PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
34730397-3	2022	In this study, we identified a cluster of six arginine residues in the disordered domain of UL34 as a minimal region required for the interaction with ALIX as well as the recruitment of ALIX and an ESCRT-III protein CHMP4B to the INM in HSV-1-infected cells.	Arginine	46-54	programmed cell death 6 interacting protein	Homo sapiens	151-155
34730397-3	2022	In this study, we identified a cluster of six arginine residues in the disordered domain of UL34 as a minimal region required for the interaction with ALIX as well as the recruitment of ALIX and an ESCRT-III protein CHMP4B to the INM in HSV-1-infected cells.	Arginine	46-54	programmed cell death 6 interacting protein	Homo sapiens	186-190
34730397-5	2022	We also showed that the effect of the arginine cluster in UL34 on HSV-1 replication was dependent primarily on ALIX.	Arginine	38-46	programmed cell death 6 interacting protein	Homo sapiens	111-115
34730397-6	2022	These results indicated that the arginine cluster in the disordered domain of UL34 was required for the interaction with ALIX and the recruitment of ESCRT-III machinery to the INM to promote primary envelopment.	Arginine	33-41	programmed cell death 6 interacting protein	Homo sapiens	121-125
34730397-10	2022	In this study, we present data suggesting that the arginine cluster in the disordered domain of HSV-1 UL34 mediates the interaction with ALIX, thereby leading to the recruitment of ESCRT-III machinery to the INM for efficient primary envelopment.	Arginine	51-59	programmed cell death 6 interacting protein	Homo sapiens	137-141
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.	Proline	91-98	programmed cell death 6 interacting protein	Homo sapiens	120-124
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
35315341-8	2022	Moreover, glutamate supplementation increased exosome secretion by increasing expression of Alix, TSG101, Rab27a/b and VAMP7.	Glutamic Acid	10-19	programmed cell death 6 interacting protein	Homo sapiens	92-96
34346309-7	2021	Finally, ACBs retain a population of ALIX, and their presence correlates with delayed abscission and delayed recruitment of ALIX to the midbody where it would normally promote abscission.	acbs	9-13	programmed cell death 6 interacting protein	Homo sapiens	37-41
34346309-7	2021	Finally, ACBs retain a population of ALIX, and their presence correlates with delayed abscission and delayed recruitment of ALIX to the midbody where it would normally promote abscission.	acbs	9-13	programmed cell death 6 interacting protein	Homo sapiens	124-128
34211388-10	2021	Most surprisingly, the decreased expression of Alix was attenuated after the treatment of Memantine in different AD animal models.	Memantine	90-99	programmed cell death 6 interacting protein	Homo sapiens	47-51
33781846-3	2021	Characterization of keratinocyte-derived EVs after poly(I:C) treatment (poly(I:C)-EVs) showed slight differences in levels of EV markers TSG101 and Alix, a loss of CD63 and were positive for autophagosome marker LC3b-II and the cytokine IL36gamma compared to EVs from unstimulated keratinocytes (control-EVs).	poly(i:c)-evs	72-85	programmed cell death 6 interacting protein	Homo sapiens	148-152
35052621-6	2022	Briefly, YRL1091-induced cell death was associated with upregulation of microtubule-associated protein 1 light chain 3B, downregulation of multifunctional adapter protein Alix, and activation of extracellular signal-regulated kinase 1/2 and c-Jun N-terminal kinase.	yrl1091	9-16	programmed cell death 6 interacting protein	Homo sapiens	171-175
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
32659447-6	2020	Noteworthy, BMP was associated with extracellular vesicles (EVs) isolated from human urines and extracellular medium of human embryonic kidney HEK293 cells and co-localizing with classical EV protein markers CD63 and ALIX.	bis(monoacylglyceryl)phosphate	12-15	programmed cell death 6 interacting protein	Homo sapiens	217-221
32917811-0	2020	Proline-rich domain of human ALIX contains multiple TSG101-UEV interaction sites and forms phosphorylation-mediated reversible amyloids.	Proline	0-7	programmed cell death 6 interacting protein	Homo sapiens	29-33
33521905-9	2021	RESULTS: RIF-EVs and FER-EVs were bilayer membrane vesicles, ranging from 100 to 150 nm in size, that expressed the classic EV markers Alix and CD9.	rif-evs	9-16	programmed cell death 6 interacting protein	Homo sapiens	135-139
33521905-9	2021	RESULTS: RIF-EVs and FER-EVs were bilayer membrane vesicles, ranging from 100 to 150 nm in size, that expressed the classic EV markers Alix and CD9.	fer-evs	21-28	programmed cell death 6 interacting protein	Homo sapiens	135-139
33756122-6	2021	Interestingly, MIM-containing l-EV production was promoted by in vivo equivalent external forces and by the suppression of ALIX, suggesting an alternative mechanism of vesicle formation to s-EVs.	l-ev	30-34	programmed cell death 6 interacting protein	Homo sapiens	123-127
33525864-12	2021	RT-PCR analysis of EV biogenesis markers (CD63, CD81, Alix, TSG101, Syntenin1, ADAM10, RAB27b, and Syndecan) showed differential expression between the iron-oxide-treated cultures and nontreated cultures, as well as between adherent and nonadherent 3D cultures.	ferric oxide	152-162	programmed cell death 6 interacting protein	Homo sapiens	54-58
33139753-7	2020	These results indicate that the ALIX-mediated ESCRT-III pathway plays a suppressive role in progerin-induced NM deformation and suggest that autophagy down-regulates progerin-induced NM deformation in a manner dependent on ESCRT-III machinery.	progerin	92-100	programmed cell death 6 interacting protein	Homo sapiens	32-36
