count	source_label	source_id	relationship	target_label	target_id	entity_type	solr_id	publication_id	sentences
3		MESH:D035683	decreases	PIGV	UNIPROT:Q9NUD9	Phenotype	5221451c-c7be-11ee-b346-0050569a791b	PMC10388210	To investigate how miR 449c-5p suppressed PIGV level, we performed the reporter assays in the 293T cells by treating the cells either transfected with a WT PIGV-3′UTR or a mutated PIGV-3′UTR with miR 449c-5p (Fig. 5F).|||The miR then reduces the level of PIGV mRNA (Figs.
3		MESH:D035683	inhibits	PIGV	UNIPROT:Q9NUD9	Phenotype	5221451c-c7be-11ee-b346-0050569a791b	PMC10388210	Thus, ER stress–induced miR 449c-5p suppresses the mRNA of PIGV, disrupting the GPI modification process and leading to the accumulation of pro-PrP, which confers migration and invasion advantages of AsPC-1 cells.|||The results showed that miR 449c-5p mimic could repress the luciferase activity of WT PIGV 3′-UTR but not the mutated one (Fig. 5F).|||The results showed that only inhibitor of miR 449c-5p significantly enhanced PIGV transcripts, while mimic of 449c-5p significantly suppressed PIGV transcripts (Fig. 5C).
2	PIGV	UNIPROT:Q9NUD9	activates		UNIPROT:P04280	Protein	42d2920e-0daa-11f0-b759-0050569a791b	10.1016/S0022-1910(98)00110-3	Furthermore, the presence of an enhancin-type gene was recently reported fromLymantria disparnuclear polyhedrosis virus (Bischoff and Slavicek, 1997) suggesting that other similar nuclear polyhedrosis viruses (NPVs) may carry enhancin genes.Begon et al. (1993)reportedPlodia interpunctellaGV (PiGV) OBs caused dramatic and significant effects of the PM structure from the same species and concluded that the PM provided a barrier to PiGV infection at lower virus doses.
2	PIGV	UNIPROT:Q9NUD9	inhibits		UNIPROT:F7VJQ1	Protein	5221451c-c7be-11ee-b346-0050569a791b	PMC10388210	We found that decreasing mouse PIGV levels also significantly reduced cell surface PrP sensitivity to PI-PLC (Fig. 2E).|||Collectively, these results strongly support the conclusion that Tg treatment decreased PIGV protein expression causing the accumulation of pro-PrP.
1	PIGV	UNIPROT:Q9NUD9	decreases		UNIPROT:Q9NUD9	Protein	5221451c-c7be-11ee-b346-0050569a791b	PMC10388210	Immunoblot analysis further confirmed that the inhibitor of miR 449c-5p increased the protein level of PIGV, while the mimic of miR 449c-5p decreased the protein level of PIGV (Figs.
1	PIGV	UNIPROT:Q9NUD9	activates		UNIPROT:Q13363	Protein	9d636c72-c483-11e5-85e4-001a4ae51246	PMC3307314	In contrast, a substantially higher amount of PLAP was secreted into the culture medium from PIGV-deficient mutant cells than from PIGV-rescued cells (Fig. 2B,black bars).
1	PIGV	UNIPROT:Q9NUD9	activates		UNIPROT:P18850	Protein	5221451c-c7be-11ee-b346-0050569a791b	PMC10388210	ATF6–miR449c-5p–PIGV axis also contributes to PDAC in humans and are makers of prognosis in patients with PDAC To investigate the clinical relevance of the ATF6–miR449c-5p–PIGV axis in human PDAC tumorigenesis, we first performed a prognosis analysis for patients with PDAC (https://kmplot.com/analysis/) (28).
1	PIGV	UNIPROT:Q9NUD9	activates		UNIPROT:P06744	Protein	5221451c-c7be-11ee-b346-0050569a791b	PMC10388210	A reduction in PIGV protein disrupts the GPI modification process (Figs.
1	PIGV	UNIPROT:Q9NUD9	inhibits		UNIPROT:P06744	Protein	8f15fb58-bbfa-11e5-8abe-001a4ae51246	10.1016/j.bbalip.2012.01.004	In addition, autosomal recessive mutations inPIG-M,PIG-V, andPIG-Nhave been reported to cause inherited GPI deficiency[8,16,17].
