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FLASH GENE

Symbol

LDLRAD3

contributors: mct - updated : 17-04-2023

HGNC name	low density lipoprotein receptor class A domain containing 3
HGNC id	27046

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

RNA

TRANSCRIPTS	type	messenger

identification nb exons type bp product Protein kDa AA specific expression Year Pubmed NM_174902 6 - 2969 NP_777562 50 345 - 2020 33208938 NM_001304264 6 - 3783 NP_001291193 - 224 - 2020 33208938 NM_001304263 5 - 3667 NP_001291192 - 296 - 2020 33208938

EXPRESSION

Type

expressed in	(based on citations)
organ(s)	System Organ level 1 Organ level 2 Organ level 3 Organ level 4 Level Pubmed Species Stage Rna symbol Nervous brain         Homo sapiens   brain forebrain cerebral cortex     Homo sapiens   brain limbic system hippocampus     Homo sapiens

cells

System Cell Pubmed Species Stage Rna symbol Nervous neuron Homo sapiens

cell lineage

cell lines

fluid/secretion

at STAGE

PROTEIN

PHYSICAL PROPERTIES

STRUCTURE

motifs/domains	an ectodomain containing three LDLa repeats
	a transmembrane domain, and a cytoplasmic domain containing a conserved dileucine internalization motif and two polyproline motifs

conjugated

LipoP

HOMOLOGY

Homologene

FAMILY

LDLR family

CATEGORY

receptor

SUBCELLULAR LOCALIZATION	plasma membrane
text	type I transmembrane receptor

basic FUNCTION	its expression significantly decreases the cellular half-life of mature APP
	is a receptor for Venezuelan equine encephalitis virus

CELLULAR PROCESS

PHYSIOLOGICAL PROCESS

PATHWAY

metabolism

signaling

a component

INTERACTION

DNA

RNA

small molecule

protein	influences APP processing, raising the possibility that LRAD3 alters APP function in neurons, including its downstream signaling
	DPP4, AGTR2, SLC4A1, KREMEN1, ASGR1, ANP, TMEM30A, CLEC4G, and LDLRAD3, along with ACE2 facilitate SARS-CoV-2. virus entry and transmission

cell & other

REGULATION

ASSOCIATED DISORDERS

corresponding disease(s)

Susceptibility

Variant & Polymorphism

Candidate gene

Marker

Therapy target

ANIMAL & CELL MODELS

pathogenesis of VEEV infection is abrogated in mice with deletions in Ldlrad3