PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
29461425-1	2018	PURPOSE OF REVIEW: Analysis of antiribosomal P protein autoantibodies (anti-P) pathogenicity in diffuse brain manifestations of neuropsychiatric lupus, emphasizing cognitive dysfunction and the recently emerged role of cross-reacting neuronal surface P antigen (NSPA) in alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid and N-Methyl-D-Aspartate receptor glutamatergic transmission.	SCHEMBL4437207	285-327	OCA2 melanosomal transmembrane protein	Homo sapiens	45-54
31315583-14	2019	However, conditional and haplotype-based analyses indicate the presence of other variants with independent effects on melanin levels in OCA2 and APBA2.	Melanins	118-125	OCA2 melanosomal transmembrane protein	Homo sapiens	136-140
30835348-5	2019	The mutation of c.819+3insATATGCC in TYR and the mutation of c.1870G>C in OCA2 are first reported in this study.	Tyrosine	37-40	OCA2 melanosomal transmembrane protein	Homo sapiens	77-81
30576860-7	2019	In the presence of leptomycin B, P protein is retained in the nucleus, indicating that it contains a CRM1-dependent NES.	leptomycin B	19-31	OCA2 melanosomal transmembrane protein	Homo sapiens	33-42
30238347-0	2019	1H, 15N and 13C resonance assignments of the C-terminal domain of the P protein of the Nishigahara strain of rabies virus.	Hydrogen	0-2	OCA2 melanosomal transmembrane protein	Homo sapiens	70-79
30238347-0	2019	1H, 15N and 13C resonance assignments of the C-terminal domain of the P protein of the Nishigahara strain of rabies virus.	15n	4-7	OCA2 melanosomal transmembrane protein	Homo sapiens	70-79
30238347-0	2019	1H, 15N and 13C resonance assignments of the C-terminal domain of the P protein of the Nishigahara strain of rabies virus.	13c	12-15	OCA2 melanosomal transmembrane protein	Homo sapiens	70-79
30238347-2	2019	Here we report the 1H, 13C and 15N chemical shift assignments of this domain from P protein of the Nishigahara strain of rabies virus, a pathogenic laboratory strain well established for studies of virulence functions of rabies virus proteins, including P protein.	Hydrogen	19-21	OCA2 melanosomal transmembrane protein	Homo sapiens	82-91
30238347-2	2019	Here we report the 1H, 13C and 15N chemical shift assignments of this domain from P protein of the Nishigahara strain of rabies virus, a pathogenic laboratory strain well established for studies of virulence functions of rabies virus proteins, including P protein.	13c	23-26	OCA2 melanosomal transmembrane protein	Homo sapiens	82-91
30238347-2	2019	Here we report the 1H, 13C and 15N chemical shift assignments of this domain from P protein of the Nishigahara strain of rabies virus, a pathogenic laboratory strain well established for studies of virulence functions of rabies virus proteins, including P protein.	15n	31-34	OCA2 melanosomal transmembrane protein	Homo sapiens	82-91
30816852-2	2019	Protein Kinase C (PKC)-alpha Activation Inhibits PKC-zeta and Mediates the Action of PED/PEA-15 on Glucose Transport in the L6 Skeletal Muscle Cells.	Glucose	99-106	OCA2 melanosomal transmembrane protein	Homo sapiens	85-88
25809079-5	2015	RESULTS: Two nonsynonymous variants selected within the OCA2 gene, rs1800414 (His615Arg) and rs74653330 (Ala481Thr), were significantly associated with melanin levels in the sample.	Melanins	152-159	OCA2 melanosomal transmembrane protein	Homo sapiens	56-60
25681551-6	2015	(2) The mean electrostatic force exerted on the ligand by the water molecules polarized by E(ext) is thought to result from the dielectric polarization (P(protein)) in the region occupied by the protein, where P(protein) is proportional to -E(ext).	Water	62-67	OCA2 melanosomal transmembrane protein	Homo sapiens	153-163
25681551-6	2015	(2) The mean electrostatic force exerted on the ligand by the water molecules polarized by E(ext) is thought to result from the dielectric polarization (P(protein)) in the region occupied by the protein, where P(protein) is proportional to -E(ext).	Water	62-67	OCA2 melanosomal transmembrane protein	Homo sapiens	210-220
29231794-14	2018	Conclusion The ratio of MCA to ICA transit time decreases following PED treatment and decreases more in patients with DIPH.	diph	118-122	OCA2 melanosomal transmembrane protein	Homo sapiens	68-71
29109245-1	2017	Protein Kinase C (PKC)-alpha Activation Inhibits PKC-zeta and Mediates the Action of PED/PEA-15 on Glucose Transport in the L6 Skeletal Muscle Cells.	Glucose	99-106	OCA2 melanosomal transmembrane protein	Homo sapiens	85-88
27892580-3	2017	Without CSA, the analogous complex RdH(HCl)3 is a luminogen with aggregation-caused quenching (ACQ) properties.	acenaphthenequinone	95-98	OCA2 melanosomal transmembrane protein	Homo sapiens	39-44
25937519-9	2015	Subsequently, the nucleic acid sequence of the viral P-protein was cloned and transfected into the macrophage cell line; the effect of this transfection on staurosporine-induced apoptosis was evaluated by assaying for cell viability and caspases-8 and -9 activity.	Staurosporine	156-169	OCA2 melanosomal transmembrane protein	Homo sapiens	53-62
25236473-2	2014	Among various genes, the OCA2 is being essential for proper melanin synthesis, and mutation or deletion of this gene leads to oculocutaneous albinism type 2.	Melanins	60-67	OCA2 melanosomal transmembrane protein	Homo sapiens	25-29
25513726-5	2014	Here we used direct patch-clamp of skin and eye melanosomes to identify a novel chloride-selective anion conductance mediated by OCA2 and required for melanin production.	Melanins	151-158	OCA2 melanosomal transmembrane protein	Homo sapiens	129-133
25513726-6	2014	Expression of OCA2 increases organelle pH, suggesting that the chloride channel might regulate melanin synthesis by modulating melanosome pH.	Melanins	95-102	OCA2 melanosomal transmembrane protein	Homo sapiens	14-18
24665080-1	2014	The most stable complexes between squaric acid and its sulfur- and selenium-containing analogues (C4X4H2 ; X = O, S, Se) with BeY2 (Y = H, F) were studied by means of the Gaussian 04 (G4) composite ab initio theory.	squaric acid	34-46	OCA2 melanosomal transmembrane protein	Homo sapiens	126-130
24665080-1	2014	The most stable complexes between squaric acid and its sulfur- and selenium-containing analogues (C4X4H2 ; X = O, S, Se) with BeY2 (Y = H, F) were studied by means of the Gaussian 04 (G4) composite ab initio theory.	c4x4h2	98-104	OCA2 melanosomal transmembrane protein	Homo sapiens	126-130
24665080-3	2014	The relative stability of the C4X4H2 BeY2 (X = O, S, Se; Y = H, F) complexes changes with the nature of the chalcogen atom; but more importantly, the formation of the C4X4H2 BeF2 complexes results in a substantial acidity enhancement of the squaric moiety owing to the dramatic electron-density redistribution undergone by the system when the beryllium bond is formed.	Beryllium	343-352	OCA2 melanosomal transmembrane protein	Homo sapiens	37-41
23824587-1	2014	Oculocutaneous albinism type 2 (OCA2), caused by mutations of OCA2 gene, is an autosomal recessive disorder characterized by reduced biosynthesis of melanin pigment in the skin, hair, and eyes.	Melanins	149-156	OCA2 melanosomal transmembrane protein	Homo sapiens	0-30
24501400-0	2014	Roles of serine and threonine residues of mumps virus P protein in viral transcription and replication.	Serine	9-15	OCA2 melanosomal transmembrane protein	Homo sapiens	54-63
24501400-0	2014	Roles of serine and threonine residues of mumps virus P protein in viral transcription and replication.	Threonine	20-29	OCA2 melanosomal transmembrane protein	Homo sapiens	54-63
24387780-2	2014	The OCA2 protein plays a central role in melanosome biogenesis, and it is a strong determinant of the eumelanin content in melanocytes.	eumelanin	102-111	OCA2 melanosomal transmembrane protein	Homo sapiens	4-8
23824587-1	2014	Oculocutaneous albinism type 2 (OCA2), caused by mutations of OCA2 gene, is an autosomal recessive disorder characterized by reduced biosynthesis of melanin pigment in the skin, hair, and eyes.	Melanins	149-156	OCA2 melanosomal transmembrane protein	Homo sapiens	32-36
23824587-1	2014	Oculocutaneous albinism type 2 (OCA2), caused by mutations of OCA2 gene, is an autosomal recessive disorder characterized by reduced biosynthesis of melanin pigment in the skin, hair, and eyes.	Melanins	149-156	OCA2 melanosomal transmembrane protein	Homo sapiens	62-66
23165166-5	2013	RESULTS: OCA2 A481T (p=6.18x10(-8)) and, OCA2 H615R (p=5.72x10(-6)) were strongly associated with the melanin index.	Melanins	102-109	OCA2 melanosomal transmembrane protein	Homo sapiens	9-13
23962237-4	2013	We therefore investigated adaptive mechanisms in Oculocutaneous albinism type 2 (Oca2)-null melanocytes where UPR signaling is arrested despite continued tyrosinase accumulation leading to resistance to the chemical ER stressor thapsigargin.	Thapsigargin	228-240	OCA2 melanosomal transmembrane protein	Homo sapiens	81-85
23962237-7	2013	Gadd34-complex inhibition blocked eIF2alpha dephosphorylation and significantly increased Oca2-null melanocyte sensitivity to thapsigargin.	Thapsigargin	126-138	OCA2 melanosomal transmembrane protein	Homo sapiens	90-94
23165166-5	2013	RESULTS: OCA2 A481T (p=6.18x10(-8)) and, OCA2 H615R (p=5.72x10(-6)) were strongly associated with the melanin index.	Melanins	102-109	OCA2 melanosomal transmembrane protein	Homo sapiens	41-45
