PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
34635505-0	2022	GATM-Mediated Creatine Biosynthesis Enables Maintenance of FLT3-ITD-Mutant Acute Myeloid Leukemia.	Creatine	14-22	glycine amidinotransferase	Homo sapiens	0-4	
34635505-4	2022	In this study, we demonstrate the effects of de novo creatine biosynthesis upregulation by FLT3-ITD on AML sustainability.	Creatine	53-61	fms related receptor tyrosine kinase 3	Homo sapiens	91-95	
34635505-5	2022	Our data show that FLT3-ITD constitutively activates the STAT5 signaling pathway, which upregulates the expression of glycine amidinotransferase (GATM), the first rate-limiting enzyme of de novo creatine biosynthesis.	Glycine	118-125	fms related receptor tyrosine kinase 3	Homo sapiens	19-23	
34635505-5	2022	Our data show that FLT3-ITD constitutively activates the STAT5 signaling pathway, which upregulates the expression of glycine amidinotransferase (GATM), the first rate-limiting enzyme of de novo creatine biosynthesis.	Glycine	118-125	signal transducer and activator of transcription 5A	Homo sapiens	57-62	
34635505-5	2022	Our data show that FLT3-ITD constitutively activates the STAT5 signaling pathway, which upregulates the expression of glycine amidinotransferase (GATM), the first rate-limiting enzyme of de novo creatine biosynthesis.	Glycine	118-125	glycine amidinotransferase	Homo sapiens	146-150	
34635505-5	2022	Our data show that FLT3-ITD constitutively activates the STAT5 signaling pathway, which upregulates the expression of glycine amidinotransferase (GATM), the first rate-limiting enzyme of de novo creatine biosynthesis.	Creatine	195-203	fms related receptor tyrosine kinase 3	Homo sapiens	19-23	
34635505-5	2022	Our data show that FLT3-ITD constitutively activates the STAT5 signaling pathway, which upregulates the expression of glycine amidinotransferase (GATM), the first rate-limiting enzyme of de novo creatine biosynthesis.	Creatine	195-203	signal transducer and activator of transcription 5A	Homo sapiens	57-62	
34635505-5	2022	Our data show that FLT3-ITD constitutively activates the STAT5 signaling pathway, which upregulates the expression of glycine amidinotransferase (GATM), the first rate-limiting enzyme of de novo creatine biosynthesis.	Creatine	195-203	glycine amidinotransferase	Homo sapiens	146-150	
34635505-6	2022	Pharmacological FLT3-ITD inhibition reduces intracellular creatinine levels through transcriptional down-regulation of genes in the de novo creatine biosynthesis pathway.	Creatinine	58-68	fms related receptor tyrosine kinase 3	Homo sapiens	16-20	
34635505-6	2022	Pharmacological FLT3-ITD inhibition reduces intracellular creatinine levels through transcriptional down-regulation of genes in the de novo creatine biosynthesis pathway.	Creatine	140-148	fms related receptor tyrosine kinase 3	Homo sapiens	16-20	
34635505-7	2022	The same reduction can be achieved by cyclocreatine or genetic GATM knock down with shRNA and is reflected in significant decrease of cell proliferation and moderate increase of cell apoptosis in FLT3-ITD mutant cell lines.	cyclocreatine	38-51	fms related receptor tyrosine kinase 3	Homo sapiens	196-200	
34635505-9	2022	This study uncovers a previously uncharacterized role of creatine metabolic pathway in the maintenance of FLT3-ITD mutant AML and suggests that targeting this pathway may serve as a promising therapeutic strategy for FLT3-ITD positive AML.	Creatine	57-65	fms related receptor tyrosine kinase 3	Homo sapiens	106-110	
34635505-10	2022	Implications: FLT3-ITD mutation in AML upregulates de novo creatine biosynthesis that we show can be suppressed to diminish the proliferation and survival of blast cells.	Creatine	59-67	fms related receptor tyrosine kinase 3	Homo sapiens	14-18