33139753-7	2020	These results indicate that the ALIX-mediated ESCRT-III pathway plays a suppressive role in progerin-induced NM deformation and suggest that autophagy down-regulates progerin-induced NM deformation in a manner dependent on ESCRT-III machinery.	progerin	166-174	programmed cell death 6 interacting protein	Homo sapiens	32-36
32917811-2	2020	Using a "divide-and-conquer" approach, we present a detailed investigation of a PRD (166 residues; ~30% prolines) belonging to a human protein ALIX, a versatile adaptor protein involved in essential cellular processes including ESCRT-mediated membrane remodeling, cell adhesion, and apoptosis.	Proline	104-112	programmed cell death 6 interacting protein	Homo sapiens	143-147
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.	Congo Red	201-210	programmed cell death 6 interacting protein	Homo sapiens	88-92
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.	thioflavin T	215-227	programmed cell death 6 interacting protein	Homo sapiens	88-92
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.	thioflavin T	229-232	programmed cell death 6 interacting protein	Homo sapiens	88-92
32948012-3	2020	We report that the ESCRT proteins transiently co-localize with virions after completion of virion assembly for durations of 45 +- 30 s. We show that mutagenizing the YP domain of Gag which is the primary ALIX binding site or depleting ALIX from cells results in multiple recruitments of the full ESCRT machinery on the same virion (referred to as stuttering where the number of recruitments to the same virion >3).	Glycosaminoglycans	179-182	programmed cell death 6 interacting protein	Homo sapiens	204-208
32948012-3	2020	We report that the ESCRT proteins transiently co-localize with virions after completion of virion assembly for durations of 45 +- 30 s. We show that mutagenizing the YP domain of Gag which is the primary ALIX binding site or depleting ALIX from cells results in multiple recruitments of the full ESCRT machinery on the same virion (referred to as stuttering where the number of recruitments to the same virion >3).	Glycosaminoglycans	179-182	programmed cell death 6 interacting protein	Homo sapiens	235-239
32886660-7	2020	Imaging ATP depleted cells, we show that the disassembly of CHMP4b and ALIX observed in step 2 is ATP dependent.	Adenosine Triphosphate	8-11	programmed cell death 6 interacting protein	Homo sapiens	71-75
32886660-7	2020	Imaging ATP depleted cells, we show that the disassembly of CHMP4b and ALIX observed in step 2 is ATP dependent.	Adenosine Triphosphate	98-101	programmed cell death 6 interacting protein	Homo sapiens	71-75
29348172-6	2018	Using a lentiviral doxycycline-inducible system, we demonstrate that re-expression of ARRDC3 in invasive breast carcinoma is sufficient to restore normal PAR1 trafficking through the ALG-interacting protein X (ALIX)-dependent lysosomal degradative pathway.	Doxycycline	19-30	programmed cell death 6 interacting protein	Homo sapiens	183-208
32879635-5	2020	WGCNA analysis showed that sevoflurane anesthesia clustered into 7 functional disorder modules, including PDCD6IP, WDR3, and other core genes; propofol anesthesia clustered to form two functional disorder modules, including KCNB2 and LHX2, two core genes Enrichment analysis of the functions and pathways of interest suggests that both anesthesia-related module genes tend to function as pathways associated with ion and transmembrane transport.	Sevoflurane	27-38	programmed cell death 6 interacting protein	Homo sapiens	106-113
31969431-7	2020	Moreover, the late domain (L-domain) of Gag played a central role in Alix recruitment, which promoted endosomal sorting complex required for transport I (ESCRT-I) formation and amphisome accumulation by facilitating late endosome formation.	Glycosaminoglycans	40-43	programmed cell death 6 interacting protein	Homo sapiens	69-73
32049272-0	2020	ALIX- and ESCRT-III-dependent sorting of tetraspanins to exosomes.	Tetraspanin 24	41-53	programmed cell death 6 interacting protein	Homo sapiens	0-4
32049272-5	2020	Our data indicate that this ALIX- and ESCRT-III-dependent pathway promotes the sorting and delivery of tetraspanins to exosomes.	Tetraspanin 24	103-115	programmed cell death 6 interacting protein	Homo sapiens	28-32
31754648-6	2019	Cocaine also increases postsynaptic alpha-syn where it is needed for normal ALIX function, multivesicular body formation, and cocaine-induced exosome release indicating potentially similar alpha-syn actions for vesicle release pre- and post-synaptically.	Cocaine	0-7	programmed cell death 6 interacting protein	Homo sapiens	76-80
30824759-6	2019	We revealed that the interaction between the SH3 domain of c-Src and the proline-rich region of Alix activates ESCRT-mediated intra-luminal vesicle (ILV) formation, resulting in the upregulation of exosome secretion in c-Src-transformed cells.	Proline	73-80	programmed cell death 6 interacting protein	Homo sapiens	96-100
29571744-4	2018	To investigate the role of GagNC in this recruitment, we analysed its impact on TSG101 and ALIX localisations and interactions in cells expressing Gag.	Glycosaminoglycans	27-30	programmed cell death 6 interacting protein	Homo sapiens	91-95
32622655-12	2020	RESULT(S): RIF-EVs and FER-EVs are bilayered vesicles ~100 nm in size and enriched with TSG101, Alix, and CD9.	rif-evs	11-18	programmed cell death 6 interacting protein	Homo sapiens	96-100
