Ignet

Gene Information

Gene symbol: EIF2AK2

Gene name: eukaryotic translation initiation factor 2-alpha kinase 2

HGNC ID: 9437

Synonyms: PKR, EIF2AK1

Related Genes

#	Gene Symbol	Number of hits
1	ADA	1 hits
2	ADAR	1 hits
3	ADARB1	1 hits
4	AKT1	1 hits
5	ANXA1	1 hits
6	ATF2	1 hits
7	CALR	1 hits
8	CD40	1 hits
9	CD46	1 hits
10	CD80	1 hits
11	CD86	1 hits
12	CD8A	1 hits
13	CIITA	1 hits
14	DDX58	1 hits
15	EIF2AK3	1 hits
16	EIF2S1	1 hits
17	GTF2H2	1 hits
18	HLA-A	1 hits
19	ICAM1	1 hits
20	IFIH1	1 hits
21	IFITM3	1 hits
22	IFN1	1 hits
23	IFNA1	1 hits
24	IFNA2	1 hits
25	IFNB1	1 hits
26	IFNG	1 hits
27	IL2RB	1 hits
28	IL6R	1 hits
29	IL8RA	1 hits
30	IRF3	1 hits
31	ITGAL	1 hits
32	JUN	1 hits
33	KHDRBS1	1 hits
34	LGALS3	1 hits
35	MAP3K7	1 hits
36	MAPK8	1 hits
37	MAPK9	1 hits
38	MRC1	1 hits
39	MX1	1 hits
40	MYD88	1 hits
41	NFKB1	1 hits
42	NFKBIA	1 hits
43	NOS2A	1 hits
44	OAS1	1 hits
45	OAS2	1 hits
46	PIK3CA	1 hits
47	PTX3	1 hits
48	RSAD2	1 hits
49	TICAM1	1 hits
50	TLR2	1 hits
51	TLR4	1 hits

Related Sentences

#	PMID	Sentence
1	12228285	Infection of mice with Dam(+) Salmonella resulted in the induction of host genes known to be indicators of IFN bioactivity and regulated by either IFN-alpha/beta (Mx1) or IFN-gamma (class II transactivator protein [CIITA] and inducible nitric oxide synthase [iNOS]) or by both IFN-alpha/beta and IFN-gamma (RNA-specific adenosine deaminase [ADAR1] and RNA-dependent protein kinase [PKR]) in a tissue-specific manner compared to uninfected animals.
2	12228285	Since the Mx1 promoter is IFN-alpha/beta specific and the Mx1 gene is not inducible directly by IFN-gamma, these data suggest a role of IFN-alpha/beta in the host response to Salmonella infection.
3	12228285	Finally, although no Dam(-) organisms were recovered from the liver or spleen after oral infection of mice, ADAR, PKR, Mx, and CIITA expression levels were elevated in these tissues relative to those in uninfected mice, suggestive of the distant action of a signaling molecule(s) in the activation of ISG expression.
4	12228285	Infection of mice with Dam(+) Salmonella resulted in the induction of host genes known to be indicators of IFN bioactivity and regulated by either IFN-alpha/beta (Mx1) or IFN-gamma (class II transactivator protein [CIITA] and inducible nitric oxide synthase [iNOS]) or by both IFN-alpha/beta and IFN-gamma (RNA-specific adenosine deaminase [ADAR1] and RNA-dependent protein kinase [PKR]) in a tissue-specific manner compared to uninfected animals.
5	12228285	Since the Mx1 promoter is IFN-alpha/beta specific and the Mx1 gene is not inducible directly by IFN-gamma, these data suggest a role of IFN-alpha/beta in the host response to Salmonella infection.
6	12228285	Finally, although no Dam(-) organisms were recovered from the liver or spleen after oral infection of mice, ADAR, PKR, Mx, and CIITA expression levels were elevated in these tissues relative to those in uninfected mice, suggestive of the distant action of a signaling molecule(s) in the activation of ISG expression.
