PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
30232181-5	2018	Mutational studies of these domains are confounded by the fact that the Tyr residues (important for interactions of YPX1or3L peptides with ALIX) are required for efficient capsid assembly.	Tyrosine	72-75	programmed cell death 6 interacting protein	Homo sapiens	139-143	
32917811-6	2020	In contrast to the soluble N-terminal portion, the C-terminal tyrosine-rich fragment of ALIX-PRD forms amyloid fibrils and viscous gels validated using dye-binding assays with amyloid-specific probes, congo red and thioflavin T (ThT), and visualized by transmission electron microscopy.	Tyrosine	62-70	programmed cell death 6 interacting protein	Homo sapiens	88-92	
20962096-5	2011	Crystal structures revealed that anchoring tyrosines (in lightface) and nearby hydrophobic residues (underlined) contact the ALIX V domain, revealing how lentiviruses employ a diverse family of late-domain sequences to bind ALIX and promote virus budding.	Tyrosine	43-52	programmed cell death 6 interacting protein	Homo sapiens	125-129	
19143627-2	2009	Specifically, the PTAP (Pro-Thr-Ala-Pro)-type primary L domain of HIV-1 recruits ESCRT-I by binding to Tsg101 (tumour susceptibility gene 101), and an auxiliary LYPX(n)L (Leu-Tyr-Pro-Xaa(n)-Leu)-type L domain recruits the ESCRT-III-binding partner Alix [ALG-2 (apoptosis-linked gene 2)-interacting protein X].	Tyrosine	175-178	programmed cell death 6 interacting protein	Homo sapiens	248-252	
17082185-2	2006	In this study, we show that Alix interacts with the C-terminal region of the platelet-derived growth factor (PDGF) beta-receptor (PDGFRbeta) and becomes transiently tyrosine-phosphorylated in response to PDGF-BB stimulation.	Tyrosine	165-173	programmed cell death 6 interacting protein	Homo sapiens	28-32	
12588984-4	2003	We show that both PalA and AIP1/Alix recognize a protein-protein binding motif that we denote YPXL/I, where Tyr, Pro, and Leu/Ile are crucial for its interactive properties.	Tyrosine	108-111	programmed cell death 6 interacting protein	Homo sapiens	27-31	
12588984-4	2003	We show that both PalA and AIP1/Alix recognize a protein-protein binding motif that we denote YPXL/I, where Tyr, Pro, and Leu/Ile are crucial for its interactive properties.	Tyrosine	108-111	programmed cell death 6 interacting protein	Homo sapiens	32-36	
12445460-4	2002	Both the N-terminal regulatory domain of annexin XI (Anx11N) and the ALG-2-binding domain of Alix/AIP1 are rich in Pro, Gly, Ala, Tyr and Gln.	Tyrosine	130-133	programmed cell death 6 interacting protein	Homo sapiens	93-97	
12445460-4	2002	Both the N-terminal regulatory domain of annexin XI (Anx11N) and the ALG-2-binding domain of Alix/AIP1 are rich in Pro, Gly, Ala, Tyr and Gln.	Tyrosine	130-133	programmed cell death 6 interacting protein	Homo sapiens	98-102	
15557335-5	2005	Src phosphorylated Alix at a C-terminal region rich in tyrosines, an activity that was stimulated by the presence of the Alix binding partner SETA/CIN85.	Tyrosine	55-64	programmed cell death 6 interacting protein	Homo sapiens	19-23	
15557335-5	2005	Src phosphorylated Alix at a C-terminal region rich in tyrosines, an activity that was stimulated by the presence of the Alix binding partner SETA/CIN85.	Tyrosine	55-64	programmed cell death 6 interacting protein	Homo sapiens	121-125	
15456872-6	2004	Increasing the level of Alix weakened the interaction between SETA/CIN85 and Cbl and reduced the tyrosine phosphorylation of c-Cbl and the level of ubiquitination of EGFR, SETA/CIN85, and Cbls.	Tyrosine	97-105	programmed cell death 6 interacting protein	Homo sapiens	24-28	
34688656-2	2021	Here we investigate the molecular basis of these transitions and the effects of tyrosine phosphorylation on the interplay between structure, assembly, and intra- and inter-molecular interactions of ALIX.	Tyrosine	80-88	programmed cell death 6 interacting protein	Homo sapiens	198-202	
34688656-3	2021	As evidenced by transmission electron microscopy and fluorescence and CD spectroscopy, the proline-rich domain (PRD) of ALIX, which encodes binding epitopes of multiple cellular partners, formed rope-like beta-sheet-rich reversible amyloid fibrils that dissolved upon Src-mediated phosphorylation and were restored on PTP1B-mediated dephosphorylation of its conserved tyrosine residues.	Tyrosine	368-376	programmed cell death 6 interacting protein	Homo sapiens	120-124	
34688656-5	2021	These results uncover the autoinhibition mechanism that relocates ALIX to the cytosol, and the diverse roles played by tyrosine phosphorylation in cellular and membrane functions of ALIX.	Tyrosine	119-127	programmed cell death 6 interacting protein	Homo sapiens	182-186