count	source_label	source_id	relationship	target_label	target_id	entity_type	solr_id	publication_id	sentences
4	PARD6B	UNIPROT:Q9BYG5	activates		GO:0044085	Phenotype	56d6f602-bc4a-11e5-ac4e-001a4ae51246	PMC2768076	First, we found that both wild-type PAR-6C and PAR-6B efficiently rescued spine biogenesis, confirming that the defects in spine formation are specifically caused by loss of PAR-6 and are not caused by off-target effects of the shRNA.
3	PARD6B	UNIPROT:Q9BYG5	increases		UNIPROT:P12830	Protein	abaf813e-bc32-11e5-ac4e-001a4ae51246	PMC3800127	Par6b Depletion Reduces E-cadherin Protein Level Post-transcriptionally Loss of membrane-localized E-cadherin by Par6b depletion could be due either to lowere-cadherinmRNA level, reduced protein level, or failure of membrane presentation.|||Par6b Depletion Causes Loss of E-cadherin Expression and Epidermal Cell Dissociation at Tailbud Stage To understand the role of Par6b in the developing epidermis, we injected a previously validated translation-blocking morpholino oligo against Par6b (Par6b-MO)[29], at doses of 10 ng/cell, into two ventral animal blastomeres (which give rise to the epidermis) at the 8-cell stage.|||Par6b depletion reduced the total amount of E-cadherin protein in a dose-dependent fashion (Fig. 5A).
2	PARD6B	UNIPROT:Q9BYG5	activates		UNIPROT:O00254	Protein	0dedafd4-bc0f-11e5-9b9d-001a4ae51247	10.1016/j.tcb.2006.04.001	encoding Par3, Par6B or aPKC) leads to the disruption of apical–basal polarity, which could lead to EMT[13,32,60,61].
2	PARD6B	UNIPROT:Q9BYG5	inhibits		UNIPROT:Q07157	Protein	012ca0a0-c9fe-11e5-9b70-001a4ae51247	15292221	) Par6A co-localized predominantly with the tight junction marker ZO-1 at cell-cell contacts, whereas Par6B was distributed throughout the cytoplasm and disrupted ZO-1 localization (Fig. 1,AandB), as previously described (3,5).
2	PARD6B	UNIPROT:Q9BYG5	inhibits		GO:0051179	Phenotype	012ca0a0-c9fe-11e5-9b70-001a4ae51247	15292221	) Par6A co-localized predominantly with the tight junction marker ZO-1 at cell-cell contacts, whereas Par6B was distributed throughout the cytoplasm and disrupted ZO-1 localization (Fig. 1,AandB), as previously described (3,5).
2	PARD6B	UNIPROT:Q9BYG5	activates		GO:0007163	Phenotype	11bd0702-c46d-11e5-85e4-001a4ae51246	25176042	Cell polarity mediated by PARD6b and EMK1 is determined by cell-cell contacts during compaction; therefore, without compaction, polarization is never established.
2	PARD6B	UNIPROT:Q9BYG5	activates		UNIPROT:Q15672	Protein	b14a26ca-bc3d-11e5-9b9d-001a4ae51247	PMC3731222	Western blot analysis also showed that the expression of E-cadherin and Par6b was dramatically reduced inWt1-deficient SCs, however, ZO-1 and N-cadherin expression was not changed (Figure 6B).|||RNA-Seq analysis revealed that cell polarity-associated genes, such asE-cadherin, Par6b, were significantly decreased inWt1-deficient SCs.
2	PARD6B	UNIPROT:Q9BYG5	activates		GO:0009653	Phenotype	465f1f26-c478-11e5-9cc6-001a4ae51246	PMC3069449	Par6B and aPKC Control Mitotic Spindle Orientation Cdc42 promotes proper epithelial morphogenesis by orienting the mitotic spindle during cell division (Fig. 1A) (10).|||Preliminary studies using isoform-specific pools of siRNA indicated that depletion of Par6B was sufficient to disrupt Caco-2 morphogenesis (supplemental Fig. 1).