23165166-7	2013	Then five surviving variants including A481T, H615R, T387M in OCA2, D125Y in TYR, and T500P in SLC45A2, accounted for contribution to about 11% of the melanin index.	Melanins	151-158	OCA2 melanosomal transmembrane protein	Homo sapiens	62-66
23003570-3	2012	A melanin synthesizing P-MDCK cell line was developed by lentiviral transduction of human tyrosinase and p-protein genes in MDCK (NBL-2) cells.	Melanins	2-9	OCA2 melanosomal transmembrane protein	Homo sapiens	105-114
22633639-2	2012	The majority of cases are caused by mutations in P-protein, one of the four components of the glycine cleavage enzyme, glycine decarboxylase.	Glycine	94-101	OCA2 melanosomal transmembrane protein	Homo sapiens	49-58
22261077-1	2012	Non ketotic hyperglycinemia is a rare inborn error of glycine metabolism due to deficient activity of glycine cleavage system, a multienzymatic complex consisting of four protein subunits: the P-protein, the H-protein, the T-protein and the L-protein.	Glycine	17-24	OCA2 melanosomal transmembrane protein	Homo sapiens	193-202
22787212-3	2012	P protein is an unusual reverse transcriptase that initiates reverse transcription by protein priming, by which a Tyr residue in the unique terminal protein domain acts as an acceptor of the first DNA nucleotide.	Tyrosine	114-117	OCA2 melanosomal transmembrane protein	Homo sapiens	0-9
22718909-0	2012	Differential recognition of a dileucine-based sorting signal by AP-1 and AP-3 reveals a requirement for both BLOC-1 and AP-3 in delivery of OCA2 to melanosomes.	dileucine	30-39	OCA2 melanosomal transmembrane protein	Homo sapiens	140-144
22718909-4	2012	Here we exploit targeted mutagenesis of the acidic dileucine-based sorting signal in the pigment cell-specific protein OCA2 to dissect the relative roles of AP-1 and AP-3 in transport to melanosomes.	dileucine	51-60	OCA2 melanosomal transmembrane protein	Homo sapiens	119-123
21895963-2	2012	In addition to apoptosis, PED/PEA-15 is involved in the regulation of other major cellular functions, including cell adhesion, migration, proliferation and glucose metabolism.	Glucose	156-163	OCA2 melanosomal transmembrane protein	Homo sapiens	26-29
21895963-6	2012	The molecular interaction of PED/PEA-15 with 67LR was confirmed by pull-down experiments with recombinant His-tagged 37LRP on lysates of PED/PEA-15 transfected HEK-293 cells.	Histidine	106-109	OCA2 melanosomal transmembrane protein	Homo sapiens	29-32
21895963-6	2012	The molecular interaction of PED/PEA-15 with 67LR was confirmed by pull-down experiments with recombinant His-tagged 37LRP on lysates of PED/PEA-15 transfected HEK-293 cells.	Histidine	106-109	OCA2 melanosomal transmembrane protein	Homo sapiens	137-140
21895963-8	2012	PED/PEA-15 overexpression significantly increased 67LR-mediated HEK-293 cell adhesion and migration to laminin that, in turn, determined PED/PEA-15 phosphorylation both in Ser-104 and Ser-116, thus enabling cell proliferation and resistance to apoptosis.	Serine	172-175	OCA2 melanosomal transmembrane protein	Homo sapiens	0-3
21895963-8	2012	PED/PEA-15 overexpression significantly increased 67LR-mediated HEK-293 cell adhesion and migration to laminin that, in turn, determined PED/PEA-15 phosphorylation both in Ser-104 and Ser-116, thus enabling cell proliferation and resistance to apoptosis.	Serine	172-175	OCA2 melanosomal transmembrane protein	Homo sapiens	137-140
21895963-8	2012	PED/PEA-15 overexpression significantly increased 67LR-mediated HEK-293 cell adhesion and migration to laminin that, in turn, determined PED/PEA-15 phosphorylation both in Ser-104 and Ser-116, thus enabling cell proliferation and resistance to apoptosis.	Serine	184-187	OCA2 melanosomal transmembrane protein	Homo sapiens	0-3
21895963-8	2012	PED/PEA-15 overexpression significantly increased 67LR-mediated HEK-293 cell adhesion and migration to laminin that, in turn, determined PED/PEA-15 phosphorylation both in Ser-104 and Ser-116, thus enabling cell proliferation and resistance to apoptosis.	Serine	184-187	OCA2 melanosomal transmembrane protein	Homo sapiens	137-140
22200320-5	2012	Under the optimized conditions, Pd(II) could be retained on the column at pH 1.0 and quantitatively eluted by 2.5 mL of 0.01 mol L(-1) HCl-3% thiourea solution at a flow rate of 2.0 mL min(-1).	Polydioxanone	32-38	OCA2 melanosomal transmembrane protein	Homo sapiens	135-140
22200320-5	2012	Under the optimized conditions, Pd(II) could be retained on the column at pH 1.0 and quantitatively eluted by 2.5 mL of 0.01 mol L(-1) HCl-3% thiourea solution at a flow rate of 2.0 mL min(-1).	Thiourea	142-150	OCA2 melanosomal transmembrane protein	Homo sapiens	135-140
21185050-3	2011	An expression of the P domain with or without the hinge, or with an additional cysteine at either ends of the P protein resulted in P dimers and/or P particles.	Cysteine	79-87	OCA2 melanosomal transmembrane protein	Homo sapiens	110-119
22112520-5	2011	The aim of the study was to investigate the levels of 25-hydroxy vitamin D (25(OH)D), and L/A, in association with PED/PEA-15 protein abundance, in both lean and overweight/obese (o/o) women with PCOS.	25-hydroxyvitamin D	54-74	OCA2 melanosomal transmembrane protein	Homo sapiens	115-118
21436336-7	2011	Both patients presented with symptomatic acute occlusions of the PED constructs within 14 days of clopidogrel discontinuation.	Clopidogrel	98-109	OCA2 melanosomal transmembrane protein	Homo sapiens	65-68
20956287-6	2010	SHEP1 association is required for the BCR or S1P receptor(s) to induce the conversion of CasL into its serine/threonine hyperphosphorylated form, which is important for lymphocyte adhesion and motility.	Serine	103-109	OCA2 melanosomal transmembrane protein	Homo sapiens	0-5
21199270-0	2011	Phosphoprotein enriched in diabetes gene product (Ped/pea-15) is increased in omental adipose tissue of women with the polycystic ovary syndrome: ex vivo regulation of ped/pea-15 by glucose, insulin and metformin.	Glucose	182-189	OCA2 melanosomal transmembrane protein	Homo sapiens	50-53
21199270-0	2011	Phosphoprotein enriched in diabetes gene product (Ped/pea-15) is increased in omental adipose tissue of women with the polycystic ovary syndrome: ex vivo regulation of ped/pea-15 by glucose, insulin and metformin.	Glucose	182-189	OCA2 melanosomal transmembrane protein	Homo sapiens	168-171
21199270-0	2011	Phosphoprotein enriched in diabetes gene product (Ped/pea-15) is increased in omental adipose tissue of women with the polycystic ovary syndrome: ex vivo regulation of ped/pea-15 by glucose, insulin and metformin.	Metformin	203-212	OCA2 melanosomal transmembrane protein	Homo sapiens	50-53
21199270-2	2011	Phosphoprotein enriched in diabetes gene product (Ped/pea-15) regulates glucose metabolism and is increased in T2DM.	Glucose	72-79	OCA2 melanosomal transmembrane protein	Homo sapiens	50-53
21199270-5	2011	Glucose was predictive of omental AT Ped/pea-15 mRNA expression (p = 0.045).	Glucose	0-7	OCA2 melanosomal transmembrane protein	Homo sapiens	37-40
21199270-6	2011	Importantly, glucose and insulin increased whereas metformin significantly decreased Ped/pea-15 levels in human omental AT explants.	Metformin	51-60	OCA2 melanosomal transmembrane protein	Homo sapiens	85-88
20956287-6	2010	SHEP1 association is required for the BCR or S1P receptor(s) to induce the conversion of CasL into its serine/threonine hyperphosphorylated form, which is important for lymphocyte adhesion and motility.	Threonine	110-119	OCA2 melanosomal transmembrane protein	Homo sapiens	0-5
20426782-10	2010	CONCLUSIONS: Our results suggest that an OCA2 gene defect is the second most prevalent type of OCA in India after TYR.	Tyrosine	114-117	OCA2 melanosomal transmembrane protein	Homo sapiens	41-45
20406097-10	2010	Both ERK2 overexpression and genetic silencing of PED/PEA-15 by antisense oligonucleotides increased ERK nuclear accumulation and reduced CAR expression and adenoviral entry.	Oligonucleotides	74-90	OCA2 melanosomal transmembrane protein	Homo sapiens	50-53
20434461-6	2010	Additionally, a second, lower-affinity Mg(II) activates cleavage catalyzed by RNase P. Structural changes that occur upon binding Ca(II) to the ES complex were determined by time-resolved Forster resonance energy transfer measurements of the distances between donor-acceptor fluorophores introduced at specific locations on the P protein and pre-tRNA 5" leader.	mg(ii)	39-45	OCA2 melanosomal transmembrane protein	Homo sapiens	328-337
20434461-6	2010	Additionally, a second, lower-affinity Mg(II) activates cleavage catalyzed by RNase P. Structural changes that occur upon binding Ca(II) to the ES complex were determined by time-resolved Forster resonance energy transfer measurements of the distances between donor-acceptor fluorophores introduced at specific locations on the P protein and pre-tRNA 5" leader.	ca(ii)	130-136	OCA2 melanosomal transmembrane protein	Homo sapiens	328-337
20434461-7	2010	These data demonstrate that the 5" leader of pre-tRNA moves 4 to 6 A closer to the PRNA x P protein interface during the ES-to-ES* transition and suggest that the metal-dependent conformational change reorganizes the bound substrate in the active site to form a catalytically competent ES* complex.	Einsteinium	127-129	OCA2 melanosomal transmembrane protein	Homo sapiens	90-99
