PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
6153673-4	1980	On the other hand, the induction of Ts requires DNP-modified MHC determinants, since DNP-LC lysates passed over lentil lectin or specific anti-H-2 immunoabsorbent columns lost their ability to induce Ts.	2,4-Dinitrophenol	48-51	major histocompatibility complex, class I, C	Homo sapiens	61-64
34022431-7	2021	Therefore, I call for rigorous experimental methodology, employing heavy stable isotope peptides spiking into the immunoaffinity purified mixtures of natural MHC peptides and analysis by the highly reliable targeted mass spectrometry, to claim that MHC peptides are indeed spliced.	Peptides	88-96	major histocompatibility complex, class I, C	Homo sapiens	249-252
34003837-11	2021	Carvedilol, a nonselective beta-adrenergic receptor antagonist, suppressed the facilitating effects of Epi on the Atrogin-1 mRNA induction by LPS, and abolished the effects of Epi on the MHC protein loss in the presence of LPS.	Carvedilol	0-10	major histocompatibility complex, class I, C	Homo sapiens	187-190
33539638-1	2021	HLA-C*15:227 differs from HLA-C*15:02:01:01 by a single nonsynonymous change (368A   G Tyrosine 99 to Cysteine).	Tyrosine	87-95	major histocompatibility complex, class I, C	Homo sapiens	0-5
33381897-0	2021	HLA-B*08 identified as the most associated MHC locus for anti-carbamylated protein antibody-positive/anti-CCP-negative rheumatoid arthritis.	ccp	106-109	major histocompatibility complex, class I, C	Homo sapiens	43-46
33381897-12	2021	CONCLUSION: Our results identify HLA-B*08 carrying Asp-9 as the most associated MHC locus with anti-CarP+ /anti-CCP- RA.	asp-9	51-56	major histocompatibility complex, class I, C	Homo sapiens	80-83
33381897-12	2021	CONCLUSION: Our results identify HLA-B*08 carrying Asp-9 as the most associated MHC locus with anti-CarP+ /anti-CCP- RA.	ccp	112-115	major histocompatibility complex, class I, C	Homo sapiens	80-83
33381897-12	2021	CONCLUSION: Our results identify HLA-B*08 carrying Asp-9 as the most associated MHC locus with anti-CarP+ /anti-CCP- RA.	Radium	117-119	major histocompatibility complex, class I, C	Homo sapiens	80-83
33981311-7	2021	We improved it to create ERGO-II by adding the CDR3 alpha segment, the MHC typing, V and J genes, and T cell type (CD4+ or CD8+) as to the predictor.	ergo-ii	25-32	major histocompatibility complex, class I, C	Homo sapiens	71-74
33977152-0	2021	HLA-C*06:02 allele can influence clinical efficacy of certolizumab pegol?	Certolizumab Pegol	54-66	major histocompatibility complex, class I, C	Homo sapiens	0-5
33977152-0	2021	HLA-C*06:02 allele can influence clinical efficacy of certolizumab pegol?	pegol	67-72	major histocompatibility complex, class I, C	Homo sapiens	0-5
33539638-1	2021	HLA-C*15:227 differs from HLA-C*15:02:01:01 by a single nonsynonymous change (368A   G Tyrosine 99 to Cysteine).	Tyrosine	87-95	major histocompatibility complex, class I, C	Homo sapiens	26-31
33539638-1	2021	HLA-C*15:227 differs from HLA-C*15:02:01:01 by a single nonsynonymous change (368A   G Tyrosine 99 to Cysteine).	Cysteine	102-110	major histocompatibility complex, class I, C	Homo sapiens	0-5
33539638-1	2021	HLA-C*15:227 differs from HLA-C*15:02:01:01 by a single nonsynonymous change (368A   G Tyrosine 99 to Cysteine).	Cysteine	102-110	major histocompatibility complex, class I, C	Homo sapiens	26-31
32270503-11	2021	All HLA-B*14:01 carriers with TMP-SMX DILI possessed HLA-C*08:02, another significant allele (p=0.0026).	Trimethoprim, Sulfamethoxazole Drug Combination	30-37	major histocompatibility complex, class I, C	Homo sapiens	53-58
33622787-8	2021	Expression of HLA-C was inhibited by ELF3 small interfering RNAs (siRNAs) and by wrenchnolol treatment.	wrenchnolol	81-92	major histocompatibility complex, class I, C	Homo sapiens	14-19
33603436-2	2021	One of the most well-defined risk factors of allopurinol-induced SCARs is the presence of polymorphic alleles of human leukocyte antigen (HLA) genes, such as HLA-B*58:01 and HLA-C*03:02 alleles.	Allopurinol	45-56	major histocompatibility complex, class I, C	Homo sapiens	174-179