2		UNIPROT:O96013	phosphorylatesProtein	PARD6B	UNIPROT:Q9BYG5	Protein	8ebace46-3b4a-11e8-9fbf-001a4a160176	29507112	In vertebrate cells, Pak4 also regulates ZA maturation (Jin et al., 2015;Law and Sargent, 2014;Wallace et al., 2010), and its function during epithelial morphogenesis has been linked to that of the Par complex, as Pak4 phosphorylates Par6b (Jin et al., 2015;Wallace et al., 2010).
1	PARD6B	UNIPROT:Q9BYG5	activates		UNIPROT:P03372	Protein	8d7bd578-c6c9-11ee-9133-0050569a1f61	10.1016/j.bcp.2023.115907	Oxysterol 27-hydroxycholesterol has also been discovered to be enriched in ER-positive breast cancer cells and promote cell proliferation via ER-mediated signaling including ARMT1, PARD6B and GDFN-RET pathway[49].
1	PARD6B	UNIPROT:Q9BYG5	activates		UNIPROT:P57087	Protein	16b17b86-c480-11e5-9cc6-001a4ae51246	PMC2892954	Knockdown of Par3 or Par6b markedly blocks the ability of ECs to undergo these critical early events that are necessary to reach their neighbors and assemble into multicellular tube networks.11Our results reveal the same phenomenon with blockade of Jam-B and Jam-C.
1	PARD6B	UNIPROT:Q9BYG5	activates		UNIPROT:Q96TA2	Protein	a1944e94-3405-11e8-a34b-001a4a160175	28263792	Supplementary Table 8 includes genes such asISG15,VAV1,PTPRJ,HTR3A,AMPD1/AMPD2,PARD6A/PARD6B,CYP11B1/CYP11B2,ICAM5/ICAM3,IQSEC3/SAG,PDE4C/PDE8A) that were upregulated andDUSP14,YWHAQ,YME1L1,DHRS7,TUBA1A/LBPthat were down-regulated in the two studies.
1	PARD6B	UNIPROT:Q9BYG5	increases		UNIPROT:P33148	Protein	abaf813e-bc32-11e5-ac4e-001a4ae51246	PMC3800127	Similarly the total protein but not mRNA level of C-cadherin was also modestly reduced by Par6b depletion (Fig. 5A, B).
1	PARD6B	UNIPROT:Q9BYG5	activates		UNIPROT:Q9BUF7	Protein	abaf813e-bc32-11e5-ac4e-001a4ae51246	PMC3800127	We show that Par6b depletion reduced cytoplasmic Crb3 and stabilized membrane Crb3 in deep epidermal cells.
1	PARD6B	UNIPROT:Q9BYG5	activates		UNIPROT:Q92754	Protein	122cb55e-c475-11e5-91a7-001a4ae51247	PMC4419278	The expression ofCdx2transcripts and of CDX2 protein were not restored in PARD6B rescued TFAP2C KD embryos (Fig. 5A,B).
1	PARD6B	UNIPROT:Q9BYG5	activates		UNIPROT:Q9JM04	Protein	abaf813e-bc32-11e5-ac4e-001a4ae51246	PMC3800127	Par6b depletion reduces Lgl2 in both the superficial and deep layers, whilst Crb3 becomes inappropriately stabilized to the entire deep cell surfaces.
1	PARD6B	UNIPROT:Q9BYG5	activates		UNIPROT:Q71U36	Protein	a1944e94-3405-11e8-a34b-001a4a160175	28263792	Supplementary Table 8 includes genes such asISG15,VAV1,PTPRJ,HTR3A,AMPD1/AMPD2,PARD6A/PARD6B,CYP11B1/CYP11B2,ICAM5/ICAM3,IQSEC3/SAG,PDE4C/PDE8A) that were upregulated andDUSP14,YWHAQ,YME1L1,DHRS7,TUBA1A/LBPthat were down-regulated in the two studies.