7	17855554	MVA stimulation of bone marrow-derived dendritic cells (DC) showed that plasmacytoid DC were main alpha IFN (IFN-alpha) producers that were triggered independently of productive infection, viral replication, or intermediate and late viral gene expression.
8	17855554	Increased IFN-alpha levels were induced upon treatment with mildly UV-irradiated MVA, suggesting that a virus-encoded immune modulator(s) interfered with the host cytokine response.
9	17855554	Mice devoid of Toll-like receptor 9 (TLR9), the receptor for double-stranded DNA, mounted normal IFN-alpha responses upon MVA treatment.
10	17855554	Furthermore, mice devoid of the adaptors of TLR signaling MyD88 and TRIF and mice deficient in protein kinase R (PKR) showed IFN-alpha responses that were only slightly reduced compared to those of wild-type mice.
11	17855554	MVA-induced IFN-alpha responses were critically dependent on autocrine/paracrine triggering of the IFN-alpha/beta receptor and were independent of IFN-beta, thus involving "one-half" of a positive-feedback loop.
12	19596385	Modified vaccinia virus Ankara can activate NF-kappaB transcription factors through a double-stranded RNA-activated protein kinase (PKR)-dependent pathway during the early phase of virus replication.
13	19596385	In human embryonic kidney (HEK 293T) cells, the MVA-induced depletion of IkappaBalpha required to activate NF-kappaB is inhibited by UV-inactivation of the virus, and begins before viral DNA replication.
14	19596385	In mouse embryonic fibroblasts (MEFs), MVA induction of IkappaBalpha depletion is dependent on the expression of mouse or human double-stranded RNA-activated protein kinase (PKR).
15	19596385	These results demonstrate that events during the early phase of MVA replication can induce PKR-mediated processes contributing both to the activation of NF-kappaB signaling, and to processes that may restrict viral replication.
16	19596385	Modified vaccinia virus Ankara can activate NF-kappaB transcription factors through a double-stranded RNA-activated protein kinase (PKR)-dependent pathway during the early phase of virus replication.
17	19596385	In human embryonic kidney (HEK 293T) cells, the MVA-induced depletion of IkappaBalpha required to activate NF-kappaB is inhibited by UV-inactivation of the virus, and begins before viral DNA replication.
18	19596385	In mouse embryonic fibroblasts (MEFs), MVA induction of IkappaBalpha depletion is dependent on the expression of mouse or human double-stranded RNA-activated protein kinase (PKR).
19	19596385	These results demonstrate that events during the early phase of MVA replication can induce PKR-mediated processes contributing both to the activation of NF-kappaB signaling, and to processes that may restrict viral replication.
20	19596385	Modified vaccinia virus Ankara can activate NF-kappaB transcription factors through a double-stranded RNA-activated protein kinase (PKR)-dependent pathway during the early phase of virus replication.
21	19596385	In human embryonic kidney (HEK 293T) cells, the MVA-induced depletion of IkappaBalpha required to activate NF-kappaB is inhibited by UV-inactivation of the virus, and begins before viral DNA replication.
22	19596385	In mouse embryonic fibroblasts (MEFs), MVA induction of IkappaBalpha depletion is dependent on the expression of mouse or human double-stranded RNA-activated protein kinase (PKR).
23	19596385	These results demonstrate that events during the early phase of MVA replication can induce PKR-mediated processes contributing both to the activation of NF-kappaB signaling, and to processes that may restrict viral replication.
24	19846517	The enhanced IFN-inducing capacity of the C(ko) virus correlated with an enhanced activation of IFN regulatory factor 3 (IRF-3), NF-kappaB, and ATF-2 in C(ko)-infected compared to V(ko) or parental virus-infected cells.
25	19846517	Furthermore, protein kinase PKR and mitochondrial adapter IPS-1 were required for maximal C(ko)-mediated IFN-beta induction, which correlated with the PKR-mediated enhancement of mitogen-activated protein kinase and NF-kappaB activation.