32622655-12	2020	RESULT(S): RIF-EVs and FER-EVs are bilayered vesicles ~100 nm in size and enriched with TSG101, Alix, and CD9.	fer-evs	23-30	programmed cell death 6 interacting protein	Homo sapiens	96-100
32326345-2	2020	Galectin-3 (Gal3), a beta-galactose binding lectin, has been reported to interact with Alix and regulate HIV-1 subtype B budding.	Galactose	26-35	programmed cell death 6 interacting protein	Homo sapiens	87-91
31479773-5	2019	METHODS: The presence of exosomes in human and calcium phosphate (CaPO4)-induced AAA tissues was determined by immunofluorescence staining of CD63 and Alix.	capo4	66-71	programmed cell death 6 interacting protein	Homo sapiens	151-155
31444311-0	2019	ALIX(ir) of Life: The Pivotal Role of ALIX In Regulating Plant Responses To Abscisic Acid.	Abscisic Acid	76-89	programmed cell death 6 interacting protein	Homo sapiens	0-4
31444311-0	2019	ALIX(ir) of Life: The Pivotal Role of ALIX In Regulating Plant Responses To Abscisic Acid.	Abscisic Acid	76-89	programmed cell death 6 interacting protein	Homo sapiens	38-42
31149942-6	2019	RESULTS: Neuronal enrichment of NDE was confirmed with elevated synaptophysin and normalized to the exosomal marker, apoptosis-linked gene-2-interacting protein X (ALIX).	NDE	32-35	programmed cell death 6 interacting protein	Homo sapiens	117-162
31149942-6	2019	RESULTS: Neuronal enrichment of NDE was confirmed with elevated synaptophysin and normalized to the exosomal marker, apoptosis-linked gene-2-interacting protein X (ALIX).	NDE	32-35	programmed cell death 6 interacting protein	Homo sapiens	164-168
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
30240438-7	2018	Further, we were able to inhibit the cell protective function of ALG-2 after digitonin treatment by adding a peptide with the ALG-2 binding sequence of ALIX, which has been proposed to serve as the ALG-2 downstream target in a number of processes including cell membrane repair.	Digitonin	77-86	programmed cell death 6 interacting protein	Homo sapiens	152-156
29891975-7	2018	Notably, conserved Phenyl alanine residue (F676) in ALIX was critical for ALIX mediated release of pNL-INp6DeltaPTAP/PYRE implying the critical role of this hydrophobic patch in ALIX recruitment.	Phenylalanine	19-33	programmed cell death 6 interacting protein	Homo sapiens	52-56
29891975-7	2018	Notably, conserved Phenyl alanine residue (F676) in ALIX was critical for ALIX mediated release of pNL-INp6DeltaPTAP/PYRE implying the critical role of this hydrophobic patch in ALIX recruitment.	Phenylalanine	19-33	programmed cell death 6 interacting protein	Homo sapiens	74-78
29891975-7	2018	Notably, conserved Phenyl alanine residue (F676) in ALIX was critical for ALIX mediated release of pNL-INp6DeltaPTAP/PYRE implying the critical role of this hydrophobic patch in ALIX recruitment.	Phenylalanine	19-33	programmed cell death 6 interacting protein	Homo sapiens	74-78
29884298-10	2018	Total tSTB-EVs and STB-EXs also expressed the exosome markers such as the Apoptosis-Linked Gene 2-Interacting Protein X (Alix) and the cluster differentiation protein 9 (CD9).	stb-exs	19-26	programmed cell death 6 interacting protein	Homo sapiens	74-119
29884298-10	2018	Total tSTB-EVs and STB-EXs also expressed the exosome markers such as the Apoptosis-Linked Gene 2-Interacting Protein X (Alix) and the cluster differentiation protein 9 (CD9).	stb-exs	19-26	programmed cell death 6 interacting protein	Homo sapiens	121-125
29348172-6	2018	Using a lentiviral doxycycline-inducible system, we demonstrate that re-expression of ARRDC3 in invasive breast carcinoma is sufficient to restore normal PAR1 trafficking through the ALG-interacting protein X (ALIX)-dependent lysosomal degradative pathway.	Doxycycline	19-30	programmed cell death 6 interacting protein	Homo sapiens	210-214
28379543-9	2017	Reduction of Alix also substantially decreased PS-ASO activities without affecting total PS-ASO uptake.	ps-aso	47-53	programmed cell death 6 interacting protein	Homo sapiens	13-17
26150415-3	2015	In Alix, the Phe residue, which is located in the hydrophobic groove of the V domain, is critical for binding to the YP(X)nL motif.	Phenylalanine	13-16	programmed cell death 6 interacting protein	Homo sapiens	3-7
27280284-4	2016	Specifically, we show that Gag mutants with compromised interactions with ALIX and Tsg101, two early ESCRT factors, have an average budding delay of ~75 minutes and ~10 hours, respectively.	Glycosaminoglycans	27-30	programmed cell death 6 interacting protein	Homo sapiens	74-78
26859355-3	2016	Here we demonstrate that M phase-specific phosphorylation of the intramolecular interaction site within the proline-rich domain (PRD) of ALIX transforms cytosolic ALIX from closed to open conformation.	Proline	108-115	programmed cell death 6 interacting protein	Homo sapiens	137-141
26859355-3	2016	Here we demonstrate that M phase-specific phosphorylation of the intramolecular interaction site within the proline-rich domain (PRD) of ALIX transforms cytosolic ALIX from closed to open conformation.	Proline	108-115	programmed cell death 6 interacting protein	Homo sapiens	163-167
27244115-5	2016	We also found that Alix is required for fast endocytosis and downstream signaling of the interleukin-2 receptor giving a first indication that CIE is necessary for activation of at least some surface receptors.	chlorimuron ethyl	143-146	programmed cell death 6 interacting protein	Homo sapiens	19-23
