PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
34175824-7	2021	Based on the fact that both AKT and STAT3 are closely related to mitochondrial biogenesis and mitochondrial pathway-associated apoptosis, this study is the first time to link CLU, STAT3, AKT and mitochondrial biogenesis function after Cr(VI) exposure, to further enrich the experimental basis of Cr(VI)-induced hepatotoxicity, clarify the molecular mechanism of CLU helping cells to escape apoptosis, and also suggest that new ways can be sought to prevent and treat Cr(VI)-induced hepatotoxicity by regulating mitochondrial biosynthesis.	chromium hexavalent ion	235-241	clusterin	Homo sapiens	362-365	
34175824-7	2021	Based on the fact that both AKT and STAT3 are closely related to mitochondrial biogenesis and mitochondrial pathway-associated apoptosis, this study is the first time to link CLU, STAT3, AKT and mitochondrial biogenesis function after Cr(VI) exposure, to further enrich the experimental basis of Cr(VI)-induced hepatotoxicity, clarify the molecular mechanism of CLU helping cells to escape apoptosis, and also suggest that new ways can be sought to prevent and treat Cr(VI)-induced hepatotoxicity by regulating mitochondrial biosynthesis.	chromium hexavalent ion	467-473	clusterin	Homo sapiens	175-178	
34175824-7	2021	Based on the fact that both AKT and STAT3 are closely related to mitochondrial biogenesis and mitochondrial pathway-associated apoptosis, this study is the first time to link CLU, STAT3, AKT and mitochondrial biogenesis function after Cr(VI) exposure, to further enrich the experimental basis of Cr(VI)-induced hepatotoxicity, clarify the molecular mechanism of CLU helping cells to escape apoptosis, and also suggest that new ways can be sought to prevent and treat Cr(VI)-induced hepatotoxicity by regulating mitochondrial biosynthesis.	chromium hexavalent ion	467-473	clusterin	Homo sapiens	362-365	
31376806-1	2019	Our group found that long-term low-dose exposure to hexavalent chromium [Cr(VI)] in L-02 hepatocytes resulted in premature senescence, which accompanied by the increased expression of Clusterin (CLU), but the functional role of CLU in premature senescence has never been explored.	chromium hexavalent ion	73-79	clusterin	Homo sapiens	184-193	
31376806-1	2019	Our group found that long-term low-dose exposure to hexavalent chromium [Cr(VI)] in L-02 hepatocytes resulted in premature senescence, which accompanied by the increased expression of Clusterin (CLU), but the functional role of CLU in premature senescence has never been explored.	chromium hexavalent ion	73-79	clusterin	Homo sapiens	195-198	
31376806-1	2019	Our group found that long-term low-dose exposure to hexavalent chromium [Cr(VI)] in L-02 hepatocytes resulted in premature senescence, which accompanied by the increased expression of Clusterin (CLU), but the functional role of CLU in premature senescence has never been explored.	chromium hexavalent ion	73-79	clusterin	Homo sapiens	228-231	
31376806-4	2019	The results indicated that Cr(VI)-induced premature senescence was associated with phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway inhibition, and high expression of CLU in the senescent cells exerted its functional role of promoting cell proliferation.	chromium hexavalent ion	27-33	clusterin	Homo sapiens	186-189	
31376806-5	2019	CLU could complex with eukaryotic translation initiation factor 3 subunit I (EIF3I) and prevent its degradation, leading to the increase of AKT activity in Cr(VI)-exposed senescent hepatocytes.	chromium hexavalent ion	156-162	clusterin	Homo sapiens	0-3	
31376806-6	2019	Blockage of the PI3K/AKT pathway with its inhibitor LY294002 eliminated the inhibitory effect of CLU on Cr(VI)-induced premature senescence.	chromium hexavalent ion	104-110	clusterin	Homo sapiens	97-100	