26	19846517	Our results reveal multiple consequences of C protein expression and document an important function for PKR as an enhancer of IFN-beta induction during measles virus infection.
27	19846517	The enhanced IFN-inducing capacity of the C(ko) virus correlated with an enhanced activation of IFN regulatory factor 3 (IRF-3), NF-kappaB, and ATF-2 in C(ko)-infected compared to V(ko) or parental virus-infected cells.
28	19846517	Furthermore, protein kinase PKR and mitochondrial adapter IPS-1 were required for maximal C(ko)-mediated IFN-beta induction, which correlated with the PKR-mediated enhancement of mitogen-activated protein kinase and NF-kappaB activation.
29	19846517	Our results reveal multiple consequences of C protein expression and document an important function for PKR as an enhancer of IFN-beta induction during measles virus infection.
30	20585572	Here, we have investigated the role of PKR and Type I IFNs in regulating viral clearance and CD8+ T cell response during primary and secondary viral infections.
31	20585572	Our studies demonstrate differential requirement for PKR, in viral control versus elicitation of CD8+ T cell responses during primary infection of mice with lymphocytic choriomeningitis virus (LCMV).
32	20585572	PKR-deficient mice mounted potent CD8+ T cell responses, but failed to effectively control LCMV.
33	20585572	The compromised LCMV control in the absence of PKR was multifactorial, and linked to less effective CD8+ T cell-mediated viral suppression, enhanced viral replication in cells, and lower steady state expression levels of IFN-responsive genes.
34	20585572	Moreover, we show that despite normal expansion of memory CD8+ T cells and differentiation into effectors during a secondary response, effective clearance of LCMV but not vaccinia virus required PKR activity in infected cells.
35	20585572	Here, we have investigated the role of PKR and Type I IFNs in regulating viral clearance and CD8+ T cell response during primary and secondary viral infections.
36	20585572	Our studies demonstrate differential requirement for PKR, in viral control versus elicitation of CD8+ T cell responses during primary infection of mice with lymphocytic choriomeningitis virus (LCMV).
37	20585572	PKR-deficient mice mounted potent CD8+ T cell responses, but failed to effectively control LCMV.
38	20585572	The compromised LCMV control in the absence of PKR was multifactorial, and linked to less effective CD8+ T cell-mediated viral suppression, enhanced viral replication in cells, and lower steady state expression levels of IFN-responsive genes.
39	20585572	Moreover, we show that despite normal expansion of memory CD8+ T cells and differentiation into effectors during a secondary response, effective clearance of LCMV but not vaccinia virus required PKR activity in infected cells.
40	20585572	Here, we have investigated the role of PKR and Type I IFNs in regulating viral clearance and CD8+ T cell response during primary and secondary viral infections.
41	20585572	Our studies demonstrate differential requirement for PKR, in viral control versus elicitation of CD8+ T cell responses during primary infection of mice with lymphocytic choriomeningitis virus (LCMV).
42	20585572	PKR-deficient mice mounted potent CD8+ T cell responses, but failed to effectively control LCMV.
43	20585572	The compromised LCMV control in the absence of PKR was multifactorial, and linked to less effective CD8+ T cell-mediated viral suppression, enhanced viral replication in cells, and lower steady state expression levels of IFN-responsive genes.
44	20585572	Moreover, we show that despite normal expansion of memory CD8+ T cells and differentiation into effectors during a secondary response, effective clearance of LCMV but not vaccinia virus required PKR activity in infected cells.
45	20585572	Here, we have investigated the role of PKR and Type I IFNs in regulating viral clearance and CD8+ T cell response during primary and secondary viral infections.
46	20585572	Our studies demonstrate differential requirement for PKR, in viral control versus elicitation of CD8+ T cell responses during primary infection of mice with lymphocytic choriomeningitis virus (LCMV).
47	20585572	PKR-deficient mice mounted potent CD8+ T cell responses, but failed to effectively control LCMV.
48	20585572	The compromised LCMV control in the absence of PKR was multifactorial, and linked to less effective CD8+ T cell-mediated viral suppression, enhanced viral replication in cells, and lower steady state expression levels of IFN-responsive genes.
