Ignet

Gene Information

Gene symbol: CEBPB

Gene name: CCAAT/enhancer binding protein (C/EBP), beta

HGNC ID: 1834

Synonyms: LAP, CRP2, NFIL6, IL6DBP, C/EBP-beta

Related Genes

#	Gene Symbol	Number of hits
1	CD4	1 hits
2	CD46	1 hits
3	CSF3	1 hits
4	FOS	1 hits
5	FOXP3	1 hits
6	IFNG	1 hits
7	IL1B	1 hits
8	IL6	1 hits
9	IL8	1 hits
10	MAPK14	1 hits
11	NFKB1	1 hits
12	PDC	1 hits
13	RNF123	1 hits
14	TGFB1	1 hits
15	WARS	1 hits

Related Sentences

#	PMID	Sentence
1	10092809	Activated macrophages kill bacteria, a function known to depend on the expression of NF-IL-6.
2	10092809	Here, it is demonstrated that the attenuated Brucella abortus vaccine strain 19 replicates much better in NF-IL-6-/- than in NF-IL-6(+/+) and NF-IL-6(+/+)-activated murine macrophages and at levels comparable to those observed in normal macrophages infected with the pathogenic strain 2308.
3	10092809	The role of NF-IL-6 in the inhibition of intracellular bacterial replication is related to its control of endocytosis and membrane fusion between endosomes and Brucella-containing phagosomes.
4	10092809	Addition of the granulocyte-CSF (G-CSF), whose induction is impaired in NF-IL-6(-/-) macrophages, restores both endocytosis and the morphology of endosomes, together with bactericidal activity.
5	10092809	Regulation of membrane traffic in endocytosis by G-CSF whose expression is controlled by NF-IL-6 may explain how a host cell can control intracellular bacterial replication.
6	10092809	Activated macrophages kill bacteria, a function known to depend on the expression of NF-IL-6.
7	10092809	Here, it is demonstrated that the attenuated Brucella abortus vaccine strain 19 replicates much better in NF-IL-6-/- than in NF-IL-6(+/+) and NF-IL-6(+/+)-activated murine macrophages and at levels comparable to those observed in normal macrophages infected with the pathogenic strain 2308.
8	10092809	The role of NF-IL-6 in the inhibition of intracellular bacterial replication is related to its control of endocytosis and membrane fusion between endosomes and Brucella-containing phagosomes.
9	10092809	Addition of the granulocyte-CSF (G-CSF), whose induction is impaired in NF-IL-6(-/-) macrophages, restores both endocytosis and the morphology of endosomes, together with bactericidal activity.
10	10092809	Regulation of membrane traffic in endocytosis by G-CSF whose expression is controlled by NF-IL-6 may explain how a host cell can control intracellular bacterial replication.
11	10092809	Activated macrophages kill bacteria, a function known to depend on the expression of NF-IL-6.
12	10092809	Here, it is demonstrated that the attenuated Brucella abortus vaccine strain 19 replicates much better in NF-IL-6-/- than in NF-IL-6(+/+) and NF-IL-6(+/+)-activated murine macrophages and at levels comparable to those observed in normal macrophages infected with the pathogenic strain 2308.
13	10092809	The role of NF-IL-6 in the inhibition of intracellular bacterial replication is related to its control of endocytosis and membrane fusion between endosomes and Brucella-containing phagosomes.
14	10092809	Addition of the granulocyte-CSF (G-CSF), whose induction is impaired in NF-IL-6(-/-) macrophages, restores both endocytosis and the morphology of endosomes, together with bactericidal activity.
15	10092809	Regulation of membrane traffic in endocytosis by G-CSF whose expression is controlled by NF-IL-6 may explain how a host cell can control intracellular bacterial replication.
16	10092809	Activated macrophages kill bacteria, a function known to depend on the expression of NF-IL-6.
17	10092809	Here, it is demonstrated that the attenuated Brucella abortus vaccine strain 19 replicates much better in NF-IL-6-/- than in NF-IL-6(+/+) and NF-IL-6(+/+)-activated murine macrophages and at levels comparable to those observed in normal macrophages infected with the pathogenic strain 2308.
18	10092809	The role of NF-IL-6 in the inhibition of intracellular bacterial replication is related to its control of endocytosis and membrane fusion between endosomes and Brucella-containing phagosomes.
19	10092809	Addition of the granulocyte-CSF (G-CSF), whose induction is impaired in NF-IL-6(-/-) macrophages, restores both endocytosis and the morphology of endosomes, together with bactericidal activity.
