Human Ortholog: -

Disease: Neuropathy, Ataxia, And Retinitis Pigmentosa; Leber Optic Atrophy