Ignet

Gene Information

Gene symbol: COX8A

Gene name: cytochrome c oxidase subunit VIIIA (ubiquitous)

HGNC ID: 2294

Synonyms: COX8-2, COX8L, VIII-L, COX, VIII

Related Genes

#	Gene Symbol	Number of hits
1	CISH	1 hits
2	IL12A	1 hits
3	MMP9	1 hits
4	NOD2	1 hits
5	PTGS1	1 hits
6	PTGS2	1 hits
7	SOCS3	1 hits
8	VEGFA	1 hits

Related Sentences

#	PMID	Sentence
1	12949405	Cyclooxygenase (COX) enzymes catalyze the synthesis of prostaglandins and exist as two isoforms, COX-1 and COX-2.
2	16272346	Contrasting effects of cyclooxygenase-1 (COX-1) and COX-2 deficiency on the host response to influenza A viral infection.
3	16272346	The cyclooxygenase (COX) pathway is important in modulating immune responses and is also a major target of nonsteroidal anti-inflammatory drugs (NSAIDs) and the newer COX-2 inhibitors.
4	16272346	The purpose of the present study was to examine the effect of deficiency of COX-1 or COX-2 on the host response to influenza.
5	16272346	We used an influenza A viral infection model in wild type (WT), COX-1-/-, and COX-2-/- mice.
6	16272346	Infection induced less severe illness in COX-2-/- mice in comparison to WT and COX-1-/- mice as evidenced by body weight and body temperature changes.
7	16272346	COX-1-/- mice had enhanced inflammation and earlier appearance of proinflammatory cytokines in the BAL fluid, whereas the inflammatory and cytokine responses were blunted in COX-2-/- mice.
8	16272346	However, lung viral titers were markedly elevated in COX-2-/- mice relative to WT and COX-1-/- mice on day 4 of infection.
9	16272346	Levels of PGE2 were reduced in COX-1-/- airways whereas cysteinyl leukotrienes were elevated in COX-2-/- airways following infection.
10	16272346	Thus, deficiency of COX-1 and COX-2 leads to contrasting effects in the host response to influenza infection, and these differences are associated with altered production of prostaglandins and leukotrienes following infection.
11	16272346	COX-1 deficiency is detrimental whereas COX-2 deficiency is beneficial to the host during influenza viral infection.
12	16822852	Previous studies have shown that prostaglandin E(2) (PGE(2)) release by splenic F4/80(+) cyclooxygenase (COX)-2(+) macrophages (MØ) isolated from mice, treated with mycobacterial components, plays a major role in the regulation of immune responses.
13	16822852	However, splenic MØ, isolated from untreated mice and treated in vitro with lipopolysaccharide and interferon-gamma, express COX-1 and COX-2 within 1 day but release only minimal amounts of PGE(2) following elicitation with calcium ionophore A23187.
14	16822852	In sharp contrast, 14 days after HK-BCG treatment, PGE(2) release by COX-2(+) splenic MØ increased as much as sevenfold, and a greater increase was seen in IL-10(-/-) cells than in WT cells.
15	17159912	CpG-ODN induces the expression of cyclooxygenase (COX)-2, and its product prostaglandin (PG) E2 underlies an immunosuppressive network, therefore it is a simple strategy to use a COX-2 inhibitor for tumor vaccination with CpG-ODN.
16	17464165	Cyclo-oxygenase (COX)-2 inhibitors are also alleged to have a function in interrupting the development of HCC.
17	17473370	Vaccination efficacy can be amplified by depleting CD4;+CD25;+Foxp3;+ regulatory T cells (Treg), but the risk of inducing autoimmunity warrants new strategies to selectively amplify anti-tumor immunity when modulating Treg.
18	17473370	In the tumors, the major cyclooxygenase (COX)-2 product is prostaglandin E2(PGE2) which suppresses T and NK cells while amplifying Treg.
19	26391398	Ac2PIM-responsive miR-150 and miR-143 target receptor-interacting protein kinase 2 and transforming growth factor beta-activated kinase 1 to suppress NOD2-induced immunomodulators.
20	26391398	While Ac2PIM treatment of macrophages compromised their ability to induce NOD2-dependent immunomodulators like cyclooxygenase (COX)-2, suppressor of cytokine signaling (SOCS)-3, and matrix metalloproteinase (MMP)-9, no change in the NOD2-responsive NO, TNF-α, VEGF-A, and IL-12 levels was observed.
21	26391398	Further, genome-wide microRNA expression profiling identified Ac2PIM-responsive miR-150 and miR-143 to target NOD2 signaling adaptors, RIP2 and TAK1, respectively.
22	26391398	Interestingly, Ac2PIM was found to activate the SRC-FAK-PYK2-CREB cascade via TLR2 to recruit CBP/P300 at the promoters of miR-150 and miR-143 and epigenetically induce their expression.
23	26391398	Loss-of-function studies utilizing specific miRNA inhibitors establish that Ac2PIM, via the miRNAs, abrogate NOD2-induced PI3K-PKCδ-MAPK pathway to suppress β-catenin-mediated expression of COX-2, SOCS-3, and MMP-9.