49	20585572	Moreover, we show that despite normal expansion of memory CD8+ T cells and differentiation into effectors during a secondary response, effective clearance of LCMV but not vaccinia virus required PKR activity in infected cells.
50	20585572	Here, we have investigated the role of PKR and Type I IFNs in regulating viral clearance and CD8+ T cell response during primary and secondary viral infections.
51	20585572	Our studies demonstrate differential requirement for PKR, in viral control versus elicitation of CD8+ T cell responses during primary infection of mice with lymphocytic choriomeningitis virus (LCMV).
52	20585572	PKR-deficient mice mounted potent CD8+ T cell responses, but failed to effectively control LCMV.
53	20585572	The compromised LCMV control in the absence of PKR was multifactorial, and linked to less effective CD8+ T cell-mediated viral suppression, enhanced viral replication in cells, and lower steady state expression levels of IFN-responsive genes.
54	20585572	Moreover, we show that despite normal expansion of memory CD8+ T cells and differentiation into effectors during a secondary response, effective clearance of LCMV but not vaccinia virus required PKR activity in infected cells.
55	21464971	Co-expression of miRNA targeting the expression of PERK, but not PKR, enhances cellular immunity from an HIV-1 Env DNA vaccine.
56	21464971	Using the miR-155-expressing intron as a scaffold, we developed novel vectors for miRNA-mediated targeting of the cellular antiviral proteins PKR and PERK, which significantly down-modulated target gene expression and led to increased Env expression in vitro.
57	21464971	Finally, vaccinating BALB/c mice with a DNA vaccine vector delivering miRNA targeting PERK, but not PKR, was able to augment the generation of Env-specific T-cell immunity.
58	21464971	Co-expression of miRNA targeting the expression of PERK, but not PKR, enhances cellular immunity from an HIV-1 Env DNA vaccine.
59	21464971	Using the miR-155-expressing intron as a scaffold, we developed novel vectors for miRNA-mediated targeting of the cellular antiviral proteins PKR and PERK, which significantly down-modulated target gene expression and led to increased Env expression in vitro.
60	21464971	Finally, vaccinating BALB/c mice with a DNA vaccine vector delivering miRNA targeting PERK, but not PKR, was able to augment the generation of Env-specific T-cell immunity.
61	21464971	Co-expression of miRNA targeting the expression of PERK, but not PKR, enhances cellular immunity from an HIV-1 Env DNA vaccine.
62	21464971	Using the miR-155-expressing intron as a scaffold, we developed novel vectors for miRNA-mediated targeting of the cellular antiviral proteins PKR and PERK, which significantly down-modulated target gene expression and led to increased Env expression in vitro.
63	21464971	Finally, vaccinating BALB/c mice with a DNA vaccine vector delivering miRNA targeting PERK, but not PKR, was able to augment the generation of Env-specific T-cell immunity.
64	21543505	NSs protein of rift valley fever virus promotes posttranslational downregulation of the TFIIH subunit p62.
65	21543505	Its NSs protein has previously been identified as a major virulence factor that suppresses host defense through three distinct mechanisms: it directly inhibits beta interferon (IFN-β) promoter activity, it promotes the degradation of double-stranded RNA-dependent protein kinase (PKR), and it suppresses host transcription by disrupting the assembly of the basal transcription factor TFIIH through sequestration of its p44 subunit.
66	21543505	Here, we report that in addition to PKR, NSs also promotes the degradation of the TFIIH subunit p62.
67	21543505	These data suggest that the RVFV NSs protein is able to interact with the TFIIH subunit p62 inside infected cells and promotes its degradation, which can occur directly in the nucleus.
68	21543505	NSs protein of rift valley fever virus promotes posttranslational downregulation of the TFIIH subunit p62.
69	21543505	Its NSs protein has previously been identified as a major virulence factor that suppresses host defense through three distinct mechanisms: it directly inhibits beta interferon (IFN-β) promoter activity, it promotes the degradation of double-stranded RNA-dependent protein kinase (PKR), and it suppresses host transcription by disrupting the assembly of the basal transcription factor TFIIH through sequestration of its p44 subunit.
