MT-ATP8 Rabbit Polyclonal Antibody

MT-ATP8 Rabbit Polyclonal Antibody

Cat: APRab14201
Boyut:20μL Fiyat:$99_x000D_
Boyut:50μL Fiyat:$118_x000D_
Boyut:100μL Fiyat:$220_x000D_
Boyut:200μL Fiyat:$380_x000D_
Uygulama:IHC,ELISA
Reaktivite:Human,Rat,Mouse
Konjuge:Unconjugated
İsteğe bağlı konjugeler: Biotin, FITC (ücretsiz). Diğer 26 konjugatı görün.

Gen Adı:MT-ATP8
Category: ポリクローナル抗体 Tags: , , , , , , ,
MT-ATP8 Rabbit Polyclonal Antibody
Konjugasyon: Unconjugated
Rabbit polyclonal Antibody
Uygulama
IHC  ICC/IF  ELISA IHC,ELISA
Reaktivite
Human,Rat,Mouse
Gen Adı
MT-ATP8
Saklama
Aliquot and store at -20°C (valid for 12 months). Avoid freeze/thaw cycles.
Özet
Ürün Adı MT-ATP8 Rabbit Polyclonal Antibody
Açıklama Rabbit polyclonal Antibody
Konak Rabbit
Reaktivite Human,Rat,Mouse
Konjugasyon Unconjugated
Modifikasyon Unmodified
İzotip IgG
Klonalite Polyclonal
Form Liquid
Konsantrasyon Unconjugated
Saklama Aliquot and store at -20°C (valid for 12 months). Avoid freeze/thaw cycles.
Nakliye Ice bags.
Tampon Liquid in PBS containing 50% glycerol, 0.5% protective protein and 0.02% New type preservative N.
Saflaştırma Affinity purification
Antijen Bilgisi
Gen Adı MT-ATP8
Alternatif İsimler ATP synthase protein 8 (A6L;F-ATPase subunit 8)
Gen Kimliği 4509
SwissProt Kimliği P03928
İmmünojen Synthesized peptide derived from human MT-ATP8 AA range: 30-110
Uygulama
Uygulama IHC,ELISA
Seyreltme Oranı IHC 1:50-1:200,ELISA 1:5000-1:20000
Moleküler Ağırlık -
Araştırma Alanı
Arka Plan
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.,function: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. Part of the complex F(0) domain. Minor subunit located with subunit a in the membrane.,function:Subunits I, II and III form the functional core of the enzyme complex.,similarity:Belongs to the ATPase A chain family.,similarity:Belongs to the ATPase protein 8 family.,similarity:Belongs to the cytochrome c oxidase subunit 3 family.,subunit:F-type ATPases have 2 components, CF(1) - the catalytic core - and CF(0) - the membrane proton channel.,subunit:F-type ATPases have 2 components, CF(1) - the catalytic core - and CF(0) - the membrane proton channel. CF(1) has five subunits: alpha(3), beta(3), gamma(1), delta(1), epsilon(1). CF(0) has three main subunits: a, b and c.,disease:Defects in MT-ATP6 are a cause of infantile bilateral striatal necrosis [MIM:500003]. Bilateral striatal necrosis is a neurological disorder resembling Leigh syndrome.,disease:Defects in MT-ATP6 are a cause of Leber hereditary optic neuropathy (LHON) [MIM:535000]. 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.,disease:Defects in MT-ATP6 are a cause of Leigh syndrome (LS) [MIM:256000].
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