25667979-6	2015	On the other hand, amino acid substitution of Tyr180, a Pocket 1 residue, with Ala caused loss of binding to ALIX, but maintained binding to Sec31A.	Alanine	79-82	programmed cell death 6 interacting protein	Homo sapiens	109-113
27462417-4	2015	Our results show that calcium-dependent ALG-2 interaction with ALIX completely relieves the intramolecular interaction of ALIX and promotes CHMP4-dependent ALIX association with the membrane.	Calcium	22-29	programmed cell death 6 interacting protein	Homo sapiens	63-67
27462417-4	2015	Our results show that calcium-dependent ALG-2 interaction with ALIX completely relieves the intramolecular interaction of ALIX and promotes CHMP4-dependent ALIX association with the membrane.	Calcium	22-29	programmed cell death 6 interacting protein	Homo sapiens	122-126
27462417-4	2015	Our results show that calcium-dependent ALG-2 interaction with ALIX completely relieves the intramolecular interaction of ALIX and promotes CHMP4-dependent ALIX association with the membrane.	Calcium	22-29	programmed cell death 6 interacting protein	Homo sapiens	122-126
27462417-7	2015	These findings indicate that calcium-dependent ALG-2 interaction with ALIX is specifically responsible for generating functional ALIX that supports MVB sorting of ubiquitinated membrane receptors.	Calcium	29-36	programmed cell death 6 interacting protein	Homo sapiens	70-74
27462417-7	2015	These findings indicate that calcium-dependent ALG-2 interaction with ALIX is specifically responsible for generating functional ALIX that supports MVB sorting of ubiquitinated membrane receptors.	Calcium	29-36	programmed cell death 6 interacting protein	Homo sapiens	129-133
25759984-0	2015	Dicaine represses apoptosis-linked gene 2-interacting protein X expression to induce airway epithelial barrier dysfunction.	Tetracaine	0-7	programmed cell death 6 interacting protein	Homo sapiens	18-63
25759984-8	2015	The results of the present study demonstrated that Alix expression levels were markedly lower in Rpc cells treated with dicaine, compared with those not treated with dicaine.	Tetracaine	120-127	programmed cell death 6 interacting protein	Homo sapiens	51-55
25759984-11	2015	In conclusion, dicaine causes a decrease in expression levels of Alix, which resulted in compromise of the Rpc cell monolayer epithelial barrier function.	Tetracaine	15-22	programmed cell death 6 interacting protein	Homo sapiens	65-69
25828531-3	2015	report that trimming of heparan sulfate side chains of syndecans by endosomal heparanase facilitates sorting into exosomes by the formation of tight syndecan clusters that are recruited by the multivalent adaptor syntenin to the ALIX-ESCRT sorting machinery at endosomes.	Heparitin Sulfate	24-39	programmed cell death 6 interacting protein	Homo sapiens	229-233
25732677-10	2015	Taken together, our findings identify heparanase as a modulator of the syndecan-syntenin-ALIX pathway, fostering endosomal membrane budding and the biogenesis of exosomes by trimming the heparan sulfate chains on syndecans.	Heparitin Sulfate	187-202	programmed cell death 6 interacting protein	Homo sapiens	89-93
25988257-7	2015	UF/heparin-purified EVs from cell culture displayed the EV marker Alix, contained a diverse RNA profile, had lower levels of protein contamination, and were functional at binding to and uptake into cells.	Heparin	3-10	programmed cell death 6 interacting protein	Homo sapiens	66-70
24834918-0	2014	ALIX is recruited temporarily into HIV-1 budding sites at the end of gag assembly.	Glycosaminoglycans	69-72	programmed cell death 6 interacting protein	Homo sapiens	0-4
24996823-9	2014	We also found that the galectin-3 N-terminal domain interacts with the proline-rich region of Alix.	Proline	71-78	programmed cell death 6 interacting protein	Homo sapiens	94-98
23027949-8	2012	These Gag clusters package a fluorescent oligonucleotide, and recruit early ESCRT complexes ESCRT-I or ALIX with the appropriate dependence on the Gag PTAP and LYP(X)(n)L motifs.	Oligonucleotides	41-56	programmed cell death 6 interacting protein	Homo sapiens	103-107
22981647-0	2012	Natural deletion of L35Y36 in p6 gag eliminate LYPXnL/ALIX auxiliary virus release pathway in HIV-1 subtype C. Natural loss of L35Y36 residues in ALIX binding site of HIV-1 subtype C was found to prevent the p6 gag-ALIX interaction.	Glycosaminoglycans	33-36	programmed cell death 6 interacting protein	Homo sapiens	54-58
22981647-0	2012	Natural deletion of L35Y36 in p6 gag eliminate LYPXnL/ALIX auxiliary virus release pathway in HIV-1 subtype C. Natural loss of L35Y36 residues in ALIX binding site of HIV-1 subtype C was found to prevent the p6 gag-ALIX interaction.	Glycosaminoglycans	33-36	programmed cell death 6 interacting protein	Homo sapiens	146-150
22981647-0	2012	Natural deletion of L35Y36 in p6 gag eliminate LYPXnL/ALIX auxiliary virus release pathway in HIV-1 subtype C. Natural loss of L35Y36 residues in ALIX binding site of HIV-1 subtype C was found to prevent the p6 gag-ALIX interaction.	Glycosaminoglycans	33-36	programmed cell death 6 interacting protein	Homo sapiens	146-150
23664863-0	2013	Viral infection controlled by a calcium-dependent lipid-binding module in ALIX.	Calcium	32-39	programmed cell death 6 interacting protein	Homo sapiens	74-78
23664863-7	2013	We conclude that LBPA recruits ALIX onto late endosomes via the calcium-bound Bro1 domain, triggering a conformational change in ALIX to mediate the delivery of viral nucleocapsids to the cytosol during infection.	Calcium	64-71	programmed cell death 6 interacting protein	Homo sapiens	31-35