31376806-7	2019	We concluded that high expression of CLU suppressed Cr(VI)-induced premature senescence through activation of PI3K/AKT pathway, which will provide the experimental basis for the study of Cr(VI)-induced liver cancer, especially for the elucidation of the mechanism of liver cancer cells escaping from senescence.	chromium hexavalent ion	52-58	clusterin	Homo sapiens	37-40	
31376806-7	2019	We concluded that high expression of CLU suppressed Cr(VI)-induced premature senescence through activation of PI3K/AKT pathway, which will provide the experimental basis for the study of Cr(VI)-induced liver cancer, especially for the elucidation of the mechanism of liver cancer cells escaping from senescence.	chromium hexavalent ion	187-193	clusterin	Homo sapiens	37-40	
30713657-6	2019	By the establishment of CLU over-expression cells, we found that over-expression of CLU alleviated Cr(vi)-induced MRCC I inhibition and further rescued cell viability loss and reduced AST and ALT leakage.	chromium hexavalent ion	99-105	clusterin	Homo sapiens	84-87	
30713657-7	2019	Thus, we reached the conclusion that the CLU-induced increase of MRCC I activity protected against Cr(vi)-induced cytotoxicity.	chromium hexavalent ion	99-105	clusterin	Homo sapiens	41-44	
34175824-2	2021	We previously proved that Clusterin (CLU) can inhibit the apoptosis of L02 hepatocytes induced by Cr(VI) through mitochondrial pathway, but the associated molecular mechanism has not been further studied.	chromium hexavalent ion	98-104	clusterin	Homo sapiens	26-35	
34175824-2	2021	We previously proved that Clusterin (CLU) can inhibit the apoptosis of L02 hepatocytes induced by Cr(VI) through mitochondrial pathway, but the associated molecular mechanism has not been further studied.	chromium hexavalent ion	98-104	clusterin	Homo sapiens	37-40	
34175824-4	2021	We demonstrated in the present study that Cr(VI) triggered mitochondrial biogenesis dysfunction-associated apoptosis, and CLU delayed Cr(VI)-induced apoptosis by enhancing mitochondrial biogenesis.	chromium hexavalent ion	134-140	clusterin	Homo sapiens	122-125	
34175824-6	2021	We used the STAT3 inhibitor C188-9 and the AKT inhibitor Uprosertib to eliminate the anti-apoptotic effect of CLU, and found that CLU inhibited Cr(VI)-induced apoptosis by up-regulating AKT/STAT3 signal.	chromium hexavalent ion	144-150	clusterin	Homo sapiens	130-133	
34175824-7	2021	Based on the fact that both AKT and STAT3 are closely related to mitochondrial biogenesis and mitochondrial pathway-associated apoptosis, this study is the first time to link CLU, STAT3, AKT and mitochondrial biogenesis function after Cr(VI) exposure, to further enrich the experimental basis of Cr(VI)-induced hepatotoxicity, clarify the molecular mechanism of CLU helping cells to escape apoptosis, and also suggest that new ways can be sought to prevent and treat Cr(VI)-induced hepatotoxicity by regulating mitochondrial biosynthesis.	chromium hexavalent ion	235-241	clusterin	Homo sapiens	175-178	
34020271-3	2021	Our previous work has confirmed that premature senescent hepatocytes induced by Cr(VI) expressed high level of Clusterin (CLU) and secrete interleukin-6 (IL-6) and IL-8.	chromium hexavalent ion	80-86	clusterin	Homo sapiens	111-120	
34020271-3	2021	Our previous work has confirmed that premature senescent hepatocytes induced by Cr(VI) expressed high level of Clusterin (CLU) and secrete interleukin-6 (IL-6) and IL-8.	chromium hexavalent ion	80-86	clusterin	Homo sapiens	122-125	
32961495-0	2020	Clusterin alleviates Cr(VI)-induced mitochondrial apoptosis in L02 hepatocytes via inhibition of Ca2+-ROS-Drp1-mitochondrial fission axis.	chromium hexavalent ion	21-27	clusterin	Homo sapiens	0-9	
32961495-3	2020	In this study, we aimed to explore the effect of CLU on Cr(VI)-induced mitochondrial fission and apoptosis.	chromium hexavalent ion	56-62	clusterin	Homo sapiens	49-52	
32961495-5	2020	CLU over-expression could protect the hepatocytes from Cr(VI)-induced mitochondrial apoptosis.	chromium hexavalent ion	55-61	clusterin	Homo sapiens	0-3