1	PARD6B	UNIPROT:Q9BYG5	increases		UNIPROT:Q99626	Protein	5d8b550c-c47d-11e5-9da3-001a4ae51247	PMC2924801	"These results suggest that PARD6B acts upstream of CDX2 and is necessary to
                         up-regulate CDX2 expression in TE."
1	PARD6B	UNIPROT:Q9BYG5	activates		UNIPROT:P19544	Protein	b14a26ca-bc3d-11e5-9b9d-001a4ae51247	PMC3731222	However, functional analysis showed that both these mutated Wt1 could not induced the expression ofE-cadherin, Par6b, Wnt4, andWnt11inWt1-deficient SCs (Figure 7A), indicating that these mutations caused Wt1 protein loss of function.
1	PARD6B	UNIPROT:Q9BYG5	activates		UNIPROT:Q19266	Protein	465f1f26-c478-11e5-9cc6-001a4ae51246	PMC3069449	Strikingly, depletion of Par6B attenuated the apical enrichment of aPKC, whereas actin remained concentrated at the apical surface of each individual lumen.
1	PARD6B	UNIPROT:Q9BYG5	activates		UNIPROT:Q9BX67	Protein	16b17b86-c480-11e5-9cc6-001a4ae51246	PMC2892954	Knockdown of Par3 or Par6b markedly blocks the ability of ECs to undergo these critical early events that are necessary to reach their neighbors and assemble into multicellular tube networks.11Our results reveal the same phenomenon with blockade of Jam-B and Jam-C.
1	PARD6B	UNIPROT:Q9BYG5	inhibits		UNIPROT:P01106	Protein	7c477f0c-37eb-11e6-9aa8-001a4ae51247	PMC4800288	Loss of Par6B activity cooperates with proliferation-promoting function of oncogenic Myc, whereas loss of Par6G can interfere with the cell cycle restriction alone.
1	PARD6B	UNIPROT:Q9BYG5	activates		UNIPROT:P27348	Protein	a1944e94-3405-11e8-a34b-001a4a160175	28263792	Supplementary Table 8 includes genes such asISG15,VAV1,PTPRJ,HTR3A,AMPD1/AMPD2,PARD6A/PARD6B,CYP11B1/CYP11B2,ICAM5/ICAM3,IQSEC3/SAG,PDE4C/PDE8A) that were upregulated andDUSP14,YWHAQ,YME1L1,DHRS7,TUBA1A/LBPthat were down-regulated in the two studies.
1	PARD6B	UNIPROT:Q9BYG5	activates		UNIPROT:Q9Y394	Protein	a1944e94-3405-11e8-a34b-001a4a160175	28263792	Supplementary Table 8 includes genes such asISG15,VAV1,PTPRJ,HTR3A,AMPD1/AMPD2,PARD6A/PARD6B,CYP11B1/CYP11B2,ICAM5/ICAM3,IQSEC3/SAG,PDE4C/PDE8A) that were upregulated andDUSP14,YWHAQ,YME1L1,DHRS7,TUBA1A/LBPthat were down-regulated in the two studies.
1	PARD6B	UNIPROT:Q9BYG5	activates		GO:0007163	Phenotype	122cb55e-c475-11e5-91a7-001a4ae51247	PMC4419278	Interestingly, in the current study PARD6B rescue restored apical cell polarity, but only partially re-established position-dependent HIPPO signaling and did not rescueCdx2expression.
1	PARD6B	UNIPROT:Q9BYG5	activates		GO:0007163	Phenotype	ac69108c-bc45-11e5-ac4e-001a4ae51246	10.1016/j.mrfmmm.2007.12.004	Pard6b complexes with Par3 and PKC3 in order to modulate cell polarity[66].