19133258-5	2009	This process depends on the late endosomal lipid lysobisphosphatidic acid and its putative effector Alix/AIP1, and is presumably coupled to the invagination of the endosomal limiting membrane at the molecular level via ESCRT proteins.	bis(monoacylglyceryl)phosphate	49-73	programmed cell death 6 interacting protein	Homo sapiens	100-104
21715492-2	2011	Here, we report that the C-terminal proline-rich region (PRR) of ALIX folds back against the upstream domains and auto-inhibits V domain binding to viral late domains.	Proline	36-43	programmed cell death 6 interacting protein	Homo sapiens	65-69
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
20929444-4	2010	Our results demonstrate that an intramolecular interaction between Patch 2 in the Bro1 domain and the TSG101 (tumour susceptibility gene 101 protein)-docking site in the proline-rich domain locks ALIX into a closed conformation that renders ALIX unable to interact with CHMP4 and retroviral Gag proteins.	Proline	170-177	programmed cell death 6 interacting protein	Homo sapiens	196-200
20929444-4	2010	Our results demonstrate that an intramolecular interaction between Patch 2 in the Bro1 domain and the TSG101 (tumour susceptibility gene 101 protein)-docking site in the proline-rich domain locks ALIX into a closed conformation that renders ALIX unable to interact with CHMP4 and retroviral Gag proteins.	Proline	170-177	programmed cell death 6 interacting protein	Homo sapiens	241-245
20929444-4	2010	Our results demonstrate that an intramolecular interaction between Patch 2 in the Bro1 domain and the TSG101 (tumour susceptibility gene 101 protein)-docking site in the proline-rich domain locks ALIX into a closed conformation that renders ALIX unable to interact with CHMP4 and retroviral Gag proteins.	Glycosaminoglycans	291-294	programmed cell death 6 interacting protein	Homo sapiens	196-200
20929444-4	2010	Our results demonstrate that an intramolecular interaction between Patch 2 in the Bro1 domain and the TSG101 (tumour susceptibility gene 101 protein)-docking site in the proline-rich domain locks ALIX into a closed conformation that renders ALIX unable to interact with CHMP4 and retroviral Gag proteins.	Glycosaminoglycans	291-294	programmed cell death 6 interacting protein	Homo sapiens	241-245
20670214-6	2010	Through biophysical experiments, we then identified the PRR (proline-rich region) motif of Alix that binds Hck-SH3 and determined a dissociation constant of 34.5 muM.	Proline	61-68	programmed cell death 6 interacting protein	Homo sapiens	91-95
20691033-8	2010	Surprisingly, however, substitution of F122 with Ala or Gly, but not with Trp, increased the Alix-binding capacity in binding assays.	Alanine	49-52	programmed cell death 6 interacting protein	Homo sapiens	93-97
20691033-8	2010	Surprisingly, however, substitution of F122 with Ala or Gly, but not with Trp, increased the Alix-binding capacity in binding assays.	Glycine	56-59	programmed cell death 6 interacting protein	Homo sapiens	93-97
20471954-0	2010	Alix is involved in caspase 9 activation during calcium-induced apoptosis.	Calcium	48-55	programmed cell death 6 interacting protein	Homo sapiens	0-4
20471954-3	2010	We show here that Alix is also a critical component of caspase 9 activation and apoptosis triggered by calcium.	Calcium	103-110	programmed cell death 6 interacting protein	Homo sapiens	18-22
20471954-4	2010	Indeed, expression of Alix dominant-negative mutants or downregulation of Alix afford significant protection against cytosolic calcium elevation following thapsigargin (Tg) treatment.	Calcium	127-134	programmed cell death 6 interacting protein	Homo sapiens	22-26
20471954-4	2010	Indeed, expression of Alix dominant-negative mutants or downregulation of Alix afford significant protection against cytosolic calcium elevation following thapsigargin (Tg) treatment.	Calcium	127-134	programmed cell death 6 interacting protein	Homo sapiens	74-78
20471954-4	2010	Indeed, expression of Alix dominant-negative mutants or downregulation of Alix afford significant protection against cytosolic calcium elevation following thapsigargin (Tg) treatment.	Thapsigargin	155-167	programmed cell death 6 interacting protein	Homo sapiens	22-26
20471954-4	2010	Indeed, expression of Alix dominant-negative mutants or downregulation of Alix afford significant protection against cytosolic calcium elevation following thapsigargin (Tg) treatment.	Thapsigargin	155-167	programmed cell death 6 interacting protein	Homo sapiens	74-78
20471954-4	2010	Indeed, expression of Alix dominant-negative mutants or downregulation of Alix afford significant protection against cytosolic calcium elevation following thapsigargin (Tg) treatment.	Thapsigargin	169-171	programmed cell death 6 interacting protein	Homo sapiens	22-26
20471954-4	2010	Indeed, expression of Alix dominant-negative mutants or downregulation of Alix afford significant protection against cytosolic calcium elevation following thapsigargin (Tg) treatment.	Thapsigargin	169-171	programmed cell death 6 interacting protein	Homo sapiens	74-78
20036734-4	2010	The levels of AIP-1/Alix protein, a known inhibitor protein of paraptosis, were progressively downregulated in curcumin-treated malignant breast cancer cells, and AIP-1/Alix overexpression attenuated curcumin-induced death in these cells.	Curcumin	111-119	programmed cell death 6 interacting protein	Homo sapiens	14-19