1	PIGV	UNIPROT:Q9NUD9	activates		UNIPROT:P06744	Protein	dc081f66-bc3d-11e5-8d2d-001a4ae51247	PMC4373761	Missense mutations in genes encoding enzymes catalyzing various steps of GPI anchor biosynthesis, such as PIGW that catalyzes attachment of acyl group to phosphatidylinositiol [15,16], PIGV that catalyzes transfer of second mannose to GPI intermediate [17,18], PIGT that attaches GPI to proteins [19] and PGAP2 that modifies the phospholipid tail of PI [20] result in congenital diseases known as hyperphosphatasia mental retardation syndrome (HPMRS), Hirschprung disease, morphological malformation and renal anomalies [21,22,23,24].
1	PIGV	UNIPROT:Q9NUD9	increases		UNIPROT:P13987	Protein	9d636c72-c483-11e5-85e4-001a4ae51246	PMC3307314	PIGV mutants driven by the strong promoter rescued the surface expression of CD59 almost completely, whereas those driven by the weak promoter failed to restore (Fig. 1B).
1	PIGV	UNIPROT:Q9NUD9	activates		UNIPROT:F7VJQ1	Protein	5221451c-c7be-11ee-b346-0050569a791b	PMC10388210	Collectively, these results strongly support the conclusion that Tg treatment decreased PIGV protein expression causing the accumulation of pro-PrP.
1	PIGV	UNIPROT:Q9NUD9	inhibits		MESH:D012640	Phenotype	580afa2c-c484-11e5-9da3-001a4ae51247	23250212	Human PIGM or PIGV deficiency causes seizures (Almeida et al., 2006) or mental retardation (Krawitz et al., 2010).
1	PIGV	UNIPROT:Q9NUD9	inhibits		MESH:D008607	Phenotype	580afa2c-c484-11e5-9da3-001a4ae51247	23250212	Human PIGM or PIGV deficiency causes seizures (Almeida et al., 2006) or mental retardation (Krawitz et al., 2010).
1	PIGV	UNIPROT:Q9NUD9	activates		MESH:D011353	Phenotype	c7968298-ae94-11ec-8b2e-0050569a1f61	PMCPMC8339205	In addition, there are also many other transcription factors involved in prodigiosin synthesis including the positive regulators PigP (Fineran et al., 2005a), PigT (Fineran et al., 2005b), PigS (Gristwood et al., 2011), PigR, and PigV (Fineran et al., 2005a) and the negative regulators PigX (Fineran et al., 2007) and HexS (Tanikawa et al., 2006).
1	PIGV	UNIPROT:Q9NUD9	inhibits		MESH:D009361	Phenotype	5221451c-c7be-11ee-b346-0050569a791b	PMC10388210	The results showed that silencing PIGV significantly enhanced the mobility and invasiveness of AsPC-1 cells (Figs.
1		MESH:D035683	activates	PIGV	UNIPROT:Q9NUD9	Phenotype	5221451c-c7be-11ee-b346-0050569a791b	PMC10388210	The results showed that only inhibitor of miR 449c-5p significantly enhanced PIGV transcripts, while mimic of 449c-5p significantly suppressed PIGV transcripts (Fig. 5C).
1		MESH:D035683	increases	PIGV	UNIPROT:Q9NUD9	Phenotype	5221451c-c7be-11ee-b346-0050569a791b	PMC10388210	Immunoblot analysis further confirmed that the inhibitor of miR 449c-5p increased the protein level of PIGV, while the mimic of miR 449c-5p decreased the protein level of PIGV (Figs.
1		UNIPROT:Q9NUD9	decreases	PIGV	UNIPROT:Q9NUD9	Protein	5221451c-c7be-11ee-b346-0050569a791b	PMC10388210	Immunoblot analysis further confirmed that the inhibitor of miR 449c-5p increased the protein level of PIGV, while the mimic of miR 449c-5p decreased the protein level of PIGV (Figs.
1		UNIPROT:P18850	decreases	PIGV	UNIPROT:Q9NUD9	Protein	5221451c-c7be-11ee-b346-0050569a791b	PMC10388210	The results showed that silencing ATF6 but not XBP1 increased the level of PIGV mRNA and its protein levels (Fig. 3,BandC).
1		UNIPROT:F7VJQ1	activates	PIGV	UNIPROT:Q9NUD9	Protein	5221451c-c7be-11ee-b346-0050569a791b	PMC10388210	To establish that c-ATF6 is upstream of miR 449c-5p and inhibits PIGV abundanceviamiR 449c-5p, we treated AsPC-1-hATF6 (1–373) cells with a miR 449c-5p inhibitor and detected the effects on PIGV and PrP.