A3481

Sigma-Aldrich

Anti-ApoER2 antibody produced in rabbit

enhanced validation

affinity isolated antibody, buffered aqueous solution

Synonym(s):
Anti-Low Density Lipoprotein Receptor-Related Protein 8, Anti-Apolipoprotein E Receptor 2, Anti-LRP8
NACRES:
NA.41
Pricing and availability is not currently available.

biological source

rabbit

Quality Level

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen ~105 kDa

species reactivity

human

enhanced validation

recombinant expression
Learn more about Antibody Enhanced Validation

application(s)

western blot: 0.5-1 μg/mL using HEK-293T cells expressing human ApoER2

conjugate

unconjugated

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

Gene Information

human ... LRP8(7804)

General description

Apolipoprotein E receptor 2 (ApoER2, also known as LRP8) is expressed predominantly in the brain and placenta. This gene is located on human chromosome 1p32.
The low-density lipoprotein receptor-related protein 8 (LRP8) or ApoER2 is a member of the LDL receptor family which includes LDLR and VLDLR. These proteins are involved in the uptake of lipid rich proteins into cells and cell signaling. ApoER2 assists in endocytosis and signal transduction.

Specificity

Rabbit anti-ApoER2 antibody recognizes human ApoER2 by immunoblotting (approx. 105kDa). Staining of the ApoER2 band in immunoblotting is specifically inhibited by the ApoER2 immunizing peptide.

Immunogen

synthetic peptide corresponding to amino acids 928-945 located near the C-terminus of human ApoER2, conjugated to KLH. This sequence is identical in mouse ApoER2.

Application

Anti-ApoER2 antibody produced in rabbit has been used in western blot analysis.

Biochem/physiol Actions

Apolipoprotein E receptor 2 (ApoER2, also known as LRP8) play an important role in the endocytosis of plasma lipoproteins, including ApoE and cholesterol metabolism. In the central nervous system, ApoER2 mediates various neuronal signaling mechanisms during neuronal development, affecting neurite outgrowth, synapse formation and neuronal migration, and neuronal survival in response to acute damage. ApoER2 plays a central role in the reelin/Dab1 signaling pathway that controls neuronal positioning during brain development as well as long-term potentiation (LTP) in the adult brain.

Physical form

Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

Personal Protective Equipment

dust mask type N95 (US),Eyeshields,Gloves

RIDADR

NONH for all modes of transport

WGK Germany

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Certificate of Analysis
Certificate of Origin
Structural basis for ligand capture and release by the endocytic receptor ApoER2
Hirai H, et al.
EMBO Reports, 18(6), 982-999 (2017)
Further evidence for the association between LRP8 and schizophrenia
Xiao X, et al.
Schizophrenia Research (2017)
The reelin receptors apolipoprotein E receptor 2 (ApoER2) and VLDL receptor
Dlugosz P and Nimpf J
International Journal of Molecular Sciences, 19(10), 3090-3090 (2018)
Modulation of synaptic plasticity and memory by Reelin involves differential splicing of the lipoprotein receptor Apoer2
Beffert U, et al.
Neuron, 47(4), 567-579 (2005)
Jorge A Larios et al.
BMC neuroscience, 15, 108-108 (2014-09-23)
ApoER2 and the neurotrophin receptors Trk and p75(NTR) are expressed in the CNS and regulate key functional aspects of neurons, including development, survival, and neuronal function. It is known that both ApoER2 and p75(NTR) are processed by metalloproteinases, followed by...
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