20434461-7	2010	These data demonstrate that the 5" leader of pre-tRNA moves 4 to 6 A closer to the PRNA x P protein interface during the ES-to-ES* transition and suggest that the metal-dependent conformational change reorganizes the bound substrate in the active site to form a catalytically competent ES* complex.	Metals	163-168	OCA2 melanosomal transmembrane protein	Homo sapiens	90-99
20434461-7	2010	These data demonstrate that the 5" leader of pre-tRNA moves 4 to 6 A closer to the PRNA x P protein interface during the ES-to-ES* transition and suggest that the metal-dependent conformational change reorganizes the bound substrate in the active site to form a catalytically competent ES* complex.	Einsteinium	127-129	OCA2 melanosomal transmembrane protein	Homo sapiens	90-99
20434461-6	2010	Additionally, a second, lower-affinity Mg(II) activates cleavage catalyzed by RNase P. Structural changes that occur upon binding Ca(II) to the ES complex were determined by time-resolved Forster resonance energy transfer measurements of the distances between donor-acceptor fluorophores introduced at specific locations on the P protein and pre-tRNA 5" leader.	Einsteinium	144-146	OCA2 melanosomal transmembrane protein	Homo sapiens	328-337
20434461-7	2010	These data demonstrate that the 5" leader of pre-tRNA moves 4 to 6 A closer to the PRNA x P protein interface during the ES-to-ES* transition and suggest that the metal-dependent conformational change reorganizes the bound substrate in the active site to form a catalytically competent ES* complex.	Einsteinium	121-123	OCA2 melanosomal transmembrane protein	Homo sapiens	90-99
20671408-0	2010	Preliminary data on effects of metformin on PED/PEA-15 cellular levels in obese women with polycystic ovary syndrome.	Metformin	31-40	OCA2 melanosomal transmembrane protein	Homo sapiens	44-47
20396999-9	2010	Moreover, HNF-4alpha silencing and PED overexpression were accompanied by a significant reduction of hepatic glycogen content.	Glycogen	109-117	OCA2 melanosomal transmembrane protein	Homo sapiens	35-38
20671408-2	2010	AIM: To investigate whether metformin (MET) has additive effects on PED/PEA-15 protein levels.	Metformin	28-37	OCA2 melanosomal transmembrane protein	Homo sapiens	68-71
20221248-0	2010	Association of the OCA2 polymorphism His615Arg with melanin content in east Asian populations: further evidence of convergent evolution of skin pigmentation.	Melanins	52-59	OCA2 melanosomal transmembrane protein	Homo sapiens	19-23
18815298-7	2008	We further demonstrated that P protein blocks the trafficking of GABAR, a principal GABA-gated ion channel that plays important roles in neural transmission, to the surface of cells infected with BDV or transfected with the P gene.	gamma-Aminobutyric Acid	65-69	OCA2 melanosomal transmembrane protein	Homo sapiens	29-38
20072825-3	2010	Among these, six Ser sites and one Thr site were identified in the highly conserved C-terminal region of eight P-proteins of various P-protein subfamilies, including two P0, two P1, three P2 and one P3 protein.	Serine	17-20	OCA2 melanosomal transmembrane protein	Homo sapiens	111-120
20072825-3	2010	Among these, six Ser sites and one Thr site were identified in the highly conserved C-terminal region of eight P-proteins of various P-protein subfamilies, including two P0, two P1, three P2 and one P3 protein.	Threonine	35-38	OCA2 melanosomal transmembrane protein	Homo sapiens	111-120
19116314-0	2009	Localization to mature melanosomes by virtue of cytoplasmic dileucine motifs is required for human OCA2 function.	dileucine	60-69	OCA2 melanosomal transmembrane protein	Homo sapiens	99-103
19116314-5	2009	Mutagenized OCA2 transgenes stimulate melanin synthesis in OCA2-deficient cells when localized to melanosomes but not when specifically retained in the ER, contradicting a proposed primary function for OCA2 in the ER.	Melanins	38-45	OCA2 melanosomal transmembrane protein	Homo sapiens	12-16
19116314-6	2009	Steady-state melanosomal localization requires a conserved consensus acidic dileucine-based sorting motif within the cytoplasmic N-terminal region of OCA2.	dileucine	76-85	OCA2 melanosomal transmembrane protein	Homo sapiens	150-154
19116314-7	2009	A second dileucine signal within this region confers steady-state lysosomal localization in melanocytes, suggesting that OCA2 might traverse multiple sequential or parallel trafficking routes.	dileucine	9-18	OCA2 melanosomal transmembrane protein	Homo sapiens	121-125
19954454-1	2009	The gene for phosphoprotein (P) of CDV encodes three different proteins, P, V, and C. The P protein is involved in viral gene transcription and replication.	Cidofovir	35-38	OCA2 melanosomal transmembrane protein	Homo sapiens	90-99
19531639-4	2009	In particular, PKC phosphorylates PED/PEA-15 at Ser(104) and CAM kinase II or Akt at Ser(116), modifying its stability.	Serine	48-51	OCA2 melanosomal transmembrane protein	Homo sapiens	34-37
19531639-13	2009	Strategies are being devised to target key signaling events in PED/PEA-15 action aimed at improving glucose tolerance and at facilitating cancer cell death.	Glucose	100-107	OCA2 melanosomal transmembrane protein	Homo sapiens	63-66
18815298-8	2008	We proposed that during BDV infection, P protein binds to GABARAP, shifts the distribution of GABARAP from the cytoplasm to the nucleus, and disrupts the trafficking of GABARs to the cell membranes, which may result in the inhibition of GABA-induced currents and in the enhancement of hyperactivity and anxiety.	gabars	169-175	OCA2 melanosomal transmembrane protein	Homo sapiens	39-48
18815298-8	2008	We proposed that during BDV infection, P protein binds to GABARAP, shifts the distribution of GABARAP from the cytoplasm to the nucleus, and disrupts the trafficking of GABARs to the cell membranes, which may result in the inhibition of GABA-induced currents and in the enhancement of hyperactivity and anxiety.	gamma-Aminobutyric Acid	58-62	OCA2 melanosomal transmembrane protein	Homo sapiens	39-48
18720148-3	2008	PE-D complexes containing diltiazem HCL (DTZ) or metoprolol tartrate (MTP) and lambda carrageenan were obtained at two particle size levels (<45 microm and 75-105 microm), maintained at different values of relative humidity (RH) (11, 52, 75, and 93%), and compressed.	Diltiazem	26-35	OCA2 melanosomal transmembrane protein	Homo sapiens	0-4
18720148-3	2008	PE-D complexes containing diltiazem HCL (DTZ) or metoprolol tartrate (MTP) and lambda carrageenan were obtained at two particle size levels (<45 microm and 75-105 microm), maintained at different values of relative humidity (RH) (11, 52, 75, and 93%), and compressed.	Hydrochloric Acid	36-39	OCA2 melanosomal transmembrane protein	Homo sapiens	0-4
18720148-3	2008	PE-D complexes containing diltiazem HCL (DTZ) or metoprolol tartrate (MTP) and lambda carrageenan were obtained at two particle size levels (<45 microm and 75-105 microm), maintained at different values of relative humidity (RH) (11, 52, 75, and 93%), and compressed.	Diltiazem	41-44	OCA2 melanosomal transmembrane protein	Homo sapiens	0-4
18720148-3	2008	PE-D complexes containing diltiazem HCL (DTZ) or metoprolol tartrate (MTP) and lambda carrageenan were obtained at two particle size levels (<45 microm and 75-105 microm), maintained at different values of relative humidity (RH) (11, 52, 75, and 93%), and compressed.	Metoprolol	49-68	OCA2 melanosomal transmembrane protein	Homo sapiens	0-4
17700518-0	2008	The PEA-15/PED protein protects glioblastoma cells from glucose deprivation-induced apoptosis via the ERK/MAP kinase pathway.	Glucose	56-63	OCA2 melanosomal transmembrane protein	Homo sapiens	11-14
18614634-8	2008	Furthermore, we found that a single amino acid residue change at position 157 of the P protein from Ser (the residue in the wild-type P protein) to Phe (the residue in Pcpi-) is sufficient for elevated viral gene expression.	Serine	100-103	OCA2 melanosomal transmembrane protein	Homo sapiens	85-94
18614634-8	2008	Furthermore, we found that a single amino acid residue change at position 157 of the P protein from Ser (the residue in the wild-type P protein) to Phe (the residue in Pcpi-) is sufficient for elevated viral gene expression.	Serine	100-103	OCA2 melanosomal transmembrane protein	Homo sapiens	134-143
18614634-8	2008	Furthermore, we found that a single amino acid residue change at position 157 of the P protein from Ser (the residue in the wild-type P protein) to Phe (the residue in Pcpi-) is sufficient for elevated viral gene expression.	Phenylalanine	148-151	OCA2 melanosomal transmembrane protein	Homo sapiens	85-94
18614634-8	2008	Furthermore, we found that a single amino acid residue change at position 157 of the P protein from Ser (the residue in the wild-type P protein) to Phe (the residue in Pcpi-) is sufficient for elevated viral gene expression.	Phenylalanine	148-151	OCA2 melanosomal transmembrane protein	Homo sapiens	134-143
18636160-10	2008	Here, we provide evidence that treatment with sub-optimal concentrations of decitabine are additive to TRAIL effects in well-differentiated PCa cells whereas the same treatment shows synergistic effects in poorly-differentiated PCa cells through increased caspase-8 expression, down-modulation of Akt activation and through the expression of certain anti-apoptotic molecules including FLIP, PED/PEA-15, survivin and c-IAP-1.	Decitabine	76-86	OCA2 melanosomal transmembrane protein	Homo sapiens	391-394
18434077-10	2008	We assume, that toxic properties of Boc-Asp-CMK can be attributed to the chloromethylketone residuum in its molecule, as its analogue Boc-Asp-FMK with fluoromethylketone residuum was more than 13 times less toxic.	chloromethylketone	73-91	OCA2 melanosomal transmembrane protein	Homo sapiens	36-47
