ABCA7 Antibody [A11M15] | Primary Antibodies

Application: Reactivity: Mouse, Rat

Lane 1: Mouse brain, Lane 2: Mouse lung, Lane 3: Mouse spleen

Usage Information

Dilution
WB1:1000 IP1:200

Application
WB, IP

Reactivity
Mouse, Rat

Source
Rabbit Monoclonal Antibody

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
235 kDa

Datasheet & SDS

Biological Description

Specificity
ABCA7 Antibody [A11M15] detects endogenous levels of total ABCA7 protein.

Clone
A11M15

Synonym(s)
ATP-binding cassette sub-family A member 7; ABCA7

Background
ABCA7 belongs to the ATP-binding cassette subfamily A, a group of membrane transporters that actively translocate phospholipids across lipid bilayers using ATP hydrolysis. The protein features two transmembrane domains, each with six helices forming substrate tunnels, and two cytoplasmic nucleotide-binding domains that drive conformational changes for lipid extrusion. ABCA7 preferentially exports phosphatidylserine over phosphatidylcholine from the outer leaflet to the extracellular space, interacting with apolipoproteins to form lipoprotein particles that facilitate lipid efflux in a unidirectional manner, distinct from ABCA1's preference for phosphatidylcholine. The protein features two transmembrane domains, each with six helices forming substrate tunnels, and two cytoplasmic nucleotide-binding domains that drive conformational changes for lipid extrusion. ABCA7 preferentially exports phosphatidylserine over phosphatidylcholine from the outer leaflet to the extracellular space, interacting with apolipoproteins to form lipoprotein particles that facilitate lipid efflux in a unidirectional manner, distinct from ABCA1's preference for phosphatidylcholine. An open state presents a continuous lipid bilayer patch spanning the transmembrane domain for substrate entry, transitioning to a nucleotide-bound closed state that expels phospholipids through a small extracellular vestibule via rigid-body motions of the domains. These dynamics position ABCA7 at the interface of membrane asymmetry maintenance and lipid homeostasis, particularly enriching neuronal and microglial membranes, where it modulates phospholipid composition critical for synaptic integrity and vesicular trafficking. Loss-of-function variants disrupt this transport, elevating amyloid-β levels through impaired processing and reduced microglial phagocytosis, while altering mitochondrial phospholipid profiles that underpin energy metabolism in brain cells.

Background

ABCA7 belongs to the ATP-binding cassette subfamily A, a group of membrane transporters that actively translocate phospholipids across lipid bilayers using ATP hydrolysis. The protein features two transmembrane domains, each with six helices forming substrate tunnels, and two cytoplasmic nucleotide-binding domains that drive conformational changes for lipid extrusion. ABCA7 preferentially exports phosphatidylserine over phosphatidylcholine from the outer leaflet to the extracellular space, interacting with apolipoproteins to form lipoprotein particles that facilitate lipid efflux in a unidirectional manner, distinct from ABCA1's preference for phosphatidylcholine. The protein features two transmembrane domains, each with six helices forming substrate tunnels, and two cytoplasmic nucleotide-binding domains that drive conformational changes for lipid extrusion. ABCA7 preferentially exports phosphatidylserine over phosphatidylcholine from the outer leaflet to the extracellular space, interacting with apolipoproteins to form lipoprotein particles that facilitate lipid efflux in a unidirectional manner, distinct from ABCA1's preference for phosphatidylcholine. An open state presents a continuous lipid bilayer patch spanning the transmembrane domain for substrate entry, transitioning to a nucleotide-bound closed state that expels phospholipids through a small extracellular vestibule via rigid-body motions of the domains. These dynamics position ABCA7 at the interface of membrane asymmetry maintenance and lipid homeostasis, particularly enriching neuronal and microglial membranes, where it modulates phospholipid composition critical for synaptic integrity and vesicular trafficking. Loss-of-function variants disrupt this transport, elevating amyloid-β levels through impaired processing and reduced microglial phagocytosis, while altering mitochondrial phospholipid profiles that underpin energy metabolism in brain cells.

References
https://pubmed.ncbi.nlm.nih.gov/36484366/ https://pubmed.ncbi.nlm.nih.gov/24097981/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

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%