1	PARD6B	UNIPROT:Q9BYG5	inhibits		GO:0007155	Phenotype	abaf813e-bc32-11e5-ac4e-001a4ae51246	PMC3800127	This raised the possibility that Par6b disrupts either the expression or function of adhesion molecules that hold epidermal cells together.
1	PARD6B	UNIPROT:Q9BYG5	activates		GO:0035329	Phenotype	122cb55e-c475-11e5-91a7-001a4ae51247	PMC4419278	Interestingly, in the current study PARD6B rescue restored apical cell polarity, but only partially re-established position-dependent HIPPO signaling and did not rescueCdx2expression.
1		UNIPROT:P37275	inhibits	PARD6B	UNIPROT:Q9BYG5	Protein	5e176e18-cd2f-11ec-b6a5-0050569a1f61	PMC8219162	In support of the hypothesis that the opening of the chromatin in Runx1KO cells is due to the loss of Zeb repressors, we examined a known Zeb1 repressed target,Pard6b, that was upregulated in Runx1KO cells nearly 10-fold based on RNA-seq analysis (S6C Fig) and RT-qPCR (S6D Fig).
1		UNIPROT:P27958	activates	PARD6B	UNIPROT:Q9BYG5	Protein	12b5e756-ca02-11e5-ab20-001a4ae51246	PMC547886	"Depletion of each of the p160 coactivators partially inhibited the ability
                               of E2 to increase PARD6B (Fig. 4B) and pS2 (Fig. 4C) mRNA levels, indicating that all three SRCs contribute to E2-stimulated gene transcription."
1		FPLX:Actin	activates	PARD6B	UNIPROT:Q9BYG5	ProteinFamily	0c5e96e2-94f1-11e9-bffb-001a4a160175	10.1016/j.cell.2018.02.035	By contrast, both sealing and blastocyst formation were abolished by (1) disruption of actin rings using Pard6b downregulation, previously shown to affect cortical actin and tight junction assembly (Alarcon, 2010); (2) disruption of ring coupling to junctions using α-cat siRNAs; (3) prevention of zippering using blebbistatin and H-1152 in a time-restricted manner; and (4) disruption of tight junction formation via ZO1 knockdown (Figures 7D–7F andS6H–S6J).
1		FPLX:Adaptor:protein:II	activates	PARD6B	UNIPROT:Q9BYG5	ProteinFamily	ef5f560e-c677-11ee-9aaa-0050569a1f61	10.1016/j.lfs.2023.122348	Interestingly, Depletion of AP2γ has been showed to disrupt the expression and subcellular localization of Pard6b, Cldn4, Aqp3, Krt18, Tjp2 and F-actin [7].
1		UNIPROT:P19544	decreases	PARD6B	UNIPROT:Q9BYG5	Protein	9601eb34-f593-11eb-9728-001a4a160176	31302435	Studies have shown that WT1 deleted in mature mice SCs downregulated Par6b expression and the loss of SCs polarity characteristics [22].
1		UNIPROT:P19544	inhibits	PARD6B	UNIPROT:Q9BYG5	Protein	c44482da-acfc-11ee-ae1b-0050569a1f61	10.1007/s13237-020-00313-4	WT1 deletion produces downregulation of polarity genes Cdc42ep5 and Par6b resulting in altered cellular polarity in testicular parenchyma [188].
1		UNIPROT:Q19266	decreases	PARD6B	UNIPROT:Q9BYG5	Protein	465f1f26-c478-11e5-9cc6-001a4ae51246	PMC3069449	Depletion of aPKC, with either of two distinct duplexes, induced a corresponding down-regulation of Par6B protein expression (Fig. 7A).
1		UNIPROT:O96013	phosphorylatesProtein	PARD6B	UNIPROT:Q9BYG5	Protein	36c2dee6-ae95-11ec-b4ed-0050569a1f61	PMCPMC8423818	The polarity protein Par6B, which also binds Cdc42, can be phosphorylated by PAK4 (ref.51).