20	10092809	Regulation of membrane traffic in endocytosis by G-CSF whose expression is controlled by NF-IL-6 may explain how a host cell can control intracellular bacterial replication.
21	10092809	Activated macrophages kill bacteria, a function known to depend on the expression of NF-IL-6.
22	10092809	Here, it is demonstrated that the attenuated Brucella abortus vaccine strain 19 replicates much better in NF-IL-6-/- than in NF-IL-6(+/+) and NF-IL-6(+/+)-activated murine macrophages and at levels comparable to those observed in normal macrophages infected with the pathogenic strain 2308.
23	10092809	The role of NF-IL-6 in the inhibition of intracellular bacterial replication is related to its control of endocytosis and membrane fusion between endosomes and Brucella-containing phagosomes.
24	10092809	Addition of the granulocyte-CSF (G-CSF), whose induction is impaired in NF-IL-6(-/-) macrophages, restores both endocytosis and the morphology of endosomes, together with bactericidal activity.
25	10092809	Regulation of membrane traffic in endocytosis by G-CSF whose expression is controlled by NF-IL-6 may explain how a host cell can control intracellular bacterial replication.
26	11991987	Among the proinflammatory cytokines and their mRNAs measured (IL-6, IL-1 beta, IL-8, and tumor necrosis factor alpha), IL-8 showed the greatest change following D2V infection.
27	11991987	Nuclear factor kappa B (NF-kappa B) and nuclear factor IL-6 (NFIL-6) are primary mediators of IL-8 expression.
28	11991987	We studied the transcriptional regulation of IL-8 in the ECV304 and 293T cell lines and found that the induction of IL-8 gene expression involved the activation of NF-kappa B (P = 0.001) and, to a lesser extent, the activation of NFIL-6 in ECV304 cells only.
29	11991987	IL-8 produced by infected monocytes and also IL-8 that may be produced by endothelial or other epithelial cells is associated with the hyperacetylation of histones bound to the IL-8 promoter in addition to the activation of transcription by NF-kappa B.
30	12297327	Immune evasion by a novel family of viral PHD/LAP-finger proteins of gamma-2 herpesviruses and poxviruses.
31	12297327	Recent observations however, suggest that a conserved family of viral proteins is used by both gamma-2 herpesviruses and by poxviruses to downregulate MHC class I.
32	12502858	The PHD/LAP-domain protein M153R of myxomavirus is a ubiquitin ligase that induces the rapid internalization and lysosomal destruction of CD4.
33	12502858	Surface expression of CD4 was restored upon overexpression of Hrs, a ubiquitin interaction motif-containing protein that sorts ubiquitinated proteins into endosomes.
34	12502858	Moreover, the purified PHD/LAP zinc finger of M153R catalyzed the formation of multiubiquitin adducts in vitro.
35	12502858	The PHD/LAP-domain protein M153R of myxomavirus is a ubiquitin ligase that induces the rapid internalization and lysosomal destruction of CD4.
36	12502858	Surface expression of CD4 was restored upon overexpression of Hrs, a ubiquitin interaction motif-containing protein that sorts ubiquitinated proteins into endosomes.
37	12502858	Moreover, the purified PHD/LAP zinc finger of M153R catalyzed the formation of multiubiquitin adducts in vitro.
38	14722266	Poxviruses and gamma-2 herpesviruses share the K3 family of viral immune evasion proteins that inhibit the surface expression of glycoproteins such as major histocompatibility complex class I (MHC-I), B7.2, ICAM-1, and CD95(Fas).
39	14722266	K3 family proteins contain an amino-terminal PHD/LAP or RING-CH domain followed by two transmembrane domains.
40	14722266	Two closely related proteins, MARCH-IV and MARCH-IX, reduced surface expression of MHC-I molecules.
41	14722266	In the presence of MARCH-IV or MARCH-IX, MHC-I was ubiquitinated and rapidly internalized by endocytosis, whereas MHC-I molecules lacking lysines in their cytoplasmic tail were resistant to downregulation.
42	16103178	The majority of adenovirus serotypes utilize the coxsackievirus-adenovirus receptor (CAR) for virus-host cell attachment, but subgroup B and subgroup D (adenovirus type 37 [Ad37]) viruses recognize CD46.