20036734-4	2010	The levels of AIP-1/Alix protein, a known inhibitor protein of paraptosis, were progressively downregulated in curcumin-treated malignant breast cancer cells, and AIP-1/Alix overexpression attenuated curcumin-induced death in these cells.	Curcumin	111-119	programmed cell death 6 interacting protein	Homo sapiens	20-24
20036734-4	2010	The levels of AIP-1/Alix protein, a known inhibitor protein of paraptosis, were progressively downregulated in curcumin-treated malignant breast cancer cells, and AIP-1/Alix overexpression attenuated curcumin-induced death in these cells.	Curcumin	111-119	programmed cell death 6 interacting protein	Homo sapiens	169-173
20036734-4	2010	The levels of AIP-1/Alix protein, a known inhibitor protein of paraptosis, were progressively downregulated in curcumin-treated malignant breast cancer cells, and AIP-1/Alix overexpression attenuated curcumin-induced death in these cells.	Curcumin	200-208	programmed cell death 6 interacting protein	Homo sapiens	14-19
20036734-4	2010	The levels of AIP-1/Alix protein, a known inhibitor protein of paraptosis, were progressively downregulated in curcumin-treated malignant breast cancer cells, and AIP-1/Alix overexpression attenuated curcumin-induced death in these cells.	Curcumin	200-208	programmed cell death 6 interacting protein	Homo sapiens	20-24
20036734-4	2010	The levels of AIP-1/Alix protein, a known inhibitor protein of paraptosis, were progressively downregulated in curcumin-treated malignant breast cancer cells, and AIP-1/Alix overexpression attenuated curcumin-induced death in these cells.	Curcumin	200-208	programmed cell death 6 interacting protein	Homo sapiens	163-168
20036734-4	2010	The levels of AIP-1/Alix protein, a known inhibitor protein of paraptosis, were progressively downregulated in curcumin-treated malignant breast cancer cells, and AIP-1/Alix overexpression attenuated curcumin-induced death in these cells.	Curcumin	200-208	programmed cell death 6 interacting protein	Homo sapiens	169-173
19523902-3	2009	Structural modeling based on small angle X-ray scattering (SAXS) data reveals an elongated crescent-shaped conformation for dimeric ALIX lacking the proline-rich domain (ALIX(BRO1-V)).	Proline	149-156	programmed cell death 6 interacting protein	Homo sapiens	132-136
22641034-4	2012	We demonstrate that Hck SH3 recognizes an extended linear proline-rich region of Alix.	Proline	58-65	programmed cell death 6 interacting protein	Homo sapiens	81-85
21889351-6	2011	In particular, phenylalanine residue in position 105 (Phe105) of Alix belongs to a long loop that is unique to its Bro1 domain.	Phenylalanine	15-28	programmed cell death 6 interacting protein	Homo sapiens	65-69
19133258-5	2009	This process depends on the late endosomal lipid lysobisphosphatidic acid and its putative effector Alix/AIP1, and is presumably coupled to the invagination of the endosomal limiting membrane at the molecular level via ESCRT proteins.	bis(monoacylglyceryl)phosphate	49-73	programmed cell death 6 interacting protein	Homo sapiens	105-109
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].	Proline	24-27	programmed cell death 6 interacting protein	Homo sapiens	248-252
19393081-4	2009	RESULTS: In this study we identified ALIX as a POSH ubiquitination substrate in human cells: POSH induces the ubiquitination of ALIX that is modified on several lysine residues in vivo and in vitro.	Lysine	161-167	programmed cell death 6 interacting protein	Homo sapiens	37-41
19393081-4	2009	RESULTS: In this study we identified ALIX as a POSH ubiquitination substrate in human cells: POSH induces the ubiquitination of ALIX that is modified on several lysine residues in vivo and in vitro.	Lysine	161-167	programmed cell death 6 interacting protein	Homo sapiens	128-132
19143629-4	2009	Binding of Ca(2+) to EF3 (third EF-hand) enables the side chain of Arg(125), present in the loop connecting EF3 and EF4 (fourth EF-hand), to move sufficiently to make a primary hydrophobic pocket accessible to the critical PPYP (Pro-Pro-Tyr-Pro) motif in Alix, which partially overlaps with the GPP (Gly-Pro-Pro) motif for binding to Cep55 (centrosome protein of 55 kDa).	Arginine	67-70	programmed cell death 6 interacting protein	Homo sapiens	255-259
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].	Threonine	28-31	programmed cell death 6 interacting protein	Homo sapiens	248-252
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].	Alanine	32-35	programmed cell death 6 interacting protein	Homo sapiens	248-252
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].	Proline	36-39	programmed cell death 6 interacting protein	Homo sapiens	248-252
19143631-1	2009	Alix [ALG-2 (apoptosis-linked gene 2)-interacting protein X] is a ubiquitinous adaptor protein first described for its capacity to bind to the calcium-binding protein, ALG-2.	Calcium	143-150	programmed cell death 6 interacting protein	Homo sapiens	0-4
19143631-1	2009	Alix [ALG-2 (apoptosis-linked gene 2)-interacting protein X] is a ubiquitinous adaptor protein first described for its capacity to bind to the calcium-binding protein, ALG-2.	Calcium	143-150	programmed cell death 6 interacting protein	Homo sapiens	13-59
19143631-4	2009	We have demonstrated recently that Alix and ALG-2 form in the presence of calcium, a complex with apical caspases and with the endocytosed death receptor TNFR1 (tumour necrosis factor alpha receptor 1), thus suggesting a molecular coupling between endosomes and the cell death machinery.	Calcium	74-81	programmed cell death 6 interacting protein	Homo sapiens	35-39
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