31018729-6	2021	RESULTS: The MTT assay and colony formation assay showed that HLA-C promoted cell proliferation.	monooxyethylene trimethylolpropane tristearate	13-16	major histocompatibility complex, class I, C	Homo sapiens	62-67
33361435-1	2021	The Gag280 mutation is associated with HLA-C*01:02 but not with HLA-B*52:01 in subtype A/E-infected individuals, whereas this mutation is associated with HLA-B*52:01 but not with HLA-C*01:02 in subtype B infections.	gag280	4-10	major histocompatibility complex, class I, C	Homo sapiens	39-44
33361435-2	2021	Although it is known that the Gag280 mutant is selected by HLA-B*52:01-restricted GagRI8 (Gag275-282)-specific T-cells in subtype B infections, it remains unknown why this Gag280 mutation is associated with HLA-C*01:02 rather than HLA-B*52:01 in subtype A/E infections.	gag280	30-36	major histocompatibility complex, class I, C	Homo sapiens	207-212
33361435-2	2021	Although it is known that the Gag280 mutant is selected by HLA-B*52:01-restricted GagRI8 (Gag275-282)-specific T-cells in subtype B infections, it remains unknown why this Gag280 mutation is associated with HLA-C*01:02 rather than HLA-B*52:01 in subtype A/E infections.	gag275	90-96	major histocompatibility complex, class I, C	Homo sapiens	207-212
33361435-2	2021	Although it is known that the Gag280 mutant is selected by HLA-B*52:01-restricted GagRI8 (Gag275-282)-specific T-cells in subtype B infections, it remains unknown why this Gag280 mutation is associated with HLA-C*01:02 rather than HLA-B*52:01 in subtype A/E infections.	gag280	172-178	major histocompatibility complex, class I, C	Homo sapiens	207-212
33361435-9	2021	The present study demonstrated that a difference in the Gag280 consensus sequence influenced the elicitation of the GagYI9-specific T-cells involved in the accumulation of HLA-C*01:02-associated Gag280 mutations.IMPORTANCE HIV-1 mutations escaped from HIV-specific CD8+ T-cells are mostly detected as HLA-associated mutations.	gag280	56-62	major histocompatibility complex, class I, C	Homo sapiens	172-177
33052032-5	2021	Nevertheless, HLA-C antigens are truly immunogenic and preformed anti-HLA-C DSA are clinically relevant.	dsa	76-79	major histocompatibility complex, class I, C	Homo sapiens	70-75
33052032-6	2021	Indeed, anti-HLA-C DSA are able to bind donor cells and to activate the complement pathway both ex vivo and in vivo.	dsa	19-22	major histocompatibility complex, class I, C	Homo sapiens	13-18
33216553-9	2021	Inhibition of sialylation with the sialyltransferase inhibitor 3Fax-Neu5Ac resulted in the lower expression of MHC and suppression of myoblast fusion.	3fax-neu5ac	63-74	major histocompatibility complex, class I, C	Homo sapiens	111-114
32997515-5	2020	ATP turnover of SRX is faster in MHC IIAX fibers compared to MHC I and IIA fibers (p = 0.001).	Adenosine Triphosphate	0-3	major histocompatibility complex, class I, C	Homo sapiens	33-36
32897882-4	2020	We solved this problem by use of higher concentrations of acetonitrile (ACN) for the separation of MHC ligands and their respective complexes.	acetonitrile	58-70	major histocompatibility complex, class I, C	Homo sapiens	99-102
32897882-4	2020	We solved this problem by use of higher concentrations of acetonitrile (ACN) for the separation of MHC ligands and their respective complexes.	acetonitrile	72-75	major histocompatibility complex, class I, C	Homo sapiens	99-102
32602630-0	2020	Improvement in HLA-C typing by a new sequence-specific oligonucleotides kit.	Oligonucleotides	55-71	major histocompatibility complex, class I, C	Homo sapiens	15-20
32462789-1	2020	HLA-C*06:297 differs from C*06:02:01:01 by a single nucleotide change in codon -19 (CCC>TCC).	Chlormequat	84-87	major histocompatibility complex, class I, C	Homo sapiens	0-5
32462789-1	2020	HLA-C*06:297 differs from C*06:02:01:01 by a single nucleotide change in codon -19 (CCC>TCC).	Triclocarban	88-91	major histocompatibility complex, class I, C	Homo sapiens	0-5
32278991-5	2020	The presence of suspended kaolin particles and humic acid enhanced the antibiotic removal, speculated to be through MHC bridging of the kaolin/humic acid and antibiotic molecules.	Kaolin	26-32	major histocompatibility complex, class I, C	Homo sapiens	116-119
