Ignet

Gene Information

Gene symbol: MAPK14

Gene name: mitogen-activated protein kinase 14

HGNC ID: 6876

Synonyms: PRKM14, p38, Mxi2, PRKM15

Related Genes

#	Gene Symbol	Number of hits
1	CD4	1 hits
2	CREB3L4	1 hits
3	CSF3	1 hits
4	HIST1H3A	1 hits
5	HIST1H3H	1 hits
6	IFNA1	1 hits
7	IFNA14	1 hits
8	IFNA4	1 hits
9	IFNA5	1 hits
10	IFNA6	1 hits
11	IFNA8	1 hits
12	IFNAR1	1 hits
13	IFNG	1 hits
14	IL17A	1 hits
15	IL6	1 hits
16	IL8	1 hits
17	IRF9	1 hits
18	KCNA2	1 hits
19	KCNA3	1 hits
20	MAPK1	1 hits
21	MAPK3	1 hits
22	MAPK4	1 hits
23	MAPK6	1 hits
24	NET1	1 hits
25	NFKB1	1 hits
26	PIK3C2A	1 hits
27	SH2D1A	1 hits
28	TNF	1 hits
29	TSPAN1	1 hits

Related Sentences

#	PMID	Sentence
1	28936833	The top 10 important nodes of SAP overlapped with Salvianolate injection and aspirin included MAPK14, MAPK8, IL-6 and IL-8.
2	28936833	The important SAP nodes overlapped with Salvianolate injection alone included AKT1 and IFNG, and the important SAP nodes overlapped with aspirin included EPHB2 and TP53.
3	28611474	p38α regulates cytokine-induced IFNγ secretion via the Mnk1/eIF4E pathway in Th1 cells.
4	28611474	p38α regulates cytokine-induced IFNγ secretion via the Mnk1/eIF4E pathway in Th1 cells.
5	28611474	The p38 mitogen-activated protein kinase (MAPK) pathway is involved in the regulation of immune and inflammatory processes.
6	28611474	The p38 mitogen-activated protein kinase (MAPK) pathway is involved in the regulation of immune and inflammatory processes.
7	28611474	We used p38α-conditional, p38β-deficient and p38α/β double-null mouse models to address the role of these two p38 MAPK in CD4⁺ T cells, and found that p38α deficiency causes these cells to hyperproliferate.
8	28611474	We used p38α-conditional, p38β-deficient and p38α/β double-null mouse models to address the role of these two p38 MAPK in CD4⁺ T cells, and found that p38α deficiency causes these cells to hyperproliferate.
9	28611474	Our studies indicate that both p38α and p38β are dispensable for T helper cell type 1 (Th1) differentiation but, by controlling interferon (IFN)γ and tumor necrosis factor (TNF)α production, are critical for normal Th1 effector function.
10	28611474	Our studies indicate that both p38α and p38β are dispensable for T helper cell type 1 (Th1) differentiation but, by controlling interferon (IFN)γ and tumor necrosis factor (TNF)α production, are critical for normal Th1 effector function.
11	28611474	Our results indicate that p38α regulates IFNγ secretion through the activation of the MNK1/eIF4E pathway of translation initiation and identify specific functions for p38α and p38β in T-cell proliferation.
12	28611474	Our results indicate that p38α regulates IFNγ secretion through the activation of the MNK1/eIF4E pathway of translation initiation and identify specific functions for p38α and p38β in T-cell proliferation.
13	28581888	Accordingly, we showed that IL17A and IFNG expression in lymphocytes from tuberculosis patients correlates with disease severity.
14	28581888	Here we investigate the role of IFNG and IL17A during autophagy in monocytes infected with Mt H37Rv or the mutant MtΔRD1.
15	28581888	IL17A augmented autophagy in infected monocytes from HR patients through a mechanism that activated MAPK1/ERK2-MAPK3/ERK1 but, during infection of monocytes from LR patients, IL17A had no effect on the autophagic response.
16	28581888	In contrast, addition of IFNG to infected monocytes, increased autophagy by activating MAPK14/p38 α both in HR and LR patients.
17	28581888	Interestingly, proteins codified in the RD1 region did not interfere with IFNG and IL17A autophagy induction.
18	28581888	In contrast, both IFNG and IL17A increased autophagy levels in patients with strong immunity to Mt, promoting mycobacterial killing.
19	28239238	Bioinformatics analysis indicated that the cytokine imbalance relevant to key molecules (such as extracellular signal-regulated kinase 1/2 (ERK1/2), p38 mitogen-activated protein kinase (MAPK), tumor necrosis factor (TNF), colony-stimulating factor 3 (CSF3), interleukin- (IL-) 6, and interferon gene (IFNG)) and canonical signaling pathways (such as the complement system, antigen presentation, macropinocytosis signaling, nuclear factor-kappa B (NF-κB) signaling, and IL-17 signaling) was responsible for the common comprehensive mechanism of PS and RA.
20	25774455	Genes that were significantly regulated between VRs and VNRs were CREB3L4, HIST1H3A, HIST1H3H, IFNA1, IFNA4, IFNA5, IFNA6, IFNA8, IFNA14, IFNG, IFNAR1, IL6, IRF9, MAPK4, MAPK5, MAPK14, NET1, and PIK3C2A in the IFN array.
21	25774455	In the TLR array, only LBP and MAPK8 were found to be differentially regulated.
22	25774455	In the antigen processing array, HLA-A, HLA-C, HLA-DMA, HLA-DMB, HLA-F, PSMA5, PSMB8, and PSMB9 were differentially downregulated.
23	24935968	MAPKAP kinase 3 suppresses Ifng gene expression and attenuates NK cell cytotoxicity and Th1 CD4 T-cell development upon influenza A virus infection.
24	24935968	MAPKAP kinase 3 suppresses Ifng gene expression and attenuates NK cell cytotoxicity and Th1 CD4 T-cell development upon influenza A virus infection.
25	24935968	MK2 and MK3 are downstream targets of p38 and ERK1/2.
26	24935968	MK2 and MK3 are downstream targets of p38 and ERK1/2.
27	24935968	Using Mk-deficient and wild-type (WT) mice, we demonstrated an inhibitory effect of MK3, but not of MK2, on interferon (IFN)-γ expression in T and NK lymphocytes.
28	24935968	Using Mk-deficient and wild-type (WT) mice, we demonstrated an inhibitory effect of MK3, but not of MK2, on interferon (IFN)-γ expression in T and NK lymphocytes.
29	24935968	The results provided evidence that the inhibitory effect of MK3 is based on negative feedback phosphorylation of p38 and ERK1/2, which causes decreased binding of Stat4 to the IFN-γ promoter and reduced expression of IFN-γ mRNA and protein.
30	24935968	The results provided evidence that the inhibitory effect of MK3 is based on negative feedback phosphorylation of p38 and ERK1/2, which causes decreased binding of Stat4 to the IFN-γ promoter and reduced expression of IFN-γ mRNA and protein.
31	24935968	The reduced disease severity in the Mk3(-/-) mice was accompanied by a >10-fold reduction in viral lung titer and an increase in the number of activated NK cells and enhanced Th1 activation of CD4 T cells.
32	24935968	The reduced disease severity in the Mk3(-/-) mice was accompanied by a >10-fold reduction in viral lung titer and an increase in the number of activated NK cells and enhanced Th1 activation of CD4 T cells.