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CCL9

From Wikipedia, the free encyclopedia

Mammalian protein found in Mus musculus
Ccl9
Identifiers
Aliaseschemokine (C-C motif) ligand 9CCF18MRP-2Scya10Scya9
External IDsHomoloGene:86734;GeneCards:[1];OMA:- orthologs
Gene location (Human)
Chromosome 11 (human)
Chr.Chromosome 11 (human)
Chromosome 11 (human)
Genomic location for Ccl9
Genomic location for Ccl9
Band11 C|11 50.81 cMStart83,463,745bp
End83,469,462bp
RNA expression pattern
Bgee
HumanMouse (ortholog)
Top expressed in
  • stroma of bone marrow

  • lacrimal gland

  • crypt of lieberkuhn of small intestine

  • left lobe of liver

  • intercostal muscle

  • white adipose tissue

  • subcutaneous adipose tissue

  • Paneth cell

  • ankle joint

  • blood
    n/a
More reference expression data
BioGPS
n/a
Gene ontology
Molecular function
Cellular component
Biological process
Sources:Amigo /QuickGO
Orthologs
SpeciesHumanMouse
Entrez

20308

n/a

Ensembl

ENSMUSG00000019122

n/a

UniProt

P51670

n/a

RefSeq (mRNA)

NM_011338

n/a

RefSeq (protein)

NP_035468

n/a

Location (UCSC)Chr 11: 83.46 – 83.47 Mbn/a
PubMed search[1]n/a
Wikidata
View/Edit Human

Chemokine (C-C motif) ligand 9 (CCL9) is a smallcytokine belonging to the CCchemokine family. It is also calledmacrophage inflammatory protein-1 gamma (MIP-1γ),macrophage inflammatory protein-related protein-2 (MRP-2) and CCF18, that has been described in rodents. CCL9 has also been previously designatedCCL10, although this name is no longer in use. It is secreted byfollicle-associatedepithelium (FAE) such as that found aroundPeyer's patches, and attractsdendritic cells that possess the cell surface moleculeCD11b and thechemokine receptorCCR1.[2] CCL9 can activateosteoclasts through its receptor CCR1 (the most abundant chemokine receptor found on osteoclasts) suggesting an important role for CCL9 inbone resorption.[3] CCL9 is constitutively expressed inmacrophages andmyeloid cells.[4][5] Thegene for CCL9 is located onchromosome 11 in mice.[5]

CCL9 is a chemokine involved in the process of signaling an antileukemic response and is a potential form of immunotherapy forchronic myelogenous leukemia (CML). CML is a type of cancer in which the bone marrow produces too many red blood cells. This is caused bychromosomal translocation, a mutation in which the abnormal gene BCR-ABL, is turned into a CML cell. CML starts off as amyeloproliferative for example insickle cell anemia or extremegranulocytosis but if left untreated, it could transform into an acute form of leukemia. In order to treat CML, alpha and beta interferons (INFs) are used to regulate the process of binding the protein ICSBP to the gene BCR-ABL. CCL9 was proved to be a gene induced by ICSBP and IFN alpha and also a requirement in the expression of ICSBP in BCR-ABL transformed cells to generate an anti-leukemic immune protection via experimentation. CCL6 and CCL9 were overexpressed in BaF3 cells and injected with BCR-ABL into syngeneic mice. Although the mice still developed leukemia, it delayed the advancement of the disease by several weeks proving that CCL6 and CCL9 contribute to the creation of an anti-leukemic response within infected cells.[6][unreliable medical source]

References

[edit]
  1. ^"Human PubMed Reference:".National Center for Biotechnology Information, U.S. National Library of Medicine.
  2. ^Zhao X, Sato A, Dela Cruz C, Linehan M, Luegering A, Kucharzik T, Shirakawa A, Marquez G, Farber J, Williams I, Iwasaki A (2003)."CCL9 is secreted by the follicle-associated epithelium and recruits dome region Peyer's patch CD11b+ dendritic cells".J Immunol.171 (6):2797–803.doi:10.4049/jimmunol.171.6.2797.PMID 12960300.
  3. ^Lean J, Murphy C, Fuller K, Chambers T (2002). "CCL9/MIP-1gamma and its receptor CCR1 are the major chemokine ligand/receptor species expressed by osteoclasts".J Cell Biochem.87 (4):386–93.doi:10.1002/jcb.10319.PMID 12397598.S2CID 23954377.
  4. ^Youn B, Jang I, Broxmeyer H, Cooper S, Jenkins N, Gilbert D, Copeland N, Elick T, Fraser M, Kwon B (1995)."A novel chemokine, macrophage inflammatory protein-related protein-2, inhibits colony formation of bone marrow myeloid progenitors".J Immunol.155 (5):2661–7.doi:10.4049/jimmunol.155.5.2661.PMID 7650394.
  5. ^abHara T, Bacon K, Cho L, Yoshimura A, Morikawa Y, Copeland N, Gilbert D, Jenkins N, Schall T, Miyajima A (1995)."Molecular cloning and functional characterization of a novel member of the C-C chemokine family".J Immunol.155 (11):5352–8.doi:10.4049/jimmunol.155.11.5352.PMID 7594550.
  6. ^Nardi V, Naveiras O, Azam M, Daley GQ (April 2009)."ICSBP-mediated immune protection against BCR-ABL-induced leukemia requires the CCL6 and CCL9 chemokines".Blood.113 (16):3813–20.doi:10.1182/blood-2008-07-167189.PMC 2670796.PMID 19171873.


By family
Chemokine
CCL
CXCL
CX3CL
XCL
TNF
Interleukin
Type I
(grouped by
receptor
subunit)
γ chain
β chain
IL6 like/gp130
IL12 family/IL12RB1
Other
Type II
IL10 family
Interferon
I
II
Ig superfamily
IL17 family
Other
By function/
cell
CC
CCR1
CCR2
CCR3
CCR4
CCR5
CCR6
CCR7
CCR8
CCR9
CCR10
CCR11
Ungrouped
CXC
CXCR1
(IL-8Rα)
CXCR2
(IL-8Rβ)
CXCR3
CXCR4
CXCR5
CXCR6
CXCR7
C (XC)
XCR1
CX3C
CX3CR1
Others
CCBP2
CMKLR1


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