32602402-4	2020	The MHC composition was determined using SDS-PAGE.	Sodium Dodecyl Sulfate	41-44	major histocompatibility complex, class I, C	Homo sapiens	4-7
32460519-11	2020	MitoTEMPOL reversed sepsis mediated reductions in mitochondrial function, activation of proteolytic pathways, and decreases in MHC content.	MitoTEMPOL	0-10	major histocompatibility complex, class I, C	Homo sapiens	127-130
32571843-0	2020	Impact of Cysteine Residues on MHC Binding Predictions and Recognition by Tumor-Reactive T Cells.	Cysteine	10-18	major histocompatibility complex, class I, C	Homo sapiens	31-34
32571843-2	2020	Nevertheless, prediction algorithms appear to function poorly for epitopes containing cysteine (Cys) residues, which can oxidize and form disulfide bonds with other Cys residues under oxidizing conditions, thus potentially interfering with their ability to bind to MHC molecules.	Cysteine	86-94	major histocompatibility complex, class I, C	Homo sapiens	265-268
32571843-2	2020	Nevertheless, prediction algorithms appear to function poorly for epitopes containing cysteine (Cys) residues, which can oxidize and form disulfide bonds with other Cys residues under oxidizing conditions, thus potentially interfering with their ability to bind to MHC molecules.	Cysteine	96-99	major histocompatibility complex, class I, C	Homo sapiens	265-268
32571843-5	2020	Substitutions of AABA for Cys at putative MHC anchor positions often significantly enhanced T cell recognition, whereas substitutions at non-MHC anchor positions were neutral, except for one epitope where this modification abolished T cell recognition.	alpha-aminobutyric acid	17-21	major histocompatibility complex, class I, C	Homo sapiens	42-45
32571843-5	2020	Substitutions of AABA for Cys at putative MHC anchor positions often significantly enhanced T cell recognition, whereas substitutions at non-MHC anchor positions were neutral, except for one epitope where this modification abolished T cell recognition.	Cysteine	26-29	major histocompatibility complex, class I, C	Homo sapiens	42-45
32278991-5	2020	The presence of suspended kaolin particles and humic acid enhanced the antibiotic removal, speculated to be through MHC bridging of the kaolin/humic acid and antibiotic molecules.	Humic Substances	47-57	major histocompatibility complex, class I, C	Homo sapiens	116-119
32278991-5	2020	The presence of suspended kaolin particles and humic acid enhanced the antibiotic removal, speculated to be through MHC bridging of the kaolin/humic acid and antibiotic molecules.	Humic Substances	143-153	major histocompatibility complex, class I, C	Homo sapiens	116-119
32278991-6	2020	In the continuous flow tests involving flocculation/sedimentation-UF for 40 days, an optimal MHC achieved a much greater performance than polyaluminium chloride in terms of the overall removal of antibiotics (RE (norfloxacin) of ~90% and RE (tylosin) of ~80%) and a greatly reduced rate of membrane fouling; the latter resulting from a more porous and looser structure of cake layer, caused by a surface-modification-like effect of residual MHC on the hydrophobic PVDF membrane.	Norfloxacin	213-224	major histocompatibility complex, class I, C	Homo sapiens	93-96
32278991-6	2020	In the continuous flow tests involving flocculation/sedimentation-UF for 40 days, an optimal MHC achieved a much greater performance than polyaluminium chloride in terms of the overall removal of antibiotics (RE (norfloxacin) of ~90% and RE (tylosin) of ~80%) and a greatly reduced rate of membrane fouling; the latter resulting from a more porous and looser structure of cake layer, caused by a surface-modification-like effect of residual MHC on the hydrophobic PVDF membrane.	Tylosin	242-249	major histocompatibility complex, class I, C	Homo sapiens	93-96
32278991-6	2020	In the continuous flow tests involving flocculation/sedimentation-UF for 40 days, an optimal MHC achieved a much greater performance than polyaluminium chloride in terms of the overall removal of antibiotics (RE (norfloxacin) of ~90% and RE (tylosin) of ~80%) and a greatly reduced rate of membrane fouling; the latter resulting from a more porous and looser structure of cake layer, caused by a surface-modification-like effect of residual MHC on the hydrophobic PVDF membrane.	polyvinylidene fluoride	464-468	major histocompatibility complex, class I, C	Homo sapiens	93-96
