PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
19812251-0	2009	A mutation associated with CMT2A neuropathy causes defects in Fzo1 GTP hydrolysis, ubiquitylation, and protein turnover.	Guanosine Triphosphate	67-70	kinesin family member 1B	Homo sapiens	27-32	
19812251-5	2009	One mutation (analogous to the CMT2A I213T substitution in the GTPase domain of Mfn2) not only abolishes GTP hydrolysis and mitochondrial membrane fusion but also reduces Mdm30-mediated ubiquitylation and degradation of the mutant protein.	Guanosine Triphosphate	63-66	kinesin family member 1B	Homo sapiens	31-36	
19812251-7	2009	These studies identify diverse and unexpected effects of CMT2A mutations, including a possible role for mitofusin ubiquitylation and degradation in CMT2A pathogenesis, and provide evidence for a novel link between Fzo1 GTP hydrolysis, ubiquitylation, and mitochondrial fusion.	Guanosine Triphosphate	219-222	kinesin family member 1B	Homo sapiens	57-62