Anti-MEGF10 (extracellular) Antibody

Antibodies

Antibodies

Israel

Storage before Reconstitution: The antibody ships as a lyophilized powder at room temperature. Upon arrival, it should be stored at -20°C - Storage after Reconstitution: The reconstituted solution can be stored at 4°C for up to 1 week. For longer periods, small aliquots should be stored at -20°C. Avoid multiple freezing and thawing. Centrifuge all antibody preparations before use (10000 x g 5 min).

A rabbit polyclonal antibody to MEGF10 (extracellular)

Polyclonal

Western blot analysis

25 µl, 50 µl or 0.2 ml double distilled water (DDW), depending on the sample size.

1% BSA, 0.05% NaN3

MEGF10

Mouse

41116161

MEGF10 is a member of the multiple epidermal growth factor-like domains protein family. MEGF10 is a type I transmembrane protein that consists of 15 EGF-like domains in its extracellular region and is the mammalian homolog of Draper (a Drosophila phagocytosis apoptotic cell receptor)1.MEGF10 is a mediator for apoptotic cell phagocytosis by central nervous system (CNS) macrophages- microglia and astrocytes, through binding with high affinity to C1q, an eat-me signal, that binds phosphatidylserine expressed on the surface of apoptotic cells2. Also necessary for astrocyte-dependent apoptotic neuron clearance in the developing cerebellum2. In this regard, MEGF10 works alongside other phagocytic receptors expressed in astrocytes or microglia such as the tyrosine kinase receptors MERTK and AXL, the G-protein coupled receptors Bai1 and GPR56 or the TREM2 receptor3.MEGF10 is involved in the uptake of amyloid-β peptide (Aβ42) in the brain. Alzheimer's disease (AD) is characterized by extracellular accumulation of senile plaques, the major component of which is the amyloid-β peptide (Aβ), and the presence of neurofibrillary tangles. MEGF10 as a functional receptor that mediates the uptake of amyloid-β peptide will help elucidate the molecular mechanisms of amlyoid-β clearance in Alzheimer's disease1, 4.MEGF10 is also an essential factor in the regulation of myogenesis. It controls the balance between skeletal muscle satellite cells proliferation and differentiation through regulation of the notch signaling pathway5. In fact, mutations in the MEGF10 gene are the underlying cause of Early-onset myopathy, areflexia, respiratory distress, and dysphagia (EMARDD), a lethal congenital myopathy characterized by hypotonia with respiratory distress 5, 6.