32374795-2	2020	Nickel(ii) complexes, 1-3, of these ligands HLa-c were synthesized in good yield (approximately 70%) by the reaction of ligands : (NiCl2 6H2O) in a 1 : 1 molar ratio in methanol.	Nickel(2+)	0-10	major histocompatibility complex, class I, C	Homo sapiens	44-49
32485991-9	2020	Besides, we observed that the decreased fiber diameter and MHC levels, as well as the transition of fiber types, were all abolished by Ang-(1-7) in mice fed with DDC.	Zalcitabine	162-165	major histocompatibility complex, class I, C	Homo sapiens	59-62
32374795-2	2020	Nickel(ii) complexes, 1-3, of these ligands HLa-c were synthesized in good yield (approximately 70%) by the reaction of ligands : (NiCl2 6H2O) in a 1 : 1 molar ratio in methanol.	nicl2 6h2o	131-141	major histocompatibility complex, class I, C	Homo sapiens	44-49
32374795-2	2020	Nickel(ii) complexes, 1-3, of these ligands HLa-c were synthesized in good yield (approximately 70%) by the reaction of ligands : (NiCl2 6H2O) in a 1 : 1 molar ratio in methanol.	Methanol	169-177	major histocompatibility complex, class I, C	Homo sapiens	44-49
32374795-3	2020	The amine donor in each of the ligands HLa-c binds to the Ni(ii) centre without deprotonation.	Amines	4-9	major histocompatibility complex, class I, C	Homo sapiens	39-44
32374795-3	2020	The amine donor in each of the ligands HLa-c binds to the Ni(ii) centre without deprotonation.	Nickel(2+)	58-64	major histocompatibility complex, class I, C	Homo sapiens	39-44
32066683-7	2020	The HLA-C*07:01 allele was identified as potentially predisposing to clozapine-induced myocarditis (OR = 2.89, 95% CI: 1.11-7.53), consistent with a previous report of association of the same allele with clozapine-induced agranulocytosis.	Clozapine	69-78	major histocompatibility complex, class I, C	Homo sapiens	4-9
31977282-6	2020	We identified an amino acid substitution of threonine at position 94 of HLA-C in combination with the telomeric KIR genotype of haplotype tA01/tB01 that had significantly higher frequency (>20%) in the case population than in both control populations.	Threonine	44-53	major histocompatibility complex, class I, C	Homo sapiens	72-77
31980816-5	2020	Supporting the hypothesis that circSamd4 might complex with PUR proteins and thereby prevent their interaction with DNA, silencing circSamd4 enhanced the association of PUR proteins with the Mhc promoter, while overexpressing circSamd4 interfered with the binding of PUR proteins to the Mhc promoter.	circsamd4	31-40	major histocompatibility complex, class I, C	Homo sapiens	191-194
31980816-5	2020	Supporting the hypothesis that circSamd4 might complex with PUR proteins and thereby prevent their interaction with DNA, silencing circSamd4 enhanced the association of PUR proteins with the Mhc promoter, while overexpressing circSamd4 interfered with the binding of PUR proteins to the Mhc promoter.	circsamd4	31-40	major histocompatibility complex, class I, C	Homo sapiens	287-290
31980816-7	2020	Our results indicate that the association of PUR proteins with circSamd4 enhances myogenesis by contributing to the derepression of MHC transcription.	circsamd4	63-72	major histocompatibility complex, class I, C	Homo sapiens	132-135
32066683-7	2020	The HLA-C*07:01 allele was identified as potentially predisposing to clozapine-induced myocarditis (OR = 2.89, 95% CI: 1.11-7.53), consistent with a previous report of association of the same allele with clozapine-induced agranulocytosis.	Clozapine	204-213	major histocompatibility complex, class I, C	Homo sapiens	4-9
31843910-6	2019	Using a mouse model of MHC I-dependent (H-2Dk) virus immunity, we discovered that NK cells depend on the Ly49G2 inhibitory self-receptor to mediate virus control, which coincided with host survival during murine cytomegalovirus infection.	Hydrogen	40-45	major histocompatibility complex, class I, C	Homo sapiens	23-26
32589879-8	2020	The allele HLA-C*04:01 was the most common in the Barao community, and the allele HLA-C*07:01 in Ipiranga.	ipiranga	97-105	major histocompatibility complex, class I, C	Homo sapiens	82-87