70	21543505	Here, we report that in addition to PKR, NSs also promotes the degradation of the TFIIH subunit p62.
71	21543505	These data suggest that the RVFV NSs protein is able to interact with the TFIIH subunit p62 inside infected cells and promotes its degradation, which can occur directly in the nucleus.
72	21994357	Interestingly, we show that upon activation by anti-CD40 and gamma interferon (IFN-γ), B cells from PKR(-/-) mice show diminished major histocompatibility complex class II (MHC II), CD80, and CD86 levels on the cell surface compared to wild-type (WT) mice.
73	21994357	Our data also show that PKR is necessary for optimal expression of adhesion molecules, such as CD11a and ICAM-1, that are necessary for homotypic aggregation of B cells.
74	21994357	Furthermore, in this report we demonstrate for the first time that upon CD40 ligation, PKR is rapidly phosphorylated and activated, indicating that PKR is an early and novel downstream mediator of CD40 signaling pathways.
75	21994357	Interestingly, we show that upon activation by anti-CD40 and gamma interferon (IFN-γ), B cells from PKR(-/-) mice show diminished major histocompatibility complex class II (MHC II), CD80, and CD86 levels on the cell surface compared to wild-type (WT) mice.
76	21994357	Our data also show that PKR is necessary for optimal expression of adhesion molecules, such as CD11a and ICAM-1, that are necessary for homotypic aggregation of B cells.
77	21994357	Furthermore, in this report we demonstrate for the first time that upon CD40 ligation, PKR is rapidly phosphorylated and activated, indicating that PKR is an early and novel downstream mediator of CD40 signaling pathways.
78	21994357	Interestingly, we show that upon activation by anti-CD40 and gamma interferon (IFN-γ), B cells from PKR(-/-) mice show diminished major histocompatibility complex class II (MHC II), CD80, and CD86 levels on the cell surface compared to wild-type (WT) mice.
79	21994357	Our data also show that PKR is necessary for optimal expression of adhesion molecules, such as CD11a and ICAM-1, that are necessary for homotypic aggregation of B cells.
80	21994357	Furthermore, in this report we demonstrate for the first time that upon CD40 ligation, PKR is rapidly phosphorylated and activated, indicating that PKR is an early and novel downstream mediator of CD40 signaling pathways.
81	22001879	NYCBHΔE3L induced phosphorylation of PKR and eIF2α as well as p38, SAPK/JNK, and IRF3 which can lead to induction of proinflammatory gene transcription.
82	22083261	NSs induces a shut-off of host transcription including interferon (IFN)-beta mRNA and promotes degradation of double-stranded RNA-dependent protein kinase (PKR) at the post-translational level.
83	22083261	IFN-beta is transcriptionally upregulated by interferon regulatory factor 3 (IRF-3), NF-kB and activator protein-1 (AP-1), and the binding of IFN-beta to IFN-alpha/beta receptor (IFNAR) stimulates the transcription of IFN-alpha genes or other interferon stimulated genes (ISGs), which induces host antiviral activities, whereas host transcription suppression including IFN-beta gene by NSs prevents the gene upregulations of those ISGs in response to viral replication although IRF-3, NF-kB and activator protein-1 (AP-1) can be activated by RVFV7.
84	22265947	In the current study we report the findings of a multigenic analysis of measles vaccine immunity, indicating a role for the measles virus receptor CD46, innate pattern-recognition receptors (DDX58, TLR2, 4, 5, 7 and 8) and intracellular signaling intermediates (MAP3K7, NFKBIA), and key antiviral molecules (VISA, OAS2, MX1, PKR) as well as cytokines (IFNA1, IL4, IL6, IL8, IL12B) and cytokine receptor genes (IL2RB, IL6R, IL8RA) in the genetic control of both humoral and cellular immune responses.