18434077-10	2008	We assume, that toxic properties of Boc-Asp-CMK can be attributed to the chloromethylketone residuum in its molecule, as its analogue Boc-Asp-FMK with fluoromethylketone residuum was more than 13 times less toxic.	butyloxycarbonyl-aspartyl-fluoromethyl ketone	134-145	OCA2 melanosomal transmembrane protein	Homo sapiens	36-47
18434077-10	2008	We assume, that toxic properties of Boc-Asp-CMK can be attributed to the chloromethylketone residuum in its molecule, as its analogue Boc-Asp-FMK with fluoromethylketone residuum was more than 13 times less toxic.	fluoromethylketone	151-169	OCA2 melanosomal transmembrane protein	Homo sapiens	36-47
17699806-6	2007	Twenty-one percent of emergency physicians use MDI+S in the PED (largely concentrated at two "user sites").	mdi+s	47-52	OCA2 melanosomal transmembrane protein	Homo sapiens	60-63
17900649-2	2008	Thus, we mutated Phe 436, a bulky amino acid with aromatic side chain, at the putative dNTP-binding cleft in reverse transcriptase (RT) domain of P protein to smaller amino acids (Gly or Val), and examined RNA polymerase activity.	Phenylalanine	17-20	OCA2 melanosomal transmembrane protein	Homo sapiens	146-155
17900649-2	2008	Thus, we mutated Phe 436, a bulky amino acid with aromatic side chain, at the putative dNTP-binding cleft in reverse transcriptase (RT) domain of P protein to smaller amino acids (Gly or Val), and examined RNA polymerase activity.	Parathion	87-91	OCA2 melanosomal transmembrane protein	Homo sapiens	146-155
17900649-2	2008	Thus, we mutated Phe 436, a bulky amino acid with aromatic side chain, at the putative dNTP-binding cleft in reverse transcriptase (RT) domain of P protein to smaller amino acids (Gly or Val), and examined RNA polymerase activity.	Glycine	180-183	OCA2 melanosomal transmembrane protein	Homo sapiens	146-155
17900649-2	2008	Thus, we mutated Phe 436, a bulky amino acid with aromatic side chain, at the putative dNTP-binding cleft in reverse transcriptase (RT) domain of P protein to smaller amino acids (Gly or Val), and examined RNA polymerase activity.	Valine	187-190	OCA2 melanosomal transmembrane protein	Homo sapiens	146-155
17233754-4	2007	We identified eight genes that are associated with the melanin pathway (SLC45A2, OCA2, TYRP1, DCT, KITLG, EGFR, DRD2 and PPARD) and presented significant differences in genetic variation between Europeans, Africans and Asians.	Melanins	55-62	OCA2 melanosomal transmembrane protein	Homo sapiens	81-85
17619204-9	2007	These results confirm that OCA2 is the major human iris color gene and suggest that using an empirical database-driven system, genotypes from a modest number of SNPs within this gene can be used to accurately predict iris melanin content from DNA.	Melanins	222-229	OCA2 melanosomal transmembrane protein	Homo sapiens	27-31
17543364-6	2007	In addition, P protein inhibits nitric oxide production through regulating iNOS expression.	Nitric Oxide	32-44	OCA2 melanosomal transmembrane protein	Homo sapiens	13-22
17327429-8	2007	Islets from ped/pea-15-null mice exhibited a twofold increased activation of PKC-zeta by glucose; increased abundance of the Sur1, Kir6.2, and Foxa2 mRNAs; and enhanced glucose effect on insulin secretion.	Glucose	169-176	OCA2 melanosomal transmembrane protein	Homo sapiens	12-15
17227770-0	2007	Phorbol esters induce intracellular accumulation of the anti-apoptotic protein PED/PEA-15 by preventing ubiquitinylation and proteasomal degradation.	Phorbol Esters	0-14	OCA2 melanosomal transmembrane protein	Homo sapiens	79-82
17227770-2	2007	Exposure of untransfected C5N keratinocytes and transfected HEK293 cells to phorbol esters (12-O-tetradecanoylphorbol-13-acetate (TPA)) increased PED/PEA-15 cellular content and enhanced its phosphorylation at serine 116 in a time-dependent fashion.	Phorbol Esters	76-90	OCA2 melanosomal transmembrane protein	Homo sapiens	146-149
17227770-2	2007	Exposure of untransfected C5N keratinocytes and transfected HEK293 cells to phorbol esters (12-O-tetradecanoylphorbol-13-acetate (TPA)) increased PED/PEA-15 cellular content and enhanced its phosphorylation at serine 116 in a time-dependent fashion.	Tetradecanoylphorbol Acetate	92-128	OCA2 melanosomal transmembrane protein	Homo sapiens	146-149
17227770-2	2007	Exposure of untransfected C5N keratinocytes and transfected HEK293 cells to phorbol esters (12-O-tetradecanoylphorbol-13-acetate (TPA)) increased PED/PEA-15 cellular content and enhanced its phosphorylation at serine 116 in a time-dependent fashion.	Tetradecanoylphorbol Acetate	130-133	OCA2 melanosomal transmembrane protein	Homo sapiens	146-149
17227770-2	2007	Exposure of untransfected C5N keratinocytes and transfected HEK293 cells to phorbol esters (12-O-tetradecanoylphorbol-13-acetate (TPA)) increased PED/PEA-15 cellular content and enhanced its phosphorylation at serine 116 in a time-dependent fashion.	Serine	210-216	OCA2 melanosomal transmembrane protein	Homo sapiens	146-149
17227770-3	2007	Ser-116 --> Gly (PED(S116G)) but not Ser-104 --> Gly (PED(S104G)) substitution almost completely abolished TPA regulation of PED/PEA-15 expression.	Serine	0-3	OCA2 melanosomal transmembrane protein	Homo sapiens	20-23
17227770-3	2007	Ser-116 --> Gly (PED(S116G)) but not Ser-104 --> Gly (PED(S104G)) substitution almost completely abolished TPA regulation of PED/PEA-15 expression.	Glycine	15-18	OCA2 melanosomal transmembrane protein	Homo sapiens	20-23
17327429-8	2007	Islets from ped/pea-15-null mice exhibited a twofold increased activation of PKC-zeta by glucose; increased abundance of the Sur1, Kir6.2, and Foxa2 mRNAs; and enhanced glucose effect on insulin secretion.	Glucose	89-96	OCA2 melanosomal transmembrane protein	Homo sapiens	12-15
17227770-7	2007	At variance, the proteasome inhibitor lactacystin mimicked TPA action on PED/PEA-15 intracellular accumulation and reverted the effects of PKC-zeta and CaMK inhibition.	lactacystin	38-49	OCA2 melanosomal transmembrane protein	Homo sapiens	73-76
17227770-7	2007	At variance, the proteasome inhibitor lactacystin mimicked TPA action on PED/PEA-15 intracellular accumulation and reverted the effects of PKC-zeta and CaMK inhibition.	Tetradecanoylphorbol Acetate	59-62	OCA2 melanosomal transmembrane protein	Homo sapiens	73-76
17227770-9	2007	PED/PEA-15 ubiquitinylation was reduced by TPA and PKC-zeta overexpression and increased by KN-93 and PKC-zeta block.	Tetradecanoylphorbol Acetate	43-46	OCA2 melanosomal transmembrane protein	Homo sapiens	0-3
17227770-10	2007	Furthermore, in HEK293 cells expressing PED(S116G), TPA failed to prevent ubiquitin-dependent degradation of the protein.	Tetradecanoylphorbol Acetate	52-55	OCA2 melanosomal transmembrane protein	Homo sapiens	40-43
17227770-12	2007	Taken together, our results indicate that TPA increases PED/PEA-15 expression at the post-translational level by inducing phosphorylation at serine 116 and preventing ubiquitinylation and proteosomal degradation.	Tetradecanoylphorbol Acetate	42-45	OCA2 melanosomal transmembrane protein	Homo sapiens	56-59
17227770-12	2007	Taken together, our results indicate that TPA increases PED/PEA-15 expression at the post-translational level by inducing phosphorylation at serine 116 and preventing ubiquitinylation and proteosomal degradation.	Serine	141-147	OCA2 melanosomal transmembrane protein	Homo sapiens	56-59
17192900-7	2007	Treatment of B-CLL cells with specific PED antisense oligonucleotides, a protein synthesis inhibitor or HDAC inhibitors, induced a significant downregulation of PED and sensitized these cells to TRAIL-induced cell death.	Oligonucleotides	53-69	OCA2 melanosomal transmembrane protein	Homo sapiens	39-42
17192900-7	2007	Treatment of B-CLL cells with specific PED antisense oligonucleotides, a protein synthesis inhibitor or HDAC inhibitors, induced a significant downregulation of PED and sensitized these cells to TRAIL-induced cell death.	Oligonucleotides	53-69	OCA2 melanosomal transmembrane protein	Homo sapiens	161-164
16364304-4	2006	Deuterium exchange mass spectrometry was used to define regions that are buried when SHEP1 is in complex with Cas.	Deuterium	0-9	OCA2 melanosomal transmembrane protein	Homo sapiens	85-90
16916463-1	2006	BACKGROUND: Oculocutaneous albinism (OCA) is a genetically inherited autosomal recessive condition and OCA2, tyrosine-positive albinism, is the most prevalent type found throughout Africa.	Tyrosine	109-117	OCA2 melanosomal transmembrane protein	Homo sapiens	103-107
16364304-5	2006	The results reveal four segments in SHEP1 that are highly protected, including a region (residues 619-640) that contains a key residue, tyrosine 635, required for association with Cas.	Tyrosine	136-144	OCA2 melanosomal transmembrane protein	Homo sapiens	36-41
15784905-6	2005	Phosphatase PP1 removes phosphate at residues in the central part of the P-protein molecule, whereas those in the NH2-terminal region are removed by phosphatase PP2A.	Phosphates	24-33	OCA2 melanosomal transmembrane protein	Homo sapiens	73-82
11917030-3	2002	The hepadnaviral P protein is an unusual reverse transcriptase (RT) that initiates DNA synthesis by host-factor-dependent protein priming on a specific RNA stem-loop template, epsilon, yielding a short DNA oligonucleotide covalently attached to the RT.	Oligonucleotides	206-221	OCA2 melanosomal transmembrane protein	Homo sapiens	17-26