31589371-1	2020	HLA-C*07:780 differs from HLA-C*07:04:01:01 in exon 2 at amino acid 49; alanine to threonine substitution.	Alanine	72-79	major histocompatibility complex, class I, C	Homo sapiens	0-5
31589371-1	2020	HLA-C*07:780 differs from HLA-C*07:04:01:01 in exon 2 at amino acid 49; alanine to threonine substitution.	Alanine	72-79	major histocompatibility complex, class I, C	Homo sapiens	26-31
31589371-1	2020	HLA-C*07:780 differs from HLA-C*07:04:01:01 in exon 2 at amino acid 49; alanine to threonine substitution.	glycyl-threonine	83-92	major histocompatibility complex, class I, C	Homo sapiens	0-5
31740487-7	2020	This direct conversion to memory is associated with a selective increase in TCR sensitivity to self-peptide MHC in vivo and an enhanced response to weak agonist peptides ex vivo.	Receptor-CD3 Complex, Antigen, T-Cell	76-79	major histocompatibility complex, class I, C	Homo sapiens	108-111
31921098-7	2019	Here, we critically review new insights into: (i) the mechanisms controlling expression of HLA-C by EVT, (ii) the mechanisms by which decidual NK cells, effector T cells and regulatory T cells recognize HLA-C allo-antigens, and (iii) immune recognition of pathogen derived antigens in context of HLA-C.	EVT	100-103	major histocompatibility complex, class I, C	Homo sapiens	91-96
31468173-7	2019	Myosin heavy chain (MHC) isoform was determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis.	Sodium Dodecyl Sulfate	51-73	major histocompatibility complex, class I, C	Homo sapiens	0-18
31271820-7	2019	Ginsenoside Rg3 enhances Akt/mTOR (mammalian target of rapamycin) signaling that in turn stimulates muscle-specific gene expression such as myosin heavy chain (MHC) and Myogenin, and suppresses the expression of muscle-specific ubiquitin ligases.	Ginsenosides	0-11	major histocompatibility complex, class I, C	Homo sapiens	140-158
31271820-7	2019	Ginsenoside Rg3 enhances Akt/mTOR (mammalian target of rapamycin) signaling that in turn stimulates muscle-specific gene expression such as myosin heavy chain (MHC) and Myogenin, and suppresses the expression of muscle-specific ubiquitin ligases.	Ginsenosides	0-11	major histocompatibility complex, class I, C	Homo sapiens	160-163
31468173-7	2019	Myosin heavy chain (MHC) isoform was determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis.	Sodium Dodecyl Sulfate	51-73	major histocompatibility complex, class I, C	Homo sapiens	20-23
31468173-7	2019	Myosin heavy chain (MHC) isoform was determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis.	polyacrylamide gels	74-92	major histocompatibility complex, class I, C	Homo sapiens	0-18
31468173-7	2019	Myosin heavy chain (MHC) isoform was determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis.	polyacrylamide gels	74-92	major histocompatibility complex, class I, C	Homo sapiens	20-23
31294563-10	2019	OVA-Man exhibited minimal DC internalization, DC processing, MHC antigen presentation, and antigen-specific T cell activation, resulting in an attenuated allergic response and validating its efficacy as a potential immunotherapeutic candidate to treat egg allergy.	ova-man	0-7	major histocompatibility complex, class I, C	Homo sapiens	61-64
31122742-6	2019	The risk A-allele was associated with eight non-conservative amino acid substitutions (amino acid positions); Asp or Ser (9), Arg (14), Ala (49), Ala (73), Ala (90), Arg (97), Phe or Ser (99), and Phe or Ser (116) in the HLA-C peptide binding groove that binds peptides for presentation to cytotoxic T cells (CTL).	Serine	117-120	major histocompatibility complex, class I, C	Homo sapiens	221-226
31523674-5	2019	After mechanical measurements, single muscle fiber determined MHC isoforms using silver stain.	Silver	81-87	major histocompatibility complex, class I, C	Homo sapiens	62-65
31939156-1	2019	Major histocompatibility class I (MHC-I) molecules bind peptides derived from cellular synthesis and display them at the cell surface for recognition by receptors on T lymphocytes (TCR) or natural killer (NK) cells.	Receptor-CD3 Complex, Antigen, T-Cell	181-184	major histocompatibility complex, class I, C	Homo sapiens	34-37