18644787-2	2008	Here we report that lysobisphosphatidic acid (LBPA), an unconventional phospholipid that is only detected in late endosomes, regulates endosomal cholesterol levels under the control of Alix/AlP1, which is an LBPA-interacting protein involved in sorting into multivesicular endosomes.	bis(monoacylglyceryl)phosphate	20-44	programmed cell death 6 interacting protein	Homo sapiens	185-189
18948538-4	2008	We solved the crystal structure of EABR bound to an ALIX peptide at a resolution of 2.0 angstroms.	eabr	35-39	programmed cell death 6 interacting protein	Homo sapiens	52-56
18940611-4	2008	Based on these results, together with the results of in vitro binding assay with mutant ALG-2 and Alix proteins, we propose a Ca(2+)/EF3-driven arginine switch mechanism for ALG-2 binding to Alix.	Arginine	144-152	programmed cell death 6 interacting protein	Homo sapiens	191-195
18940611-0	2008	Structural basis for Ca2+ -dependent formation of ALG-2/Alix peptide complex: Ca2+/EF3-driven arginine switch mechanism.	Arginine	94-102	programmed cell death 6 interacting protein	Homo sapiens	56-60
18940611-4	2008	Based on these results, together with the results of in vitro binding assay with mutant ALG-2 and Alix proteins, we propose a Ca(2+)/EF3-driven arginine switch mechanism for ALG-2 binding to Alix.	Arginine	144-152	programmed cell death 6 interacting protein	Homo sapiens	98-102
18644787-2	2008	Here we report that lysobisphosphatidic acid (LBPA), an unconventional phospholipid that is only detected in late endosomes, regulates endosomal cholesterol levels under the control of Alix/AlP1, which is an LBPA-interacting protein involved in sorting into multivesicular endosomes.	bis(monoacylglyceryl)phosphate	46-50	programmed cell death 6 interacting protein	Homo sapiens	185-189
18644787-2	2008	Here we report that lysobisphosphatidic acid (LBPA), an unconventional phospholipid that is only detected in late endosomes, regulates endosomal cholesterol levels under the control of Alix/AlP1, which is an LBPA-interacting protein involved in sorting into multivesicular endosomes.	Cholesterol	145-156	programmed cell death 6 interacting protein	Homo sapiens	185-189
18644787-5	2008	Both lumenal membranes and cholesterol can be restored in Alix knockdown cells by exogenously added LBPA.	Cholesterol	27-38	programmed cell death 6 interacting protein	Homo sapiens	58-62
18644787-5	2008	Both lumenal membranes and cholesterol can be restored in Alix knockdown cells by exogenously added LBPA.	bis(monoacylglyceryl)phosphate	100-104	programmed cell death 6 interacting protein	Homo sapiens	58-62
17428861-7	2007	The ability of ALIX to rescue a PTAP mutant also depends on its C-terminal proline-rich domain (PRD), but not on the binding sites for Tsg101, endophilin, CIN85, or for the newly identified binding partner, CMS, within the PRD.	Proline	75-82	programmed cell death 6 interacting protein	Homo sapiens	15-19
17997305-1	2007	BACKGROUND: Alix/Bro1p family proteins have recently been identified as important components of multivesicular endosomes (MVEs) and are involved in the sorting of endocytosed integral membrane proteins, interacting with components of the ESCRT complex, the unconventional phospholipid LBPA, and other known endocytosis regulators.	Phospholipids	272-284	programmed cell death 6 interacting protein	Homo sapiens	12-16
17997305-1	2007	BACKGROUND: Alix/Bro1p family proteins have recently been identified as important components of multivesicular endosomes (MVEs) and are involved in the sorting of endocytosed integral membrane proteins, interacting with components of the ESCRT complex, the unconventional phospholipid LBPA, and other known endocytosis regulators.	4-boronophenylalanine	285-289	programmed cell death 6 interacting protein	Homo sapiens	12-16
18476810-3	2008	Our results show that the docking site is not available in cytosolic or recombinant Alix under native conditions and becomes available upon addition of the detergent Nonidet P40 or SDS.	Sodium Dodecyl Sulfate	181-184	programmed cell death 6 interacting protein	Homo sapiens	84-88
18477395-3	2008	Intriguingly, the deletion of the C-terminal proline-rich region of ALIX prevented detectable binding to p6.	Proline	45-52	programmed cell death 6 interacting protein	Homo sapiens	68-72
18477395-4	2008	In contrast, a four-amino acid deletion in the central hinge region of p6 increased its association with ALIX as shown by its ability to bind to ALIX lacking the proline rich domain.	Proline	162-169	programmed cell death 6 interacting protein	Homo sapiens	105-109
18477395-7	2008	Altogether, our data support a model where the C-terminal proline-rich domain of ALIX allows the access of its binding site to p6 by alleviating a conformational constraint resulting from the presence of the central p6 hinge.	Proline	58-65	programmed cell death 6 interacting protein	Homo sapiens	81-85
16978157-1	2007	The mammalian adaptor protein Alix [ALG-2 (apoptosis-linked-gene-2 product)-interacting protein X] belongs to a conserved family of proteins that have in common an N-terminal Bro1 domain and a C-terminal PRD (proline-rich domain), both of which mediate partner protein interactions.	Proline	209-216	programmed cell death 6 interacting protein	Homo sapiens	30-34
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
17174262-0	2007	HD-PTP and Alix share some membrane-traffic related proteins that interact with their Bro1 domains or proline-rich regions.	Proline	102-109	programmed cell death 6 interacting protein	Homo sapiens	11-15