15670722-2	2005	The majority of cases are caused by mutations in the P-protein, one of the four components of the glycine cleavage enzyme, also known as glycine decarboxylase (GLDC).	Glycine	98-105	OCA2 melanosomal transmembrane protein	Homo sapiens	53-62
12808093-1	2003	The antiapoptotic protein PED/PEA-15 features an Akt phosphorylation motif upstream from Ser(116).	Serine	89-92	OCA2 melanosomal transmembrane protein	Homo sapiens	26-29
12808093-3	2003	Based on Western blotting with specific phospho-Ser(116) PED/PEA-15 antibodies, Akt phosphorylation of PED/PEA-15 occurred mainly at Ser(116).	Serine	48-51	OCA2 melanosomal transmembrane protein	Homo sapiens	103-106
12808093-3	2003	Based on Western blotting with specific phospho-Ser(116) PED/PEA-15 antibodies, Akt phosphorylation of PED/PEA-15 occurred mainly at Ser(116).	Serine	133-136	OCA2 melanosomal transmembrane protein	Homo sapiens	103-106
12808093-4	2003	In addition, a mutant of PED/PEA-15 featuring the substitution of Ser(116)-->Gly (PED(S116-->G)) showed 10-fold-decreased phosphorylation by Akt.	Serine	66-69	OCA2 melanosomal transmembrane protein	Homo sapiens	25-28
12808093-4	2003	In addition, a mutant of PED/PEA-15 featuring the substitution of Ser(116)-->Gly (PED(S116-->G)) showed 10-fold-decreased phosphorylation by Akt.	Serine	66-69	OCA2 melanosomal transmembrane protein	Homo sapiens	85-88
12808093-4	2003	In addition, a mutant of PED/PEA-15 featuring the substitution of Ser(116)-->Gly (PED(S116-->G)) showed 10-fold-decreased phosphorylation by Akt.	Glycine	80-83	OCA2 melanosomal transmembrane protein	Homo sapiens	25-28
12808093-4	2003	In addition, a mutant of PED/PEA-15 featuring the substitution of Ser(116)-->Gly (PED(S116-->G)) showed 10-fold-decreased phosphorylation by Akt.	Glycine	80-83	OCA2 melanosomal transmembrane protein	Homo sapiens	85-88
12808093-5	2003	In intact 293 cells, Akt also induced phosphorylation of PED/PEA-15 at Ser(116).	Serine	71-74	OCA2 melanosomal transmembrane protein	Homo sapiens	57-60
12466480-9	2002	From these results, it is thought that the 402-13 epitope region is concealed when the P protein is present in a free form or free N-P complex but is exposed when it is associated with the NC.	asparaginyl-proline	131-134	OCA2 melanosomal transmembrane protein	Homo sapiens	87-96
12126939-0	2002	Novel mutations in the P-protein (glycine decarboxylase) gene in patients with glycine encephalopathy (non-ketotic hyperglycinemia).	Glycine	34-41	OCA2 melanosomal transmembrane protein	Homo sapiens	23-32
12126939-1	2002	Eight novel mutations were found in the P-protein (glycine decarboxylase) gene (GLDC) of the glycine cleavage system (EC 2.1.1.10) by screening five exons of the gene in patients with glycine encephalopathy (NKH).	Glycine	51-58	OCA2 melanosomal transmembrane protein	Homo sapiens	40-49
12126939-1	2002	Eight novel mutations were found in the P-protein (glycine decarboxylase) gene (GLDC) of the glycine cleavage system (EC 2.1.1.10) by screening five exons of the gene in patients with glycine encephalopathy (NKH).	Glycine	93-100	OCA2 melanosomal transmembrane protein	Homo sapiens	40-49
11917030-11	2002	Because the function of the discriminatory residue depends on its specific spatial disposition this strongly suggests a similar architecture for the P protein dNTP-binding pocket as in other RTs.	Parathion	159-163	OCA2 melanosomal transmembrane protein	Homo sapiens	149-158
11602344-5	2001	Intramelanosomal pH governed by the P-protein may act as a critical determinant of tyrosinase enzyme activity to control the initial step in melanin synthesis or TYRP complex formation to facilitate melanogenesis and melanosomal maturation.	Melanins	141-148	OCA2 melanosomal transmembrane protein	Homo sapiens	36-45
11790785-2	2002	In these cells, expression of PED to levels comparable with those occurring in normal adult cells inhibits apoptosis induced by growth factor deprivation and by exposure to H(2)O(2) or anisomycin.	Hydrogen Peroxide	173-181	OCA2 melanosomal transmembrane protein	Homo sapiens	30-33
11790785-2	2002	In these cells, expression of PED to levels comparable with those occurring in normal adult cells inhibits apoptosis induced by growth factor deprivation and by exposure to H(2)O(2) or anisomycin.	Anisomycin	185-195	OCA2 melanosomal transmembrane protein	Homo sapiens	30-33
11790785-4	2002	In 293(PED) cells, decreased apoptosis induced by anisomycin and H(2)O(2) was also accompanied by block of JNK1/2 and p38 phosphorylations, respectively.	Anisomycin	50-60	OCA2 melanosomal transmembrane protein	Homo sapiens	7-10
11790785-4	2002	In 293(PED) cells, decreased apoptosis induced by anisomycin and H(2)O(2) was also accompanied by block of JNK1/2 and p38 phosphorylations, respectively.	Hydrogen Peroxide	65-73	OCA2 melanosomal transmembrane protein	Homo sapiens	7-10
11790785-7	2002	Treatment of 293(PED) cells with the MEK inhibitor PD98059 blocked ERK1/2 phosphorylations with no effect on inhibition of JNK1/2 and p38 activities.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	51-58	OCA2 melanosomal transmembrane protein	Homo sapiens	17-20
11790785-8	2002	Complete rescue of JNK and p38 functions in 293(PED) cells by overexpressing JNK1 or p38, respectively, enabled only partial recovery of apoptotic response to growth factor deprivation and anisomycin.	Anisomycin	189-199	OCA2 melanosomal transmembrane protein	Homo sapiens	48-51
12222932-5	2002	42: 761-771) the rabies virus P protein as being composed of several components of different sizes, among which the full-sized major components were termed as p40 and p37 according to their electrophoretic mobilities, and radiolabeling studies with [32P]phosphate implied that p40 was a hyperphosphorylated form.	Phosphorus-32	250-253	OCA2 melanosomal transmembrane protein	Homo sapiens	30-39
12222932-5	2002	42: 761-771) the rabies virus P protein as being composed of several components of different sizes, among which the full-sized major components were termed as p40 and p37 according to their electrophoretic mobilities, and radiolabeling studies with [32P]phosphate implied that p40 was a hyperphosphorylated form.	Phosphates	254-263	OCA2 melanosomal transmembrane protein	Homo sapiens	30-39
10608840-3	1999	A short DNA oligonucleotide is copied from epsilon and covalently attached to P protein, and then synthesis is arrested.	Oligonucleotides	12-27	OCA2 melanosomal transmembrane protein	Homo sapiens	78-87
10998131-10	2000	As mammalian tyrosinase activity in situ is apparently dependent on low pH, we postulate that in the absence of a low pH environment brought about by ionic transport mediated by the p protein, tyrosinase activity is severely impaired, leading to the minimal production of melanin that is characteristic of p mutants.	Melanins	272-279	OCA2 melanosomal transmembrane protein	Homo sapiens	182-191
11375323-0	2001	Protein kinase C (PKC)-alpha activation inhibits PKC-zeta and mediates the action of PED/PEA-15 on glucose transport in the L6 skeletal muscle cells.	Glucose	99-106	OCA2 melanosomal transmembrane protein	Homo sapiens	85-88
11375323-1	2001	Overexpression of the PED/PEA-15 protein in muscle and adipose cells increases glucose transport and impairs further insulin induction.	Glucose	79-86	OCA2 melanosomal transmembrane protein	Homo sapiens	22-25
11375323-6	2001	Similar effects on 2-DG uptake and PKC-zeta were also achieved by 50-fold overexpression of PKC-zeta in L6(PED).	Deoxyglucose	19-23	OCA2 melanosomal transmembrane protein	Homo sapiens	104-111
11375323-11	2001	We conclude that activation of classic PKCs, mainly PKC-alpha, inhibits PKC-zeta and may mediate the action of PED on glucose uptake in L6 skeletal muscle cells.	Glucose	118-125	OCA2 melanosomal transmembrane protein	Homo sapiens	111-114
10954708-9	2000	mCutA therefore appears necessary for the localization of AChE at the cell surface; it may be part of a multicomponent complex that anchors AChE in membranes, together with the hydrophobic P protein.	mcuta	0-5	OCA2 melanosomal transmembrane protein	Homo sapiens	189-198
10846069-8	2000	Coimmunoprecipitation analysis showed that the P protein forms a stable homooligomer (perhaps a trimer) that is present in L-P and N-P complexes in the higher oligomeric forms (at least a pentamer).	Neptunium	131-134	OCA2 melanosomal transmembrane protein	Homo sapiens	47-56
10704359-9	2000	Interestingly, the ability of the multiple site mutant of P (combo mutant has eight serine residues changed to alanine residues) to support efficient virus RNA synthesis suggests that the P protein has a high flexibility at least in its sequence and perhaps also in structure.	Serine	84-90	OCA2 melanosomal transmembrane protein	Homo sapiens	188-197
10704359-9	2000	Interestingly, the ability of the multiple site mutant of P (combo mutant has eight serine residues changed to alanine residues) to support efficient virus RNA synthesis suggests that the P protein has a high flexibility at least in its sequence and perhaps also in structure.	Alanine	111-118	OCA2 melanosomal transmembrane protein	Homo sapiens	188-197
9670003-0	1998	PED/PEA-15 gene controls glucose transport and is overexpressed in type 2 diabetes mellitus.	Glucose	25-32	OCA2 melanosomal transmembrane protein	Homo sapiens	0-3
9934693-5	1999	Furthermore, synthesis of the P protein increased when rBV containing the manipulated V gene was used to infect insect cells.	Ribavirin	55-58	OCA2 melanosomal transmembrane protein	Homo sapiens	30-39