31138701-5	2019	Here, we show that KIR2DS4 has a strong preference for rare peptides carrying a Trp at position 8 (p8) of 9-mer peptides bound to HLA-C*05:01.	Tryptophan	80-83	major histocompatibility complex, class I, C	Homo sapiens	130-135
31138701-6	2019	The complex of a peptide bound to HLA-C*05:01 with a Trp at p8 was sufficient for activation of primary KIR2DS4+ NK cells, independent of activation by other receptors and of prior NK cell licensing.	Tryptophan	53-56	major histocompatibility complex, class I, C	Homo sapiens	34-39
30924846-7	2019	TCB bridging CD3epsilon and HER2 or CEACAM5 could bypass MHC class I loss, partially rescuing T cell functions in mLN.	tcb	0-3	major histocompatibility complex, class I, C	Homo sapiens	57-60
30924846-8	2019	CONCLUSION: TCB should be developed in BC to circumvent low MHC/peptide complexes.	tcb	12-15	major histocompatibility complex, class I, C	Homo sapiens	60-63
30578879-6	2019	We developed regression models of PASI90 response, examining the interaction between HLA-C*06:02 and drug type (adalimumab or ustekinumab) while accounting for potentially confounding clinical variables.	pasi90	34-40	major histocompatibility complex, class I, C	Homo sapiens	85-90
30237582-4	2019	Five out of 12 patients with XST-induced cADRs carried HLA-C*12:02, and all of them received XST via intravenous drip.	xuesetong	29-32	major histocompatibility complex, class I, C	Homo sapiens	55-60
30680818-0	2019	Endoplasmic reticulum aminopeptidase 1 polymorphism Ile276Met is associated with atopic dermatitis and affects the generation of an HLA-C associated antigenic epitope in vitro.	ile276met	52-61	major histocompatibility complex, class I, C	Homo sapiens	132-137
30680818-15	2019	CONCLUSION: Associations of HLA-C*05:01 allele and rs26618T>C (Ile276Met) ERAP1 polymorphism with AD, and a significant difference between these two ERAP1 variants in their ability to generate an epitope for the HLA-C*05:01 molecule was found.	ile276met	66-75	major histocompatibility complex, class I, C	Homo sapiens	28-33
30680818-15	2019	CONCLUSION: Associations of HLA-C*05:01 allele and rs26618T>C (Ile276Met) ERAP1 polymorphism with AD, and a significant difference between these two ERAP1 variants in their ability to generate an epitope for the HLA-C*05:01 molecule was found.	ile276met	66-75	major histocompatibility complex, class I, C	Homo sapiens	215-220
30710433-3	2019	Unfortunately, the effectiveness of current algorithms to identify MHC ligands from LC-MS/MS data is limited because the search algorithms used were originally developed for proteomics approaches detecting tryptic peptides.	Peptides	214-222	major histocompatibility complex, class I, C	Homo sapiens	67-70
30834155-4	2019	We observed that formoterol treatment strongly suppressed L6 myoblast differentiation and the expression of myosin heavy chain (MHC) in a dose- and time-dependent manner.	Formoterol Fumarate	17-27	major histocompatibility complex, class I, C	Homo sapiens	108-126
30834155-4	2019	We observed that formoterol treatment strongly suppressed L6 myoblast differentiation and the expression of myosin heavy chain (MHC) in a dose- and time-dependent manner.	Formoterol Fumarate	17-27	major histocompatibility complex, class I, C	Homo sapiens	128-131
30834155-5	2019	Showing that both long-acting agonist (formoterol) and short-acting agonist (terbutaline) inhibited the induction of MHC protein, whereas beta2-AR antagonist (ICI-118,551) upregulated MHC expression, we clearly demonstrated that beta2-AR is involved in L6 myoblast differentiation.	Formoterol Fumarate	39-49	major histocompatibility complex, class I, C	Homo sapiens	117-120
30834155-5	2019	Showing that both long-acting agonist (formoterol) and short-acting agonist (terbutaline) inhibited the induction of MHC protein, whereas beta2-AR antagonist (ICI-118,551) upregulated MHC expression, we clearly demonstrated that beta2-AR is involved in L6 myoblast differentiation.	Terbutaline	77-88	major histocompatibility complex, class I, C	Homo sapiens	117-120
