PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
35141145-6	2021	In the CAM xenograft model, DOX and PEMF exposure also synergistically reduced tumor size as well as reduced Transient Receptor Potential Canonical 1 (TRPC1) channel expression.	pemf	36-40	transient receptor potential cation channel subfamily C member 1	Homo sapiens	109-149	
35141145-8	2021	Stable overexpression of TRPC1 enhanced the vulnerability of MCF-7 cells to both DOX and PEMF exposure and promoted proliferation, whereas TRPC1 genetic silencing reduced sensitivity to both DOX and PEMF treatments and mitigated proliferation.	pemf	89-93	transient receptor potential cation channel subfamily C member 1	Homo sapiens	25-30	
35141145-8	2021	Stable overexpression of TRPC1 enhanced the vulnerability of MCF-7 cells to both DOX and PEMF exposure and promoted proliferation, whereas TRPC1 genetic silencing reduced sensitivity to both DOX and PEMF treatments and mitigated proliferation.	pemf	199-203	transient receptor potential cation channel subfamily C member 1	Homo sapiens	139-144	
35141145-9	2021	Chronic exposure to DOX depressed TRPC1 expression, proliferation, and responses to both PEMF exposure and DOX in a manner that was reversible upon removal of DOX.	pemf	89-93	transient receptor potential cation channel subfamily C member 1	Homo sapiens	34-39	
35141145-11	2021	Finally, PEMF exposure was shown to attenuate the invasiveness of MCF-7 cells in correlation with TRPC1 expression.	pemf	9-13	transient receptor potential cation channel subfamily C member 1	Homo sapiens	98-103	
35141145-12	2021	We thus demonstrate that the expression levels of TRPC1 consistently predicted breast cancer sensitivity to DOX and PEMF interventions and positively correlated to EMT status, providing an initial rationale for the use of PEMF-based therapies as an adjuvant to DOX chemotherapy for the treatment of breast cancers characterized by elevated TRPC1 expression levels.	pemf	116-120	transient receptor potential cation channel subfamily C member 1	Homo sapiens	50-55	
35141145-12	2021	We thus demonstrate that the expression levels of TRPC1 consistently predicted breast cancer sensitivity to DOX and PEMF interventions and positively correlated to EMT status, providing an initial rationale for the use of PEMF-based therapies as an adjuvant to DOX chemotherapy for the treatment of breast cancers characterized by elevated TRPC1 expression levels.	pemf	222-226	transient receptor potential cation channel subfamily C member 1	Homo sapiens	50-55	
33644848-7	2021	As brief PEMF exposure promotes in vitro differentiation by activating a TRPC1-mitochondrial axis, an opportunity to combine 2DG with developmentally targeted PEMF exposure for synergistic effects was realizable.	pemf	9-13	transient receptor potential cation channel subfamily C member 1	Homo sapiens	73-78	
33644848-8	2021	Neurogenic gene expression, neurotransmitter release, and reactive oxygen species (ROS) production were greatly enhanced by a brief (10 min) and low amplitude (2 mT) PEMF exposure timed to coincide with the highest TRPC1 expression from hDPSCs on 2DG.	pemf	166-170	transient receptor potential cation channel subfamily C member 1	Homo sapiens	215-220	
33644848-11	2021	Hence, graphene created a more conducive environment for subsequent PEMF-stimulated neurogenic induction of hDPSCs through their mutual capacity to activate TRPC1with subsequent ROS production.	pemf	68-72	transient receptor potential cation channel subfamily C member 1	Homo sapiens	157-162