PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
18597631-9	2008	Taken together with earlier in vitro evidence, these findings show that Cx43 is required for the anti-apoptotic effect of bisphosphonates on osteocytes and osteoblasts.	Diphosphonates	122-137	gap junction protein, alpha 3	Mus musculus	72-76	
20727997-6	2011	Remarkably, this Cx43-dependent survival effect of bisphosphonates is independent of gap junctions and results from opening of Cx43 hemichannels.	Diphosphonates	51-66	gap junction protein, alpha 3	Mus musculus	17-21	
27041582-4	2016	The treatment of bisphosphonate drugs, either alendronate (ALN) or zoledronic acid (ZOL), opened Cx43 hemichannels in osteocytes.	Diphosphonates	17-31	gap junction protein, alpha 3	Mus musculus	97-101	
27041582-5	2016	Conditioned media (CM) collected from MLO-Y4 osteocyte cells treated with bisphosphonates inhibited the anchorage-independent growth, migration and invasion of MDA-MB-231 human breast cancer cells and Py8119 mouse mammary carcinoma cells, and this inhibitory effect was attenuated with Cx43(E2), a specific hemichannel-blocking antibody.	Diphosphonates	74-89	gap junction protein, alpha 3	Mus musculus	286-290	
20727997-6	2011	Remarkably, this Cx43-dependent survival effect of bisphosphonates is independent of gap junctions and results from opening of Cx43 hemichannels.	Diphosphonates	51-66	gap junction protein, alpha 3	Mus musculus	127-131