85	22278222	Adenosine deaminase acting on RNA 1 (ADAR1) suppresses the induction of interferon by measles virus.
86	22278222	ADAR1, the interferon (IFN)-inducible adenosine deaminase acting on RNA, catalyzes the C-6 deamination of adenosine (A) to produce inosine (I) in RNA substrates with a double-stranded character.
87	22278222	Because double-stranded RNA is a known inducer of IFN, we tested the role of ADAR1 in IFN induction following virus infection.
88	22278222	HeLa cells made stably deficient in ADAR1 (ADAR1(kd)) were compared to vector control (CON(kd)) and protein kinase PKR-deficient (PKR(kd)) cells for IFN-β induction following infection with either parental (wild-type [WT]) recombinant Moraten vaccine strain measles virus (MV) or isogenic knockout mutants deficient for either V (V(ko)) or C (C(ko)) protein expression.
89	22278222	We observed potent IFN-β transcript induction in ADAR1(kd) cells by all three viruses; in contrast, in ADAR1-sufficient CON(kd) cells, only the C(ko) mutant virus was an effective inducer and the IFN-β RNA induction was amplified by PKR.
90	22278222	The enhanced IFN-β transcript-inducing capacity of the WT and V(ko) viruses seen in ADAR1-deficient cells correlated with the enhanced activation of PKR, IFN regulatory factor IRF3, and activator of transcription ATF2, reaching levels similar to those seen in C(ko) virus-infected cells.
91	22278222	These results suggest that ADAR1 functions as an important suppressor of MV-mediated responses, including the activation of PKR and IRF3 and the induction of IFN-β RNA.
92	22278222	Our findings further implicate a balanced interplay between PKR and ADAR1 in modulating IFN-β protein production following virus infection.
93	22278222	Adenosine deaminase acting on RNA 1 (ADAR1) suppresses the induction of interferon by measles virus.
94	22278222	ADAR1, the interferon (IFN)-inducible adenosine deaminase acting on RNA, catalyzes the C-6 deamination of adenosine (A) to produce inosine (I) in RNA substrates with a double-stranded character.
95	22278222	Because double-stranded RNA is a known inducer of IFN, we tested the role of ADAR1 in IFN induction following virus infection.
96	22278222	HeLa cells made stably deficient in ADAR1 (ADAR1(kd)) were compared to vector control (CON(kd)) and protein kinase PKR-deficient (PKR(kd)) cells for IFN-β induction following infection with either parental (wild-type [WT]) recombinant Moraten vaccine strain measles virus (MV) or isogenic knockout mutants deficient for either V (V(ko)) or C (C(ko)) protein expression.
97	22278222	We observed potent IFN-β transcript induction in ADAR1(kd) cells by all three viruses; in contrast, in ADAR1-sufficient CON(kd) cells, only the C(ko) mutant virus was an effective inducer and the IFN-β RNA induction was amplified by PKR.
98	22278222	The enhanced IFN-β transcript-inducing capacity of the WT and V(ko) viruses seen in ADAR1-deficient cells correlated with the enhanced activation of PKR, IFN regulatory factor IRF3, and activator of transcription ATF2, reaching levels similar to those seen in C(ko) virus-infected cells.
99	22278222	These results suggest that ADAR1 functions as an important suppressor of MV-mediated responses, including the activation of PKR and IRF3 and the induction of IFN-β RNA.
100	22278222	Our findings further implicate a balanced interplay between PKR and ADAR1 in modulating IFN-β protein production following virus infection.
101	22278222	Adenosine deaminase acting on RNA 1 (ADAR1) suppresses the induction of interferon by measles virus.
102	22278222	ADAR1, the interferon (IFN)-inducible adenosine deaminase acting on RNA, catalyzes the C-6 deamination of adenosine (A) to produce inosine (I) in RNA substrates with a double-stranded character.
103	22278222	Because double-stranded RNA is a known inducer of IFN, we tested the role of ADAR1 in IFN induction following virus infection.
