Ignet

Gene Information

Gene symbol: PDIA3

Gene name: protein disulfide isomerase family A, member 3

HGNC ID: 4606

Synonyms: P58, ERp61, ERp57, ERp60, GRP57, PI-PLC, HsT17083

Related Genes

#	Gene Symbol	Number of hits
1	ATP6V1E1	1 hits
2	CALR	1 hits
3	CANX	1 hits
4	CCNH	1 hits
5	DNALI1	1 hits
6	GPI	1 hits
7	HSPA14	1 hits
8	HSPA1A	1 hits
9	HSPA8	1 hits
10	IL12A	1 hits
11	NPY6R	1 hits
12	PDIA2	1 hits
13	PKLR	1 hits
14	PLCB1	1 hits
15	PLCB4	1 hits
16	PLCXD1	1 hits
17	PPA1	1 hits
18	PRKCA	1 hits
19	PRR6	1 hits
20	PSMB5	1 hits
21	PSMB8	1 hits
22	PSMB9	1 hits
23	TAPBP	1 hits
24	TKT	1 hits
25	VIM	1 hits

Related Sentences

#	PMID	Sentence
1	7499830	Glycosylphosphatidylinositol (GPI)-modified variants of murine B7-1 and B7-2 cell surface costimulators were produced via chimerization with alternative GPI-modification signal sequences from decay-accelerating factor (DAF).
2	7499830	GPI anchorage was verified by demonstrating phosphatidylinositol-specific phospholipase C (PI-PLC) sensitivity of the chimeric polypeptides in both immunofluorescence/flow-cytometric and immunoprecipitation analyses.
3	7499830	The various GPI-modified chimeric B7-1:DAF and B7-2:DAF polypeptides were shown to retain costimulator function, in both an in vitro proliferation assay and an in vivo triggering of cytotoxicity assay.
4	7499830	Moreover, the functionality of the GPI-modified variants in enhancing the immunogenicity of the murine T lymphoma line EL-4 suggests a novel route for generating APC-centered immunotherapeutics, including cellular cancer vaccines, that is based upon protein transfer of GPI-modified costimulators.
5	10878054	Of the 18 protein bands analyzed, 8 were found to be significantly different (P<0.05) between the two groups. p93, p34, p31, and p28 occurred with increased frequency in vaccinated dogs, while p58, p37, p35, and p30 occurred more frequently in naturally infected dogs.
6	15272405	Phospholipase C (alpha -toxin) is the virulence factor most responsible for these pathologies.
7	16814434	Two types of recombinant Plasmodium falciparum MSP1p19 (PfMSP1p19) expressed in baculovirus/insect cells are described here: (1) a soluble, secreted form (PfMSP1p19S) and (2) detergent soluble cellular form(s) (PfMSP1p19+A), released from the infected cell surface by treatment with GPI specific phosphatidyl-inositol phospholipase C (PI-PLC).
8	17285277	Leukemic cells were stimulated (or not) with CD40L and IL-4.
9	17285277	Elements of the antigen-processing machinery (MB1, LMP2, LMP7, LMP10, TAP1, TAP2, calnexin, calreticulin, tapasin, ERp57, zeta, delta) were determined by real-time PCR technique.
10	17285277	The expression of important costimulatory and adhesion molecules considered as DC markers (CD40, CD54, CD80, CD83, CD86) were determined at the mRNA (PCR) and protein (flow cytometry) levels.
11	17562331	In this study, we demonstrated that the phosphoinositide-phospholipase C (PI-PLC) downstream signaling pathway is involved in M. bovis BCG-induced CXCL8 release, since A549 cells pretreated with U73122, a PI-PLC inhibitor, inhibited CXCL8 release, whereas U73343 the inactive analog had no effect.
12	17562331	In addition, our results demonstrated that M. bovis BCG-induced CXCL8 production by A549 cells was significantly blocked by using neomycin (another well-described inhibitor of PI-PLC with a different mechanism of action), Ro-32-0432 and Ro-31-8220 (two PKCalpha inhibitors), PP1 and PP2 (two potent and selective inhibitors of the Src-family tyrosine kinases), and Bay 11-7082 (an IkappaB phosphorylation inhibitor).
13	17562331	We also demonstrated that M. bovis BCG can rapidly induce translocation of PKCalpha from the cytosol to the membrane, and that treatment of cells with M. bovis BCG caused time-dependent increases in phosphorylation of c-Src at tyrosine 416.
14	17562331	Finally, our studies revealed that M. bovis BCG induced the association of c-Src and IKKalphabeta during the interaction of PKCalpha and IKKalphabeta.
15	17562331	Altogether, these results represent the first evidence to date suggesting that M. bovis BCG activates the PI-PLC/PKCalpha/c-Src/IKKalphabeta signaling pathway to induce CXCL8 release in human epithelial cells.
16	17562331	In this study, we demonstrated that the phosphoinositide-phospholipase C (PI-PLC) downstream signaling pathway is involved in M. bovis BCG-induced CXCL8 release, since A549 cells pretreated with U73122, a PI-PLC inhibitor, inhibited CXCL8 release, whereas U73343 the inactive analog had no effect.