9670003-6	1998	Transfection of PED/PEA-15 in differentiating L6 skeletal muscle cells increases the content of Glut1 transporters on the plasma membrane and inhibits insulin-stimulated glucose transport and cell-surface recruitment of Glut4, the major insulin-sensitive glucose transporter.	Glucose	170-177	OCA2 melanosomal transmembrane protein	Homo sapiens	16-19
9670003-6	1998	Transfection of PED/PEA-15 in differentiating L6 skeletal muscle cells increases the content of Glut1 transporters on the plasma membrane and inhibits insulin-stimulated glucose transport and cell-surface recruitment of Glut4, the major insulin-sensitive glucose transporter.	Glucose	255-262	OCA2 melanosomal transmembrane protein	Homo sapiens	16-19
9670003-8	1998	Overexpression of the PED/PEA-15 gene may contribute to insulin resistance in glucose uptake in type 2 diabetes.	Glucose	78-85	OCA2 melanosomal transmembrane protein	Homo sapiens	22-25
8614993-0	1996	Sendai virus P protein is constitutively phosphorylated at serine249: high phosphorylation potential of the P protein.	serine249	59-68	OCA2 melanosomal transmembrane protein	Homo sapiens	13-22
8932398-2	1996	RNAs from pools of end-labeled, partially hydrolyzed transcripts that bound to in vitro translated His-tagged P protein were isolated using immobilized Ni2+-ions.	Nickel(2+)	152-156	OCA2 melanosomal transmembrane protein	Homo sapiens	110-119
8551618-4	1996	Deletion mutant analysis of the P protein gene indicated that its C-terminal end was essential for interacting with N. This conclusion was strengthened by the finding that an anti-P monoclonal antibody (021/12P), reacting with a 21-residue P protein C-terminal peptide, apparently displaced N from N-P complexes.	asparaginyl-proline	298-301	OCA2 melanosomal transmembrane protein	Homo sapiens	32-41
8551618-6	1996	However, sequence requirements for the P protein C-terminal end were not absolute, and mutants with the substitution Ser-237-->Ala or Ser-237-->Thr were as efficient as the wild type in interacting with N. In addition, P and N proteins from strains of different HRSV antigenic groups, with sequence differences in the P protein C-terminal end, were able to coimmunoprecipitate and formed cytoplasmic inclusions.	Serine	117-120	OCA2 melanosomal transmembrane protein	Homo sapiens	39-48
8551618-6	1996	However, sequence requirements for the P protein C-terminal end were not absolute, and mutants with the substitution Ser-237-->Ala or Ser-237-->Thr were as efficient as the wild type in interacting with N. In addition, P and N proteins from strains of different HRSV antigenic groups, with sequence differences in the P protein C-terminal end, were able to coimmunoprecipitate and formed cytoplasmic inclusions.	Alanine	130-133	OCA2 melanosomal transmembrane protein	Homo sapiens	39-48
8551618-6	1996	However, sequence requirements for the P protein C-terminal end were not absolute, and mutants with the substitution Ser-237-->Ala or Ser-237-->Thr were as efficient as the wild type in interacting with N. In addition, P and N proteins from strains of different HRSV antigenic groups, with sequence differences in the P protein C-terminal end, were able to coimmunoprecipitate and formed cytoplasmic inclusions.	Serine	137-140	OCA2 melanosomal transmembrane protein	Homo sapiens	39-48
8551618-6	1996	However, sequence requirements for the P protein C-terminal end were not absolute, and mutants with the substitution Ser-237-->Ala or Ser-237-->Thr were as efficient as the wild type in interacting with N. In addition, P and N proteins from strains of different HRSV antigenic groups, with sequence differences in the P protein C-terminal end, were able to coimmunoprecipitate and formed cytoplasmic inclusions.	Threonine	150-153	OCA2 melanosomal transmembrane protein	Homo sapiens	39-48
8614993-0	1996	Sendai virus P protein is constitutively phosphorylated at serine249: high phosphorylation potential of the P protein.	serine249	59-68	OCA2 melanosomal transmembrane protein	Homo sapiens	108-117
8614993-1	1996	Previously we showed that the Sendai virus P protein (568 aa) in virus-infected cells and in virions was primarily and constitutively phosphorylated on serine(s) in a single tryptic phosphopeptide TP1.	Serine	152-158	OCA2 melanosomal transmembrane protein	Homo sapiens	43-52
8614993-2	1996	By two-dimensional thin-layer electrophoresis and chromatography analysis of tryptic phosphopeptides of several deletion and point mutants of the P protein, we now show that the sole phosphorylation site in TP1 is serine249.	serine249	214-223	OCA2 melanosomal transmembrane protein	Homo sapiens	146-155
8614993-5	1996	Mutagenesis of proline250 to alanine abrogated phosphorylation at serine249 suggesting that proline250 is essential for the primary phosphorylation of the P protein.	serine249	66-75	OCA2 melanosomal transmembrane protein	Homo sapiens	155-164
8614993-5	1996	Mutagenesis of proline250 to alanine abrogated phosphorylation at serine249 suggesting that proline250 is essential for the primary phosphorylation of the P protein.	proline250	15-25	OCA2 melanosomal transmembrane protein	Homo sapiens	155-164
11831729-3	1995	In contrast, cell-free phosphorylation of the P protein with virion-associated protein kinase (VAPK) occurred at both threonine and serine.	Threonine	118-127	OCA2 melanosomal transmembrane protein	Homo sapiens	46-55
7645214-6	1995	The results indicate that Ser 86, Ser 151, and Ser 180 located within the N-terminal half of the P protein are involved in the CKII-mediated phosphorylation of the P protein.	Serine	26-29	OCA2 melanosomal transmembrane protein	Homo sapiens	97-106
7645214-6	1995	The results indicate that Ser 86, Ser 151, and Ser 180 located within the N-terminal half of the P protein are involved in the CKII-mediated phosphorylation of the P protein.	Serine	26-29	OCA2 melanosomal transmembrane protein	Homo sapiens	164-173
7645214-6	1995	The results indicate that Ser 86, Ser 151, and Ser 180 located within the N-terminal half of the P protein are involved in the CKII-mediated phosphorylation of the P protein.	Serine	34-37	OCA2 melanosomal transmembrane protein	Homo sapiens	97-106
7645214-6	1995	The results indicate that Ser 86, Ser 151, and Ser 180 located within the N-terminal half of the P protein are involved in the CKII-mediated phosphorylation of the P protein.	Serine	34-37	OCA2 melanosomal transmembrane protein	Homo sapiens	164-173
7645214-6	1995	The results indicate that Ser 86, Ser 151, and Ser 180 located within the N-terminal half of the P protein are involved in the CKII-mediated phosphorylation of the P protein.	Serine	34-37	OCA2 melanosomal transmembrane protein	Homo sapiens	97-106
7645214-6	1995	The results indicate that Ser 86, Ser 151, and Ser 180 located within the N-terminal half of the P protein are involved in the CKII-mediated phosphorylation of the P protein.	Serine	34-37	OCA2 melanosomal transmembrane protein	Homo sapiens	164-173
11831729-3	1995	In contrast, cell-free phosphorylation of the P protein with virion-associated protein kinase (VAPK) occurred at both threonine and serine.	Serine	132-138	OCA2 melanosomal transmembrane protein	Homo sapiens	46-55
11831729-6	1995	Inhibition of cellular phosphatases (PP1 and PP2A) by okadaic acid (OA) in virus-infected cells caused a sixfold increase in the P protein phosphorylation, solely at serine residues.	Okadaic Acid	54-66	OCA2 melanosomal transmembrane protein	Homo sapiens	129-138
11831729-6	1995	Inhibition of cellular phosphatases (PP1 and PP2A) by okadaic acid (OA) in virus-infected cells caused a sixfold increase in the P protein phosphorylation, solely at serine residues.	Okadaic Acid	68-70	OCA2 melanosomal transmembrane protein	Homo sapiens	129-138
11831729-6	1995	Inhibition of cellular phosphatases (PP1 and PP2A) by okadaic acid (OA) in virus-infected cells caused a sixfold increase in the P protein phosphorylation, solely at serine residues.	Serine	166-172	OCA2 melanosomal transmembrane protein	Homo sapiens	129-138
7975241-5	1994	Through deletions and site-directed mutagenesis, the site of CKII phosphorylation was mapped to a single serine residue (Ser237) near the C-terminal end of the P protein.	Serine	105-111	OCA2 melanosomal transmembrane protein	Homo sapiens	160-169
7887411-1	1995	Tyrosinase-positive oculocutaneous albinism (OCA2), an autosomal recessive disorder of the melanin biosynthetic pathway, is the most common recessive disorder occurring in southern African Bantu-speaking Negroids, with an overall prevalence of 1/3,900.	Melanins	91-98	OCA2 melanosomal transmembrane protein	Homo sapiens	45-49
1547784-6	1992	These findings strengthen the possibility that amyloid P protein has a central role in amyloidogenic processes: first in formation of focal concentrations of lysosomal enzymes including proteases that generate fibril-forming peptides from amyloidogenic proteins, and second in formation of multicomponent complexes that include sulphoglycolipids as well as glycosaminoglycans.	Glycosaminoglycans	357-375	OCA2 melanosomal transmembrane protein	Homo sapiens	55-64
8126452-1	1994	P protein, the structural phosphoprotein of the Long strain of respiratory syncytial (RS) virus, is phosphorylated at serine residues.	Serine	118-124	OCA2 melanosomal transmembrane protein	Homo sapiens	0-9