104	22278222	HeLa cells made stably deficient in ADAR1 (ADAR1(kd)) were compared to vector control (CON(kd)) and protein kinase PKR-deficient (PKR(kd)) cells for IFN-β induction following infection with either parental (wild-type [WT]) recombinant Moraten vaccine strain measles virus (MV) or isogenic knockout mutants deficient for either V (V(ko)) or C (C(ko)) protein expression.
105	22278222	We observed potent IFN-β transcript induction in ADAR1(kd) cells by all three viruses; in contrast, in ADAR1-sufficient CON(kd) cells, only the C(ko) mutant virus was an effective inducer and the IFN-β RNA induction was amplified by PKR.
106	22278222	The enhanced IFN-β transcript-inducing capacity of the WT and V(ko) viruses seen in ADAR1-deficient cells correlated with the enhanced activation of PKR, IFN regulatory factor IRF3, and activator of transcription ATF2, reaching levels similar to those seen in C(ko) virus-infected cells.
107	22278222	These results suggest that ADAR1 functions as an important suppressor of MV-mediated responses, including the activation of PKR and IRF3 and the induction of IFN-β RNA.
108	22278222	Our findings further implicate a balanced interplay between PKR and ADAR1 in modulating IFN-β protein production following virus infection.
109	22278222	Adenosine deaminase acting on RNA 1 (ADAR1) suppresses the induction of interferon by measles virus.
110	22278222	ADAR1, the interferon (IFN)-inducible adenosine deaminase acting on RNA, catalyzes the C-6 deamination of adenosine (A) to produce inosine (I) in RNA substrates with a double-stranded character.
111	22278222	Because double-stranded RNA is a known inducer of IFN, we tested the role of ADAR1 in IFN induction following virus infection.
112	22278222	HeLa cells made stably deficient in ADAR1 (ADAR1(kd)) were compared to vector control (CON(kd)) and protein kinase PKR-deficient (PKR(kd)) cells for IFN-β induction following infection with either parental (wild-type [WT]) recombinant Moraten vaccine strain measles virus (MV) or isogenic knockout mutants deficient for either V (V(ko)) or C (C(ko)) protein expression.
113	22278222	We observed potent IFN-β transcript induction in ADAR1(kd) cells by all three viruses; in contrast, in ADAR1-sufficient CON(kd) cells, only the C(ko) mutant virus was an effective inducer and the IFN-β RNA induction was amplified by PKR.
114	22278222	The enhanced IFN-β transcript-inducing capacity of the WT and V(ko) viruses seen in ADAR1-deficient cells correlated with the enhanced activation of PKR, IFN regulatory factor IRF3, and activator of transcription ATF2, reaching levels similar to those seen in C(ko) virus-infected cells.
115	22278222	These results suggest that ADAR1 functions as an important suppressor of MV-mediated responses, including the activation of PKR and IRF3 and the induction of IFN-β RNA.
116	22278222	Our findings further implicate a balanced interplay between PKR and ADAR1 in modulating IFN-β protein production following virus infection.
117	22278222	Adenosine deaminase acting on RNA 1 (ADAR1) suppresses the induction of interferon by measles virus.
118	22278222	ADAR1, the interferon (IFN)-inducible adenosine deaminase acting on RNA, catalyzes the C-6 deamination of adenosine (A) to produce inosine (I) in RNA substrates with a double-stranded character.
119	22278222	Because double-stranded RNA is a known inducer of IFN, we tested the role of ADAR1 in IFN induction following virus infection.
120	22278222	HeLa cells made stably deficient in ADAR1 (ADAR1(kd)) were compared to vector control (CON(kd)) and protein kinase PKR-deficient (PKR(kd)) cells for IFN-β induction following infection with either parental (wild-type [WT]) recombinant Moraten vaccine strain measles virus (MV) or isogenic knockout mutants deficient for either V (V(ko)) or C (C(ko)) protein expression.
121	22278222	We observed potent IFN-β transcript induction in ADAR1(kd) cells by all three viruses; in contrast, in ADAR1-sufficient CON(kd) cells, only the C(ko) mutant virus was an effective inducer and the IFN-β RNA induction was amplified by PKR.