17	17562331	In addition, our results demonstrated that M. bovis BCG-induced CXCL8 production by A549 cells was significantly blocked by using neomycin (another well-described inhibitor of PI-PLC with a different mechanism of action), Ro-32-0432 and Ro-31-8220 (two PKCalpha inhibitors), PP1 and PP2 (two potent and selective inhibitors of the Src-family tyrosine kinases), and Bay 11-7082 (an IkappaB phosphorylation inhibitor).
18	17562331	We also demonstrated that M. bovis BCG can rapidly induce translocation of PKCalpha from the cytosol to the membrane, and that treatment of cells with M. bovis BCG caused time-dependent increases in phosphorylation of c-Src at tyrosine 416.
19	17562331	Finally, our studies revealed that M. bovis BCG induced the association of c-Src and IKKalphabeta during the interaction of PKCalpha and IKKalphabeta.
20	17562331	Altogether, these results represent the first evidence to date suggesting that M. bovis BCG activates the PI-PLC/PKCalpha/c-Src/IKKalphabeta signaling pathway to induce CXCL8 release in human epithelial cells.
21	17562331	In this study, we demonstrated that the phosphoinositide-phospholipase C (PI-PLC) downstream signaling pathway is involved in M. bovis BCG-induced CXCL8 release, since A549 cells pretreated with U73122, a PI-PLC inhibitor, inhibited CXCL8 release, whereas U73343 the inactive analog had no effect.
22	17562331	In addition, our results demonstrated that M. bovis BCG-induced CXCL8 production by A549 cells was significantly blocked by using neomycin (another well-described inhibitor of PI-PLC with a different mechanism of action), Ro-32-0432 and Ro-31-8220 (two PKCalpha inhibitors), PP1 and PP2 (two potent and selective inhibitors of the Src-family tyrosine kinases), and Bay 11-7082 (an IkappaB phosphorylation inhibitor).
23	17562331	We also demonstrated that M. bovis BCG can rapidly induce translocation of PKCalpha from the cytosol to the membrane, and that treatment of cells with M. bovis BCG caused time-dependent increases in phosphorylation of c-Src at tyrosine 416.
24	17562331	Finally, our studies revealed that M. bovis BCG induced the association of c-Src and IKKalphabeta during the interaction of PKCalpha and IKKalphabeta.
25	17562331	Altogether, these results represent the first evidence to date suggesting that M. bovis BCG activates the PI-PLC/PKCalpha/c-Src/IKKalphabeta signaling pathway to induce CXCL8 release in human epithelial cells.
26	21919206	The resulting antigenic molecules included calreticulin (CRT), ERp57, Vimentin, HSP70-4, tubulin β5 chain, coronin-1A, pyruvate kinase, ATP synthase β chain and transketolase most of which belong to so-called damage-associated molecular pattern molecules (DAMPs).
27	21919206	CRT, ERp57 and vementin were further examined by Western blot and cellular ELISA to identify molecular targets which may be involved in the TCV immunotherapy.
28	21919206	On the basis of our results, γ-radiation induced the activated T cells "immunogenic apoptosis" and exposed/secreted DAMPs (CRT, ERp57 and Vementin) played an important role in TCV therapy.
29	21919206	The resulting antigenic molecules included calreticulin (CRT), ERp57, Vimentin, HSP70-4, tubulin β5 chain, coronin-1A, pyruvate kinase, ATP synthase β chain and transketolase most of which belong to so-called damage-associated molecular pattern molecules (DAMPs).
30	21919206	CRT, ERp57 and vementin were further examined by Western blot and cellular ELISA to identify molecular targets which may be involved in the TCV immunotherapy.
31	21919206	On the basis of our results, γ-radiation induced the activated T cells "immunogenic apoptosis" and exposed/secreted DAMPs (CRT, ERp57 and Vementin) played an important role in TCV therapy.
32	21919206	The resulting antigenic molecules included calreticulin (CRT), ERp57, Vimentin, HSP70-4, tubulin β5 chain, coronin-1A, pyruvate kinase, ATP synthase β chain and transketolase most of which belong to so-called damage-associated molecular pattern molecules (DAMPs).
33	21919206	CRT, ERp57 and vementin were further examined by Western blot and cellular ELISA to identify molecular targets which may be involved in the TCV immunotherapy.
34	21919206	On the basis of our results, γ-radiation induced the activated T cells "immunogenic apoptosis" and exposed/secreted DAMPs (CRT, ERp57 and Vementin) played an important role in TCV therapy.
35	24037197	ECwt infection of mice increased expression of cyclooxygenase-2, ERp57, Hsc70, NF-κB, Hsp70, protein disulphide isomerase (PDI) and PPARγ in intestinal villus cells.
36	24037197	NAC treatment of ECwt-infected mice reduced Hsc70 and PDI expression to levels similar to those observed in villi from uninfected control mice.