43	16103178	CD46 is a ubiquitously expressed receptor that serves as a cofactor for the inactivation of the complement components C3b and C4b, and it also serves as a receptor for diverse microbial pathogens.
44	16103178	A reported consequence of CD46 engagement is a reduced capability of human immune cells to express interleukin-12 (IL-12), a cytokine involved in both the innate and adaptive immune responses.
45	16103178	Subgroup B (Ad16 and -35) and Ad37, but not Ad2 or -5, significantly reduced IL-12 production by human peripheral blood mononuclear cells stimulated with gamma interferon (IFN-gamma) and lipopolysaccharide.
46	16103178	IL-12 mRNA (p35 and p40 subunits) levels as well as other cytokine mRNA levels (IL-1alpha and -beta, IL-1Ra, and IL-6) were decreased upon interaction with CD46-utilizing Ads.
47	16103178	Analysis of transcription factor activity required for cytokine expression indicated that CD46-utilizing Ads preferentially inhibited IFN-gamma-induced C/EBPbeta protein expression, consequently reducing its ability to form DNA complexes.
48	16103178	Interference with IFN-gamma signaling events by CD46-utilizing Ads, but not CAR-utilizing Ads, reveals a potentially critical difference in the host immune response against distinct Ad vectors, a situation that has implications for gene delivery and vaccine development.
49	16399630	Chlorophyllin suppresses interleukin-1 beta expression in lipopolysaccharide-activated RAW 264.7 cells.
50	16399630	Furthermore, CHL attenuated the activation of NF-kappaB, NF-IL6 and AP-1, which are known to be responsible for IL-1beta gene expression, as determined by an electrophoretic mobility shift assay and an in vitro transfection assay using p(NF-kappaB)3-CAT, p(NF-IL6)3-CAT, and p(AP-1)3-CAT, respectively.
51	16399630	The immunoblot experiment demonstrated that CHL also caused a substantial decrease in the phosphorylation of p38 MAP kinase in LPS-stimulated RAW 264.7.
52	16399630	These results suggest that CHL inhibits IL-1beta production in macrophages stimulated with LPS at transcriptional level by blocking the phosphorylation of p38 and by suppressing the activation of transcription factors, NF-kappaB, NF-IL6, and AP-1.
53	16399630	Chlorophyllin suppresses interleukin-1 beta expression in lipopolysaccharide-activated RAW 264.7 cells.
54	16399630	Furthermore, CHL attenuated the activation of NF-kappaB, NF-IL6 and AP-1, which are known to be responsible for IL-1beta gene expression, as determined by an electrophoretic mobility shift assay and an in vitro transfection assay using p(NF-kappaB)3-CAT, p(NF-IL6)3-CAT, and p(AP-1)3-CAT, respectively.
55	16399630	The immunoblot experiment demonstrated that CHL also caused a substantial decrease in the phosphorylation of p38 MAP kinase in LPS-stimulated RAW 264.7.
56	16399630	These results suggest that CHL inhibits IL-1beta production in macrophages stimulated with LPS at transcriptional level by blocking the phosphorylation of p38 and by suppressing the activation of transcription factors, NF-kappaB, NF-IL6, and AP-1.
57	19050244	Mucosal administration of Ag conjugated to cholera toxin B subunit (CTB) can efficiently induce peripheral immunologic tolerance, so-called oral tolerance, associated with development of Foxp3(+)CD25(+)CD4(+) regulatory T (Treg) cells.
58	19050244	B cells from OVA/CTB-treated mice expressed more IL-10 and less CD86 than control B cells.
59	19050244	Adoptive transfer of these cells before parenteral immunization with OVA led to efficient suppression of proliferation and to induction of apoptotic depletion of Ag-specific CD25(-)CD4(+) effector T cells associated with the expansion of Treg cells.
60	19050244	However, also OVA/CTB-treated microMT(-/-) mice could suppress the immune response to parenteral immunization with OVA, which was associated with a strong increase in Foxp3(-)CD4(+) T cells expressing LAP/TGF-beta.
61	19050244	Our results indicate that mucosal tolerance comprises at least two separate pathways: one being B cell dependent and associated with expansion of Treg cells and Treg-mediated suppression and depletion of effector T cells, and one being B cell independent and associated with development of Foxp3(-)LAP(+)TGF-beta(+) regulatory T cells.