CCL9

Ccl9
Identifikatori
Aliasi
Vanjski ID-jevi	HomoloGene: 86734 GeneCards: [1]
Lokacija gena (čovjek)
Hrom.	Hromosom 11 (čovjek)
Kraj	83,469,462 bp
Ontologija gena
Molekularna funkcija	• CCR chemokine receptor binding; • chemokine activity; • cytokine activity;
Ćelijska komponenta	• extracellular region; • Vanćelijsko;
Biološki proces	• neutrophil chemotaxis; • negative regulation of myoblast differentiation; • cellular response to tumor necrosis factor; • positive regulation of ERK1 and ERK2 cascade; • inflammatory response; • GO:0032320, GO:0032321, GO:0032855, GO:0043089, GO:0032854 positive regulation of GTPase activity; • G protein-coupled receptor signaling pathway; • lymphocyte chemotaxis; • monocyte chemotaxis; • cellular response to interferon-gamma; • cellular response to interleukin-1; • GO:0046730, GO:0046737, GO:0046738, GO:0046736 Imuni odgovor; • chemokine-mediated signaling pathway; • Hemotaksija; • regulation of signaling receptor activity; • eosinophil chemotaxis;
	Izvori:Amigo / QuickGO
Ortolozi
	20308
	n/a
	ENSMUSG00000019122
	n/a
	P51670
	n/a
	NM_011338
	n/a
	NP_035468
	n/a
	Wikipodaci
Pogledaj/uredi – čovjek

Hemokinski (C-C motivni) ligand 9 (CCL9) je mali citokin koji pripada porodici CC hemokina. Nazivaju ga i upalni protein-1 gama makrofaga (MIP-1γ), protein-2 povezan s upalnim proteinom makrofaga-2 (MRP-2) i CCF18, koji je opisan kod glodara. CCL9 je također ranije bio označen kao CCL10, iako se ovaj naziv više ne koristi. Izlučuju ga s folikulima vezani epitel (FAE), poput onog koji se nalazi oko Peyerovih pjega i privlači dendritske ćelije koje posjeduju molekule ćelijske površine CD11b i hemokinski receptor CCR1.^[2] CCL9 može aktivirati osteoklaste preko svog receptora CCR1 (najzastupljeniji receptor hemokina koji se nalazi na osteoklastima) što ukazuje na važnu ulogu CCL9 u resorpciji kosti.^[3] CCL9 je konstitutivno izražen u makrofazima i mijeloidnim ćelijama.^[4]^[5] Kod ljudi, gen za CCL9 nalazi se na hrohromosomu 11.^[5]

CCL9 je hemokin uključen u proces signaliziranja antileuhemijskog odgovora i potencijalni je oblik imunoterapije za hroničnu mijeloidnu leukemiju (CML). CML je tip raka u kojem koštana srž proizvodi previše crvenih krvnih zrnaca. To je uzrokovano translokacijskom mutacijom u kojoj se abnormalni gen BCR-ABL pretvara u CML ćeliju. CML počinje kao mijeloproliferativna, naprimjer u anemiji srpastih eritrocita ili ekstremna granulocitoza, ali ako se ne liječi, može se transformirati u akutni oblik leukemije. Za liječenje CML-a, koriste se alfa i beta interferoni (INF) za regulaciju procesa vezivanja proteina ICSBP za gen BCR-ABL. Dokazano je da je gen CCL9 induciran ICSBP-om i IFN-alfa-om, a također i zahtjev u ekspresiji ICSBP-a u BCR-ABL transformiranim ćelijama za generiranje eksperimentalne antileukemijske imunske zaštite. CCL6 i CCL9 bili su prekomjerno eksprimirani u BaF3 ćelijama i ubrizgani BCR-ABL u singene miševe. Iako su miševi još uvijek razvili leukemiju, to je odložilo napredovanje bolesti za nekoliko sedmica, dokazujući da CCL6 i CCL9 doprinose stvaranju antileukemijskog odgovora unutar zaraženih ćelija.^[6]

Reference

^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^ 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.
^ 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.
^ 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. PMID 7650394.
^ ^a ^b Hara 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. PMID 7594550.
^ 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.

[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. PMID 7650394.

[hara-5] Hara 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. PMID 7594550.

[pmid19171873-6] 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.

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