29507106-7	2018	Collectively, our results indicate that vaccination with Thr4-p3P significantly enhances T cell recognition of targets presenting the wild-type TEIPP epitope and that higher immunogenicity is not necessarily directly related to MHC/peptide complex stability, opening for the possibility to design novel peptide vaccines with reduced MHC/peptide complex stability.	thr4-p3p	57-65	major histocompatibility complex, class I, C	Homo sapiens	333-336
30076588-7	2018	METHODS: The patient was typed for the HLA-C locus at high resolution via polymerase chain reaction sequence-specific oligonucleotide probes (PCR-SSOP) using a commercial kit (LAB Type, One Lambda Inc., Canoga Park, CA, USA).	Oligonucleotides	118-133	major histocompatibility complex, class I, C	Homo sapiens	39-44
29997937-14	2018	PQQ (a naturally occurring antioxidant) administration inhibited C2C12 myotubes atrophy induced by TNF-alpha, as evidenced by the increase of the diameter of C2C12 myotubes, together with increased MHC levels and decreased ROS, MAFbx and MuRF-1 levels.	PQQ Cofactor	0-3	major histocompatibility complex, class I, C	Homo sapiens	198-201
28508505-9	2018	Pronounced depletion of glycogen in the MHC IIX fibers of the exercised leg verifies that the type IIX fibers were active during the heavy load contractions.	Glycogen	24-32	major histocompatibility complex, class I, C	Homo sapiens	40-43
28873544-4	2018	On the other hand, in gels made with added salt, MHC polymerization occurred, as evidenced by the electrophoresis, and the gelation resulted in a well-stabilized protein network with good physicochemical properties.	Salts	43-47	major histocompatibility complex, class I, C	Homo sapiens	49-52
28489338-5	2017	Indeed, NK cells of Treg-treated BM recipients reshaped their receptor repertoire in the presence of donor MHC in a manner suggesting attenuated donor reactivity.	treg	20-24	major histocompatibility complex, class I, C	Homo sapiens	107-110
29472733-6	2017	The cross sectional area and MHC expression were significantly higher in SHAM+EX, DHT+SED, and DHT+EX than in SHAM+SED.	Dihydrotestosterone	82-85	major histocompatibility complex, class I, C	Homo sapiens	29-32
29472733-6	2017	The cross sectional area and MHC expression were significantly higher in SHAM+EX, DHT+SED, and DHT+EX than in SHAM+SED.	Dihydrotestosterone	95-98	major histocompatibility complex, class I, C	Homo sapiens	29-32
28855257-4	2017	We found that HLA-C*06:02 predominantly presents nonamer peptides with dominant arginine anchors at the P2 and P7 positions and a preference for small hydrophobic residues at the C terminus (POmega).	Arginine	80-88	major histocompatibility complex, class I, C	Homo sapiens	14-19
27739112-5	2017	BFlh exhibited a balanced MHC distribution [mean +- SD (min-max); 47.1 +- 9.1% (32.6-71.0%) MHC-I, 35.5 +- 8.5% (21.5-60.0%) MHC-IIA, 17.4 +- 9.1% (0.0-30.9%) MHC-IIX].	bflh	0-4	major histocompatibility complex, class I, C	Homo sapiens	26-29
27739112-5	2017	BFlh exhibited a balanced MHC distribution [mean +- SD (min-max); 47.1 +- 9.1% (32.6-71.0%) MHC-I, 35.5 +- 8.5% (21.5-60.0%) MHC-IIA, 17.4 +- 9.1% (0.0-30.9%) MHC-IIX].	bflh	0-4	major histocompatibility complex, class I, C	Homo sapiens	92-95
27739112-5	2017	BFlh exhibited a balanced MHC distribution [mean +- SD (min-max); 47.1 +- 9.1% (32.6-71.0%) MHC-I, 35.5 +- 8.5% (21.5-60.0%) MHC-IIA, 17.4 +- 9.1% (0.0-30.9%) MHC-IIX].	bflh	0-4	major histocompatibility complex, class I, C	Homo sapiens	92-95
27739112-5	2017	BFlh exhibited a balanced MHC distribution [mean +- SD (min-max); 47.1 +- 9.1% (32.6-71.0%) MHC-I, 35.5 +- 8.5% (21.5-60.0%) MHC-IIA, 17.4 +- 9.1% (0.0-30.9%) MHC-IIX].	bflh	0-4	major histocompatibility complex, class I, C	Homo sapiens	92-95
28855257-6	2017	These structures revealed that HLA-C*06:02 possesses a deep peptide-binding groove comprising two electronegative B- and E-pockets that coincide with the preference for P2 and P7 arginine anchors.	Arginine	179-187	major histocompatibility complex, class I, C	Homo sapiens	31-36
28620932-4	2017	Insight into the functional specialization of the PB can be provided through investigating the proportions of type I and type II muscle fibers by staining for myosin heavy chain (MHC) isoforms using immunohistochemical methods.	pladienolide B	50-52	major histocompatibility complex, class I, C	Homo sapiens	159-177