122	22278222	The enhanced IFN-β transcript-inducing capacity of the WT and V(ko) viruses seen in ADAR1-deficient cells correlated with the enhanced activation of PKR, IFN regulatory factor IRF3, and activator of transcription ATF2, reaching levels similar to those seen in C(ko) virus-infected cells.
123	22278222	These results suggest that ADAR1 functions as an important suppressor of MV-mediated responses, including the activation of PKR and IRF3 and the induction of IFN-β RNA.
124	22278222	Our findings further implicate a balanced interplay between PKR and ADAR1 in modulating IFN-β protein production following virus infection.
125	22426325	At the injection site, 594 genes were differentially expressed, including up-regulation of the cytokines osteopontin (SPP1), IL-10 and IL-18 and the chemokines CCL2, CCL19 and CXCL16.
126	22426325	Of the 362 genes differentially expressed in the lymph node, IL-1β and CXCL11 were up-regulated whereas IL18, CCL15 and CXCL12 were down-regulated.
127	22426325	ISCOM-Matrix also modulated genes for pattern recognition receptors at the injection site (TLR2, TLR4, MRC1, PTX3, LGALS3) and in the lymph node (TLR4, RIG-I, MDA5, OAS1, EIF2AK2, LGALS3).
128	22438548	The double-stranded RNA bluetongue virus induces type I interferon in plasmacytoid dendritic cells via a MYD88-dependent TLR7/8-independent signaling pathway.
129	22438548	Other inflammatory cytokines, including tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), and IL-12p40, were also induced by UV-BTV in primary pDCs.
130	22438548	In contrast, pathways involving the MyD88 adaptor and kinases dsRNA-activated protein kinase (PKR) and stress-activated protein kinase (SAPK)/Jun N-terminal protein kinase (JNK) were implicated.
131	23251389	Wogonin induced calreticulin/annexin A1 exposure dictates the immunogenicity of cancer cells in a PERK/AKT dependent manner.
132	23251389	Here we demonstrated for the first time that wogonin elicits a potent antitumor immunity effect by inducing the translocation of calreticulin (CRT) and Annexin A1 to cell plasma membrane as well as the release of high-mobility group protein 1 (HMGB1) and ATP.
133	23251389	We found that wogonin-induced reactive oxygen species (ROS) production causes an endoplasmic reticulum (ER) stress response, including the phosphorylation of PERK (PKR-like endoplasmic reticulum kinase)/PKR (protein kinase R) and eIF2α (eukaryotic initiation factor 2α), which served as upstream signal for the activation of phosphoinositide 3-kinase (PI3K)/AKT, inducing calreticulin (CRT)/Annexin A1 cell membrane translocation.
134	23251389	P22/CHP, a Ca(2+)-binding protein, was associated with CRT and was required for CRT translocation to cell membrane.
135	23251389	In conclusion, the activation of PI3K pathway elicited by ER stress induced CRT/Annexin A1 translocation ("eat me" signal) and HMGB1 release, mediating wogonin-induced immunity of tumor cell vaccine.
136	23487469	ICP34.5β is unable to counteract PKR-mediated eIF2 phosphorylation but does not interfere with ICP34.5α's function in this process.
137	23523764	A major virulence factor of RVFV is the NSs protein, which inhibits host transcription including the interferon (IFN)-β gene and promotes the degradation of dsRNA-dependent protein kinase, PKR.
138	23638202	MP-12 was manufactured as an Investigational New Drug vaccine by using MRC-5 cells and encodes a functional NSs gene, the major virulence factor of RVFV which 1) induces a shutoff of the host transcription, 2) inhibits interferon (IFN)-β promoter activation, and 3) promotes the degradation of dsRNA-dependent protein kinase (PKR).
139	26238721	Moreover, the expression of several candidate genes, such as type I interferons, PKR, OAS, viperin and IFITM3 was quantified at 3, 8 and 18h post-treatment with TLR ligands.