count	source_label	source_id	relationship	target_label	target_id	entity_type	solr_id	publication_id	sentences
2	SLITRK4	UNIPROT:Q8IW52	activates		GO:0090398	Phenotype	d3f3c67a-1b53-11f0-b759-0050569a791b	10.1016/j.arr.2024.102314	According to gene expression profiling conducted byXie et al. (2018)on UFS, which were induced to undergo replication (passaging) or stress-induced (MK2206) senescence, the overexpression of WD repeat domain, phosphoinositide interacting 1 and SLIT and NTRK-like protein 4 precursor genes induced cellular senescence in UF spheroids, and the administration of ABT263 (a BH3 mimetic) effectively reduced the senescent cells induced in UF spheroids.
2	SLITRK4	UNIPROT:Q8IW52	activates		UNIPROT:P02774	Protein	3d7c32b4-7478-11ee-9458-0050569a1f61	10.1007/s13402-023-00795-9	**p< 0.01 CNPY3/SLITRK4 axis promoted GC proliferation and migration To explore the effect of CNPY3 on the progression of GC cells, we first knocked downCNPY3in BGC823 and MKN28 cells and found thatCNPY3knockdown could inhibit the proliferation, migration and invasion of GC cellsin vitro(Supplement Figure2).|||Data are presented as the mean ± S.D SLITRK4 directly interacted with CNPY3 in GC cells and tumour tissues To further explore the mechanism of SLITRK4-mediated GC invasion and metastasis, we performed co-immunoprecipitation (Co-IP) experiments to screen and identify SLITRK4-binding proteins and combined the results of bioinformatics predictions (Fig.4A and supplement Figure1A).
1	SLITRK4	UNIPROT:Q8IW52	inhibits		UNIPROT:Q16620	Protein	3d7c32b4-7478-11ee-9458-0050569a1f61	10.1007/s13402-023-00795-9	Our study demonstrated that interference with SLITRK4 expression can inhibit the internalization and recovery of TrkB in GC.
1	SLITRK4	UNIPROT:Q8IW52	activates		UNIPROT:P42771	Protein	a5cacf25-6ff7-11e9-bb0c-001a4a160175	PMC6265265	Interestingly, WIPI1 overexpression increased p21 but not p16 expression, and SLITRK4 overexpression increased p16 but p21 expression (Suppl Figure 5).
1	SLITRK4	UNIPROT:Q8IW52	activates		UNIPROT:Q9BT09	Protein	3d7c32b4-7478-11ee-9458-0050569a1f61	10.1007/s13402-023-00795-9	**p< 0.01 CNPY3/SLITRK4 axis promoted GC proliferation and migration To explore the effect of CNPY3 on the progression of GC cells, we first knocked downCNPY3in BGC823 and MKN28 cells and found thatCNPY3knockdown could inhibit the proliferation, migration and invasion of GC cellsin vitro(Supplement Figure2).
1	SLITRK4	UNIPROT:Q8IW52	inhibits		CHEBI:45296	Chemical	e62e933e-bbee-11e5-9b9d-001a4ae51247	PMC3372679	These data suggest that DM1 causes disruption of a neuronal development program in the CNS that is mediated by loss of SLITRK4 expression.
1	SLITRK4	UNIPROT:Q8IW52	activates		GO:0008283	Phenotype	3d7c32b4-7478-11ee-9458-0050569a1f61	10.1007/s13402-023-00795-9	**p< 0.01 CNPY3/SLITRK4 axis promoted GC proliferation and migration To explore the effect of CNPY3 on the progression of GC cells, we first knocked downCNPY3in BGC823 and MKN28 cells and found thatCNPY3knockdown could inhibit the proliferation, migration and invasion of GC cellsin vitro(Supplement Figure2).
1	SLITRK4	UNIPROT:Q8IW52	inhibits		GO:0030154	Phenotype	26053cd2-5c76-11e7-8b40-001a4ae51247	PMC5143318	In this study, the SLITRK4 expression was diminished in the PB-MSCs after treatment, suggesting the differentiation of PB-MSCs into neuronal cells.
1	SLITRK4	UNIPROT:Q8IW52	activates		GO:0090398	Phenotype	a5cacf25-6ff7-11e9-bb0c-001a4a160175	PMC6265265	In our study, overexpression of either WIPI1 or SLITRK4 induced senescence in ULM and myometrial (data not shown) cells demonstrating their major role in cellular senescence.
1	SLITRK4	UNIPROT:Q8IW52	activates		GO:0007165	Phenotype	3d7c32b4-7478-11ee-9458-0050569a1f61	10.1007/s13402-023-00795-9	We supposed that CNPY3, as a secreted protein, acts as a signalling molecule and combines with SLITRK4, which causes changes in the SLITRK4 downstream signalling pathway.
1	SLITRK4	UNIPROT:Q8IW52	activates		GO:1904861	Phenotype	16e91d94-c466-11e5-85e4-001a4ae51246	PMC3593915	"Interestingly, overexpression of Slitrk1, Slitrk2, Slitrk4, or Slitrk5 specifically promoted excitatory synapse formation,
                                  whereas overexpression of Slitrk3 did not (Fig. 2BandDandFig."
1	SLITRK4	UNIPROT:Q8IW52	inhibits		IP:IPR001359	ProteinFamily	7bc2f34e-ab14-11e6-807f-001a4ae51247	PMC5071332	Similar to the results of heterologous synapse-formation assays, expression of shRNA-resistant Slitrk1 mutants (N400I or T418S) or Slitrk4 mutants (V206I or I578V) failed to reverse the reduction in the density of synapsin clusters induced by knockdown of Slitrk1 or Slitrk4 (Figures8A,B).
1		UNIPROT:P01374	increases	SLITRK4	UNIPROT:Q8IW52	Protein	c959e3e4-bc39-11e5-8abe-001a4ae51246	PMC3503294	For instance, LT preferentially induced the expression of mRNAs for histone genes, alpha-fetoprotein (afp), amy2, cd24a, prom1/CD133, h19, sox4, peg3, bex1, igf2 and c-Myc, while 17kT preferentially induced the expression of slitrk4, lmln, acot1, ak1 sulf2, ces5, psrc1/DDA3 and eda2r (Supplementary Table S3).
1		UNIPROT:Q13253	decreases	SLITRK4	UNIPROT:Q8IW52	Protein	26053cd2-5c76-11e7-8b40-001a4ae51247	PMC5143318	In contrast to GABRA3 and MECP2, treatment with Noggin decreased SLITRK4 expression in PBMSCs as compared with untreated cells.