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FLASH GENE

Symbol

CCR2

contributors: mct - updated : 25-04-2016

HGNC name	chemokine (C-C motif) receptor 2
HGNC id	1603

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

ASSOCIATED DISORDERS

corresponding disease(s)

Other morbid association(s)

Type Gene Modification Chromosome rearrangement Protein expression Protein Function constitutional     --over   in polymyositis and in inclusion body myositis constitutional     --low   leads to decreased microglial accumulation in the Alzheimer disease brain, resulting in increased A deposition particularly in and around blood vessels constitutional     --low   could play a potential role in the etiology of Alzheimer's disease, a neurodegenerative pathology that could be treated by a genetic upregulation of the transgene in monocytoid cells tumoral       gain of function of CCL2/CCR2 axis promotes prostate cancer growth in bone constitutional     --over   expression of CCR1 and CCR2 is up-regulated in peripheral blood B cells upon EBV infection

Susceptibility

HIV-1 infection for bone mass especially in middle-aged man and postmenopausal women to myocardial infarction and heart failure in patient sunder 65 years to Alzheimer disease to abdominal aortic aneurysms

Variant & Polymorphism	V64I increasing the risk of myocardial infarction and heart failure
	chronic CCR2 inhibition may hasten the progression of Alzheimer disease in susceptible individuals
	Significant relationship was observed between CCR2 V64I polymorphism and presence of abdominal aortic aneurysms

Candidate gene	a dominant protective effect of the CCR2-641 mutation
Marker
Therapy target
	System Type Disorder Pubmed miscelleaneous pain   antagonists of CCL2/CCR2 are promising agents from treating neuropathic pain immunology inflammatory   CCR2 antagonists are currently undergoing clinical trials for the treatment of a variety of chronic inflammatory diseases miscelleaneous pain   targeting CCL2-CCR2 signaling may be a potentially important new treatment strategy for trigeminal neuralgia diabete type 1   blocking CCR2 could be a novel therapeutic approach in the treatment of diabetic nephropathy

ANIMAL & CELL MODELS

	Ccr2 deficiency accelerates early disease progression and markedly impairs microglial accumulation in a transgenic mouse model of Alzheimer disease (Tg2576)
	locomotor sensitization is significantly reduced in CCR2(-/-) mice as well as the dopamine transporter regulation and the cocaine-induced p-ERK striatal activation
	mice with CCR2 deficiency are protected from insulin resistance but only after long periods of high-fat diet (HFD) feeding, despite the virtual absence of circulating inflammatory monocytes
	mice that lack Ccr2 developed mechanical allodynia, but this started to resolve from 8 wk onwards