8126452-5	1994	The P protein is modified in vitro by this activity mainly at serine residues located near the C terminus, which are also modified during virus infection.	Serine	62-68	OCA2 melanosomal transmembrane protein	Homo sapiens	4-13
34825823-1	2021	The overexpression of PED/PEA15, the phosphoprotein enriched in diabetes/phosphoprotein enriched in the astrocytes 15 protein (here referred simply to as PED), observed in some forms of type II diabetes, reduces the transport of insulin-stimulated glucose by binding to the phospholipase D1 (PLD1).	Glucose	248-255	OCA2 melanosomal transmembrane protein	Homo sapiens	22-25
1713063-4	1991	Bilayer membranes were formed from N"-(1,2-dimyristoyl-sn-glycero-3-phosphoethyl)-N-((m-3- trifluoromethyldiazirine)phenyl)thiourea (C14-PED), a head-group photosensitive phospholipid.	n"-(1,2-dimyristoyl-sn-glycero-3-phosphoethyl)-n-((m-3- trifluoromethyldiazirine)phenyl)thiourea	35-131	OCA2 melanosomal transmembrane protein	Homo sapiens	133-140
1847456-2	1991	NP proteins from virus particles and from infected cells retained 35S-P protein equally well.	Sulfur-35	66-69	OCA2 melanosomal transmembrane protein	Homo sapiens	1-10
34825823-1	2021	The overexpression of PED/PEA15, the phosphoprotein enriched in diabetes/phosphoprotein enriched in the astrocytes 15 protein (here referred simply to as PED), observed in some forms of type II diabetes, reduces the transport of insulin-stimulated glucose by binding to the phospholipase D1 (PLD1).	Glucose	248-255	OCA2 melanosomal transmembrane protein	Homo sapiens	154-157
34825823-2	2021	The inhibition of the PED/PLD1 interaction was shown to restore basal glucose transport, indicating PED as a pharmacological target for the development of drugs capable of improving insulin sensitivity and glucose tolerance.	Glucose	70-77	OCA2 melanosomal transmembrane protein	Homo sapiens	22-25
34825823-2	2021	The inhibition of the PED/PLD1 interaction was shown to restore basal glucose transport, indicating PED as a pharmacological target for the development of drugs capable of improving insulin sensitivity and glucose tolerance.	Glucose	70-77	OCA2 melanosomal transmembrane protein	Homo sapiens	100-103
34825823-2	2021	The inhibition of the PED/PLD1 interaction was shown to restore basal glucose transport, indicating PED as a pharmacological target for the development of drugs capable of improving insulin sensitivity and glucose tolerance.	Glucose	206-213	OCA2 melanosomal transmembrane protein	Homo sapiens	100-103
34825823-3	2021	We here report the identification and selection of PED ligands by means of NMR screening of a library of small organic molecules, NMR characterization of the PED/PLD1 interaction in lysates of cells expressing PLD1, and modulation of such interactions using BPH03, the best selected ligand.	bph03	258-263	OCA2 melanosomal transmembrane protein	Homo sapiens	51-54
34563978-4	2021	The SERS immunoassay integrates the interference-free Raman response of high wavenumber region (2212 cm-1) and specific capture antibody with high affinity to selectively recognize P-protein from complicated sample.	sers	4-8	OCA2 melanosomal transmembrane protein	Homo sapiens	181-190
34563978-5	2021	Meanwhile, the target-induced near-field coupling effect between localized surface plasmon resonances of individual SERS immunoprobe and capture substrate enables the detection of P-protein as low as pg/mL level, and the limit of detection can reach 0.329 pg/mL that is about 6 orders of magnitude lower than the limit defined protein residue (causing penicillin allergy).	sers	116-120	OCA2 melanosomal transmembrane protein	Homo sapiens	180-189
34563978-5	2021	Meanwhile, the target-induced near-field coupling effect between localized surface plasmon resonances of individual SERS immunoprobe and capture substrate enables the detection of P-protein as low as pg/mL level, and the limit of detection can reach 0.329 pg/mL that is about 6 orders of magnitude lower than the limit defined protein residue (causing penicillin allergy).	Penicillins	352-362	OCA2 melanosomal transmembrane protein	Homo sapiens	180-189
34563978-6	2021	With the ultrasensitivity and specific selectivity, the proposed SERS immunoassay platform can precisely evaluate the content of P-protein in blood sample or penicillin drugs.	sers	65-69	OCA2 melanosomal transmembrane protein	Homo sapiens	129-138
7153213-8	1982	The inactivation of the P-protein appears to represent a suicide reaction of the P-protein as a side reaction of the glycine decarboxylation, which is supposed to involve the formation of a ternary complex of P-protein, aminomethyl moiety of glycine and H-protein through a Schiff base linkage of the H-protein-bound amino-methyl moiety with the pyridoxal phosphate of P-protein.	Glycine	117-124	OCA2 melanosomal transmembrane protein	Homo sapiens	81-90
34707637-1	2021	Background: Tyrosinase-positive oculocutaneous albinism (OCA, type II, OCA2) is an autosomal recessive genetic disease in which the biosynthesis of melanin decreases in the skin, hair, and eyes.	Melanins	148-155	OCA2 melanosomal transmembrane protein	Homo sapiens	71-75
35259189-3	2022	Then a residue in the central epsilon bulge directs the covalent linkage of a complementary dNMP to a Tyr sidechain in P protein s Terminal Protein (TP) domain.	dnmp	92-96	OCA2 melanosomal transmembrane protein	Homo sapiens	119-128
35259189-3	2022	Then a residue in the central epsilon bulge directs the covalent linkage of a complementary dNMP to a Tyr sidechain in P protein s Terminal Protein (TP) domain.	Tyrosine	102-105	OCA2 melanosomal transmembrane protein	Homo sapiens	119-128
2434487-2	1987	In order to learn more about these protein-metal binding interactions, calcium-free human salivary and porcine pancreatic amylase [P(protein)] were obtained by carboxymethylcellulose chromatography of the partially purified proteins.	Calcium	71-78	OCA2 melanosomal transmembrane protein	Homo sapiens	131-141
6336599-0	1983	Nonketotic hyperglycinemia: two patients with primary defects of P-protein and T-protein, respectively, in the glycine cleavage system.	Glycine	16-23	OCA2 melanosomal transmembrane protein	Homo sapiens	65-74
6336599-3	1983	In one patient, the disturbance of the glycine cleavage system was due to absence of activity of the P-protein.	Glycine	39-46	OCA2 melanosomal transmembrane protein	Homo sapiens	101-110
7153213-1	1982	Glycine decarboxylase, tentatively called P-protein, was inactivated when it was incubated with glycine in the presence of the aminomethyl carrier protein, called H-protein.	Glycine	96-103	OCA2 melanosomal transmembrane protein	Homo sapiens	42-51
7153213-2	1982	The inactivation was accompanied by a spectral change in the P-protein as a pyridoxal phosphate enzyme; the spectrum became unusual, with a peak at 330 nm.	Pyridoxal Phosphate	76-95	OCA2 melanosomal transmembrane protein	Homo sapiens	61-70
7153213-4	1982	Such a spectral change and concomitant inactivation of the P-protein could be completely prevented by the addition of sodium bicarbonate, which initiates the glycine-CO2 exchange in the reaction mixture.	Sodium Bicarbonate	118-136	OCA2 melanosomal transmembrane protein	Homo sapiens	59-68
7153213-4	1982	Such a spectral change and concomitant inactivation of the P-protein could be completely prevented by the addition of sodium bicarbonate, which initiates the glycine-CO2 exchange in the reaction mixture.	Glycine	158-165	OCA2 melanosomal transmembrane protein	Homo sapiens	59-68
7153213-4	1982	Such a spectral change and concomitant inactivation of the P-protein could be completely prevented by the addition of sodium bicarbonate, which initiates the glycine-CO2 exchange in the reaction mixture.	N2,N6-bis(4-(2-aminoethoxy)quinolin-2-yl)-4-((4-fluorobenzyl)oxy)pyridine-2,6-dicarboxamide	166-169	OCA2 melanosomal transmembrane protein	Homo sapiens	59-68
7153213-5	1982	The inactivated P-protein was associated with H-protein and the methylene carbon of glycine, but not the carboxyl carbon, in a manner not separable by gel filtration, although the molar ratios of those three components were not constant.	Carbon	74-80	OCA2 melanosomal transmembrane protein	Homo sapiens	16-25
7153213-5	1982	The inactivated P-protein was associated with H-protein and the methylene carbon of glycine, but not the carboxyl carbon, in a manner not separable by gel filtration, although the molar ratios of those three components were not constant.	Glycine	84-91	OCA2 melanosomal transmembrane protein	Homo sapiens	16-25
7153213-8	1982	The inactivation of the P-protein appears to represent a suicide reaction of the P-protein as a side reaction of the glycine decarboxylation, which is supposed to involve the formation of a ternary complex of P-protein, aminomethyl moiety of glycine and H-protein through a Schiff base linkage of the H-protein-bound amino-methyl moiety with the pyridoxal phosphate of P-protein.	Glycine	117-124	OCA2 melanosomal transmembrane protein	Homo sapiens	24-33
7153213-8	1982	The inactivation of the P-protein appears to represent a suicide reaction of the P-protein as a side reaction of the glycine decarboxylation, which is supposed to involve the formation of a ternary complex of P-protein, aminomethyl moiety of glycine and H-protein through a Schiff base linkage of the H-protein-bound amino-methyl moiety with the pyridoxal phosphate of P-protein.	Glycine	117-124	OCA2 melanosomal transmembrane protein	Homo sapiens	81-90
