ATPIF1 Antibody [P8F22]

Catalog No.: F4093

Application: Reactivity: Human, Monkey

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代表番号: 045-509-1970|電子メール：sales@selleck.co.jp

使用情報

Dilution
WB1:1000 IP1:100 IHC1:1600 IF1:3200

Application
WB, IP, IHC, IF

Source
Rabbit Monoclonal Antibody

Reactivity
Human, Monkey

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
12 kDa

Datasheet & SDS

生物学的記述

Specificity
ATPIF1 Antibody [P8F22] detects endogenous levels of total ATPIF1 protein.

Clone
P8F22

Synonym(s)
ATPase inhibitor, mitochondrial; ATP synthase F1 subunit epsilon; Inhibitor of F(1)F(o)-ATPase (IF(1); IF1); ATP5IF1; ATPI; ATPIF1

Background
ATPIF1 (ATPase Inhibitory Factor 1, also IF1) is a small mitochondrial regulatory protein that physiologically inhibits the H+-ATP synthase (Complex V) to prevent ATP hydrolysis under conditions of impaired respiration or acidosis. ATPIF1 exists as an intrinsically disordered monomer in solution that undergoes disorder-to-order transition upon binding, forming two α-helices: an N-terminal helix inserting into the catalytic interface between αDP/βDP subunits of the F1 domain to sterically block rotary catalysis, and a C-terminal anti-parallel coiled-coil stabilizing IF1 homodimers. ATPIF1 binds pH-dependently to the F1 sector during ATP hydrolysis (not synthesis), locking the enzyme in the DP:IF1 conformation to preserve cellular ATP while promoting ATP synthase oligomerization (dimers/tetramers) that shapes cristae architecture and inhibits permeability transition pore (PTP) opening via OSCP subunit interaction. It triggers retrograde signaling, inducing aerobic glycolysis (Warburg effect) in cancer cells and modulates mitohormesis/apoptosis resistance. Overexpression in carcinomas drives oncogenesis, metabolic reprogramming, and tumor survival; deficiency disrupts cristae/mitochondrial structure, linking to pathologies like heart failure.

Background

ATPIF1 (ATPase Inhibitory Factor 1, also IF1) is a small mitochondrial regulatory protein that physiologically inhibits the H+-ATP synthase (Complex V) to prevent ATP hydrolysis under conditions of impaired respiration or acidosis. ATPIF1 exists as an intrinsically disordered monomer in solution that undergoes disorder-to-order transition upon binding, forming two α-helices: an N-terminal helix inserting into the catalytic interface between αDP/βDP subunits of the F1 domain to sterically block rotary catalysis, and a C-terminal anti-parallel coiled-coil stabilizing IF1 homodimers. ATPIF1 binds pH-dependently to the F1 sector during ATP hydrolysis (not synthesis), locking the enzyme in the DP:IF1 conformation to preserve cellular ATP while promoting ATP synthase oligomerization (dimers/tetramers) that shapes cristae architecture and inhibits permeability transition pore (PTP) opening via OSCP subunit interaction. It triggers retrograde signaling, inducing aerobic glycolysis (Warburg effect) in cancer cells and modulates mitohormesis/apoptosis resistance. Overexpression in carcinomas drives oncogenesis, metabolic reprogramming, and tumor survival; deficiency disrupts cristae/mitochondrial structure, linking to pathologies like heart failure.

References
[1] Domínguez-Zorita S, et al. Front Physiol. 2022 Mar 18;13:868820. [2] Carroll J, et al. J Biol Chem. 2024 Mar;300(3):105690.

PVDFメンブレン孔径参考表

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%