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	HGNC	UniGene	Nucleotide	OMIM	UCSC

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FLASH GENE

Symbol

CCL3

contributors: mct - updated : 28-04-2020

HGNC name	chemokine (C-C motif) ligand 3
HGNC id	10627

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 tumoral     --over   in myeloma Bone marrow (BM) positively correlated with the percentage of BM-infiltrating macrophages tumoral     --over   in the plasma of acute myeloid leukemia (AML) patients, and CCL3 inhibited erythroid differentiation of hematopoietic stem cells, common myeloid progenitors and especially megakaryocytic-erythroid progenitors constitutional     --over   in Chronic Obstructive Pulmonary Disease (COPD) sputum constitutional     --over   CCL2 and CCL3 are upregulated in the injured peripheral nerve through epigenetic histone modification in infiltrating immune cells such as macrophages

Susceptibility

to multiple sclerosis to HIV/acquired immunodeficiency syndrome (AIDS) (Omim: 609423)

Variant & Polymorphism SNP	increasing the risk of multiple sclerosis
	influencing HIV Type 1 transmission and AIDS disease progression

Candidate gene
Marker	autoantibody against CCL3 is associated with human type 1 diabetes mellitus (T1DM) and serves as a novel biomarker for its diagnosis
	specifically predicts future cardiovascular events, and may serve as a predictive biomarker
	CCL2 and CCL3 are associated with progression of oral squamous cell carcinoma (OSCC) and may be potential biomarkers
	decreased preclinical CCL3 and CCL4 levels might be associated with a subsequently increased risk of nasopharyngeal carcinoma
Therapy target
	System Type Disorder Pubmed diabete type 1   preferential target for therapy of T1DM immunology infectious   Pharmacological modulation of the CCL3 pathways might, therefore, represent a future therapeutic option to manage Streptococcus pneumoniae meningitis cancer hemopathy   inhibition of MIP-1α may thus provide a new therapeutic approach to control tumor progression and bone destruction in patients with multiple myeloma (MM)

ANIMAL & CELL MODELS

	homozygous knockout mice
	CCL3-/- mice had loss of mature myeloid populations, while myeloid progenitors and HSPCs were increased, and microenvironmental populations were unchanged