7153213-8	1982	The inactivation of the P-protein appears to represent a suicide reaction of the P-protein as a side reaction of the glycine decarboxylation, which is supposed to involve the formation of a ternary complex of P-protein, aminomethyl moiety of glycine and H-protein through a Schiff base linkage of the H-protein-bound amino-methyl moiety with the pyridoxal phosphate of P-protein.	Glycine	117-124	OCA2 melanosomal transmembrane protein	Homo sapiens	81-90
7153213-8	1982	The inactivation of the P-protein appears to represent a suicide reaction of the P-protein as a side reaction of the glycine decarboxylation, which is supposed to involve the formation of a ternary complex of P-protein, aminomethyl moiety of glycine and H-protein through a Schiff base linkage of the H-protein-bound amino-methyl moiety with the pyridoxal phosphate of P-protein.	Glycine	242-249	OCA2 melanosomal transmembrane protein	Homo sapiens	24-33
7153213-8	1982	The inactivation of the P-protein appears to represent a suicide reaction of the P-protein as a side reaction of the glycine decarboxylation, which is supposed to involve the formation of a ternary complex of P-protein, aminomethyl moiety of glycine and H-protein through a Schiff base linkage of the H-protein-bound amino-methyl moiety with the pyridoxal phosphate of P-protein.	Glycine	242-249	OCA2 melanosomal transmembrane protein	Homo sapiens	81-90
7153213-8	1982	The inactivation of the P-protein appears to represent a suicide reaction of the P-protein as a side reaction of the glycine decarboxylation, which is supposed to involve the formation of a ternary complex of P-protein, aminomethyl moiety of glycine and H-protein through a Schiff base linkage of the H-protein-bound amino-methyl moiety with the pyridoxal phosphate of P-protein.	Glycine	242-249	OCA2 melanosomal transmembrane protein	Homo sapiens	81-90
7153213-8	1982	The inactivation of the P-protein appears to represent a suicide reaction of the P-protein as a side reaction of the glycine decarboxylation, which is supposed to involve the formation of a ternary complex of P-protein, aminomethyl moiety of glycine and H-protein through a Schiff base linkage of the H-protein-bound amino-methyl moiety with the pyridoxal phosphate of P-protein.	Glycine	242-249	OCA2 melanosomal transmembrane protein	Homo sapiens	81-90
7153213-8	1982	The inactivation of the P-protein appears to represent a suicide reaction of the P-protein as a side reaction of the glycine decarboxylation, which is supposed to involve the formation of a ternary complex of P-protein, aminomethyl moiety of glycine and H-protein through a Schiff base linkage of the H-protein-bound amino-methyl moiety with the pyridoxal phosphate of P-protein.	Schiff Bases	274-285	OCA2 melanosomal transmembrane protein	Homo sapiens	24-33
7153213-8	1982	The inactivation of the P-protein appears to represent a suicide reaction of the P-protein as a side reaction of the glycine decarboxylation, which is supposed to involve the formation of a ternary complex of P-protein, aminomethyl moiety of glycine and H-protein through a Schiff base linkage of the H-protein-bound amino-methyl moiety with the pyridoxal phosphate of P-protein.	Schiff Bases	274-285	OCA2 melanosomal transmembrane protein	Homo sapiens	81-90
7153213-8	1982	The inactivation of the P-protein appears to represent a suicide reaction of the P-protein as a side reaction of the glycine decarboxylation, which is supposed to involve the formation of a ternary complex of P-protein, aminomethyl moiety of glycine and H-protein through a Schiff base linkage of the H-protein-bound amino-methyl moiety with the pyridoxal phosphate of P-protein.	Schiff Bases	274-285	OCA2 melanosomal transmembrane protein	Homo sapiens	81-90
7153213-8	1982	The inactivation of the P-protein appears to represent a suicide reaction of the P-protein as a side reaction of the glycine decarboxylation, which is supposed to involve the formation of a ternary complex of P-protein, aminomethyl moiety of glycine and H-protein through a Schiff base linkage of the H-protein-bound amino-methyl moiety with the pyridoxal phosphate of P-protein.	Schiff Bases	274-285	OCA2 melanosomal transmembrane protein	Homo sapiens	81-90
7153213-8	1982	The inactivation of the P-protein appears to represent a suicide reaction of the P-protein as a side reaction of the glycine decarboxylation, which is supposed to involve the formation of a ternary complex of P-protein, aminomethyl moiety of glycine and H-protein through a Schiff base linkage of the H-protein-bound amino-methyl moiety with the pyridoxal phosphate of P-protein.	Pyridoxal Phosphate	346-365	OCA2 melanosomal transmembrane protein	Homo sapiens	24-33
7153213-8	1982	The inactivation of the P-protein appears to represent a suicide reaction of the P-protein as a side reaction of the glycine decarboxylation, which is supposed to involve the formation of a ternary complex of P-protein, aminomethyl moiety of glycine and H-protein through a Schiff base linkage of the H-protein-bound amino-methyl moiety with the pyridoxal phosphate of P-protein.	Pyridoxal Phosphate	346-365	OCA2 melanosomal transmembrane protein	Homo sapiens	81-90
7153213-8	1982	The inactivation of the P-protein appears to represent a suicide reaction of the P-protein as a side reaction of the glycine decarboxylation, which is supposed to involve the formation of a ternary complex of P-protein, aminomethyl moiety of glycine and H-protein through a Schiff base linkage of the H-protein-bound amino-methyl moiety with the pyridoxal phosphate of P-protein.	Pyridoxal Phosphate	346-365	OCA2 melanosomal transmembrane protein	Homo sapiens	81-90
7153213-8	1982	The inactivation of the P-protein appears to represent a suicide reaction of the P-protein as a side reaction of the glycine decarboxylation, which is supposed to involve the formation of a ternary complex of P-protein, aminomethyl moiety of glycine and H-protein through a Schiff base linkage of the H-protein-bound amino-methyl moiety with the pyridoxal phosphate of P-protein.	Pyridoxal Phosphate	346-365	OCA2 melanosomal transmembrane protein	Homo sapiens	81-90
6790577-3	1981	The activities of glycine decarboxylase (P-protein) and the aminomethyl carrier protein (H-protein), two of the four protein components of the glycine cleavage system, were considerably reduced in both the liver and brain; the extent of reduction was greater in the H-protein.	Glycine	18-25	OCA2 melanosomal transmembrane protein	Homo sapiens	41-50
6790577-8	1981	Partial inactivation of P-protein could result secondarily from impaired metabolism of glycine resulting from deficiency in the activity of H-protein.	Glycine	87-94	OCA2 melanosomal transmembrane protein	Homo sapiens	24-33
6790577-9	1981	However, the H-protein from the patient could stimulate the P-protein catalyzed exchange of the carboxyl carbon of glycine with 14CO2, although the specific activity of the purified H-protein from the patient was only 4% of that of control human H-protein.	14co2	128-133	OCA2 melanosomal transmembrane protein	Homo sapiens	60-69
6790577-9	1981	However, the H-protein from the patient could stimulate the P-protein catalyzed exchange of the carboxyl carbon of glycine with 14CO2, although the specific activity of the purified H-protein from the patient was only 4% of that of control human H-protein.	Carbon	105-111	OCA2 melanosomal transmembrane protein	Homo sapiens	60-69
6790577-9	1981	However, the H-protein from the patient could stimulate the P-protein catalyzed exchange of the carboxyl carbon of glycine with 14CO2, although the specific activity of the purified H-protein from the patient was only 4% of that of control human H-protein.	Glycine	115-122	OCA2 melanosomal transmembrane protein	Homo sapiens	60-69
32966160-4	2020	SLC45A2 expressed ectopically in HeLa cells localizes to lysosomes and raises lysosomal pH, suggesting that in melanocytes, SLC45A2 expression, like OCA2 expression, results in the deacidification of maturing melanosomes to support melanin synthesis.	Melanins	232-239	OCA2 melanosomal transmembrane protein	Homo sapiens	149-153
33574916-2	2021	Phosphoprotein enriched in diabetes/phosphoprotein enriched in astrocytes-15 (PED/PEA-15) is a protein involved in the metabolism of glucose that regulates numerous cellular processes, including cell division, apoptosis and migration in numerous types of cancer.	Glucose	133-140	OCA2 melanosomal transmembrane protein	Homo sapiens	78-81
33124154-9	2021	We also found seven novel variants: c.731G > A, c.741C > A, c.867C > A, and c.1037-2A > T in TYR, c.695dupT and c.1054A > G in OCA2, and c.9C > A in HPS1.	Tyrosine	93-96	OCA2 melanosomal transmembrane protein	Homo sapiens	127-131
6777459-2	1980	Inward calcium currents were eliminated by using Co2+, Cd2+, or OCa2+ EGTA in the bathing solution.	Calcium	7-14	OCA2 melanosomal transmembrane protein	Homo sapiens	64-68
6777459-2	1980	Inward calcium currents were eliminated by using Co2+, Cd2+, or OCa2+ EGTA in the bathing solution.	Egtazic Acid	70-74	OCA2 melanosomal transmembrane protein	Homo sapiens	64-68
32259106-6	2020	Genomic sequencing revealed a biallelic p.L312I mutation in TYR and a homozygous p.S788L mutation in OCA2, both of which were further confirmed to affect melanin biosynthesis via in vitro assays.	Melanins	154-161	OCA2 melanosomal transmembrane protein	Homo sapiens	101-105