17174262-2	2007	HD-PTP is a paralog of Alix and a putative protein tyrosine phosphatase (PTP) that contains a Bro1 domain, coiled-coils, a proline-rich region (PRR) in addition to a PTP domain.	Proline	123-130	programmed cell death 6 interacting protein	Homo sapiens	23-27
16966331-4	2006	In cell-free systems, Alix directly interacts with F-actin at both the N-terminal Bro1 domain and the C-terminal proline-rich domain.	Proline	113-120	programmed cell death 6 interacting protein	Homo sapiens	22-26
15557335-4	2005	A proline-rich region in the C terminus of Alix bound the Src SH3 domain, but this interaction was dependent on the release of the Src SH2 domain from its Src internal ligand either by interaction with Alix Tyr319 or by mutation of Src Tyr527.	Proline	2-9	programmed cell death 6 interacting protein	Homo sapiens	43-47
16868030-5	2006	The diversity of Alix functions is due to its proline-rich C-terminus, which provides multiple protein-binding sites.	Proline	46-53	programmed cell death 6 interacting protein	Homo sapiens	17-21
15914539-5	2005	Quantitative immunoelectron microscopy showed that multivesicular endosomes of Alix-depleted cells contained normal amounts of CD63, whereas their levels of lysobisphosphatidic acid were reduced.	bis(monoacylglyceryl)phosphate	157-181	programmed cell death 6 interacting protein	Homo sapiens	79-83
16354163-1	2006	Alix/AIP1 (ALG-2-interacting protein X/apoptosis-linked-gene-2-interacting protein 1) is an adaptor protein that was first described for its capacity to bind to the calcium-binding protein ALG-2 (apoptosis-linked gene 2), the expression of which seemed necessary for cell death.	Calcium	165-172	programmed cell death 6 interacting protein	Homo sapiens	0-4
16354163-1	2006	Alix/AIP1 (ALG-2-interacting protein X/apoptosis-linked-gene-2-interacting protein 1) is an adaptor protein that was first described for its capacity to bind to the calcium-binding protein ALG-2 (apoptosis-linked gene 2), the expression of which seemed necessary for cell death.	Calcium	165-172	programmed cell death 6 interacting protein	Homo sapiens	5-9
16354163-5	2006	Mammalian Alix may have a similar function and has been shown to bind to lyso(bis)phosphatidic acid, ESCRT (endosomal sorting complex required for transport) proteins, endophilins and CIN85 (Cbl-interacting protein of 85 kDa), which are all main regulators of the endosomal system.	bis(monoacylglyceryl)phosphate	73-99	programmed cell death 6 interacting protein	Homo sapiens	10-14
15757670-0	2005	Dictyostelium discoideum requires an Alix/AIP1 homolog, DdAlix, for morphogenesis in alkaline environments.	ddalix	56-62	programmed cell death 6 interacting protein	Homo sapiens	37-41
15757670-2	2005	In this study, we found that development of Dictyostelium discoideum Alix (DdAlix) deletion mutant (alx-) cells was impaired in alkaline pH environments.	ddalix	75-81	programmed cell death 6 interacting protein	Homo sapiens	69-73
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
12860994-1	2003	Alix (ALG-2-interacting protein X) is a 95-kDa protein that interacts with an EF-hand type Ca(2+)-binding protein, ALG-2 (apoptosis-linked gene 2), through its C-terminal proline-rich region.	Proline	171-178	programmed cell death 6 interacting protein	Homo sapiens	0-4
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
15170857-0	2004	ALIX-ing phospholipids with endosome biogenesis.	Phospholipids	9-22	programmed cell death 6 interacting protein	Homo sapiens	0-4
14999017-3	2004	The region corresponding to amino acid residues 794 to 827 in the carboxy-terminal proline-rich region of Alix was sufficient to confer the ability to interact directly with ALG-2.	Proline	83-90	programmed cell death 6 interacting protein	Homo sapiens	106-110
14751282-0	2004	Early increase of apoptosis-linked gene-2 interacting protein X in areas of kainate-induced neurodegeneration.	Kainic Acid	76-83	programmed cell death 6 interacting protein	Homo sapiens	18-63
12860994-1	2003	Alix (ALG-2-interacting protein X) is a 95-kDa protein that interacts with an EF-hand type Ca(2+)-binding protein, ALG-2 (apoptosis-linked gene 2), through its C-terminal proline-rich region.	Proline	171-178	programmed cell death 6 interacting protein	Homo sapiens	6-33
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.	Proline	115-118	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.	Proline	115-118	programmed cell death 6 interacting protein	Homo sapiens	98-102
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.	Glycine	120-123	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.	Glycine	120-123	programmed cell death 6 interacting protein	Homo sapiens	98-102
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.	Alanine	125-128	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.	Alanine	125-128	programmed cell death 6 interacting protein	Homo sapiens	98-102
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
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.	Glutamine	138-141	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.	Glutamine	138-141	programmed cell death 6 interacting protein	Homo sapiens	98-102
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
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.	Proline	113-116	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.	Proline	113-116	programmed cell death 6 interacting protein	Homo sapiens	32-36
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.	Leucine	122-125	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.	Leucine	122-125	programmed cell death 6 interacting protein	Homo sapiens	32-36