28620932-4	2017	Insight into the functional specialization of the PB can be provided through investigating the proportions of type I and type II muscle fibers by staining for myosin heavy chain (MHC) isoforms using immunohistochemical methods.	pladienolide B	50-52	major histocompatibility complex, class I, C	Homo sapiens	179-182
28654264-5	2017	Here, we provide evidence that phytol can indeed affect the diversity of muscle fiber types both in vitro and in vivo and demonstrate that phytol can increase the expression of MHC I (p < 0.05), likely by upgrading the expression of PPARdelta, PGC-1alpha, and related miRNAs.	Phytol	139-145	major histocompatibility complex, class I, C	Homo sapiens	177-180
29056010-0	2017	[Predictive value of single nucleotide polymorphisms of HLA-C and UBE2L3 in evaluating the effect of telbivudine antiviral therapy during pregnancy].	Telbivudine	101-112	major histocompatibility complex, class I, C	Homo sapiens	56-61
29056010-1	2017	Objective: To investigate the association between single nucleotide polymorphisms (SNPs) of rs3130542 and rs4821116 in the HLA-C and UBE2L3 genes and the effect of telbivudine antiviral therapy during pregnancy in HBeAg-positive mothers through a large-sample control study, and to provide a basis for the development of individualized blocking strategies for pregnant women with a high viral load.	Telbivudine	164-175	major histocompatibility complex, class I, C	Homo sapiens	123-128
29056010-5	2017	Results: Mothers with an AA/AG genotype of rs3130542 in the HLA-C gene had a significantly higher probability of HBV DNA load >=10(3) IU/ml at the time of delivery (P < 0.05) and a significantly higher risk of failure in the prevention of mother-to-child transmission, no matter whether they started to take telbivudine at week 24 or 28 of pregnancy.	Telbivudine	314-325	major histocompatibility complex, class I, C	Homo sapiens	60-65
28807001-10	2017	Combination of anti-CTLA-4 with selumetinib negated this up-regulation of Cox-2 and Arg1, reduced the frequency of CD11+ Ly6G+ myeloid cells, and led to the accumulation of differentiating monocytes at the Ly6C+ MHC+ intermediate state in the tumor.	AZD 6244	32-43	major histocompatibility complex, class I, C	Homo sapiens	212-215
28729889-9	2017	In addition, we identified a large independent DMR at MHC, whereby 11 CpGs in RNF39 were hypermethylated in MS cases compared to controls (max.	aspartylmethionylarginine	47-50	major histocompatibility complex, class I, C	Homo sapiens	54-57
28366003-8	2017	Three different PTMs: acetylation, methylation, and trimethylation were identified in human beta-MHC and the corresponding sites were localized to the N-terminal Gly, Lys34, and Lys129, respectively, by electron capture dissociation (ECD).	Glycine	162-165	major histocompatibility complex, class I, C	Homo sapiens	97-100
28185362-5	2017	RESULTS: HLA-G, HLA-C, and HLA-F were expressed by 1st-trimester EVT and became intracellular and weaker as gestation progressed.	EVT	65-68	major histocompatibility complex, class I, C	Homo sapiens	16-21
28185362-10	2017	These results were confirmed in EVT outgrowths and Swan71 trophoblast which showed that HLA-F and HLA-G are increased on the cell surface of migrating EVT, while HLA-C was internalized.	EVT	32-35	major histocompatibility complex, class I, C	Homo sapiens	162-167
28185362-12	2017	HLA-C"s limited expression to the proliferative EVT suggests a protective role in the earliest events of implantation but not in active EVT invasion.	EVT	48-51	major histocompatibility complex, class I, C	Homo sapiens	0-5
27500470-2	2017	We have previously shown that in MHC-matched nonhuman primates (NHPs), a busulfan plus combined belatacept and anti-CD154-based regimen could induce long-lived myeloid chimerism, but without T cell chimerism.	Busulfan	73-81	major histocompatibility complex, class I, C	Homo sapiens	33-36
28438823-10	2017	CONCLUSION: A strong association was found between HLA-A*33:03 and HLA-C*03:02 alleles and allopurinol-induced SJS or TEN, especially in an Asian population.	Allopurinol	91-102	major histocompatibility complex, class I, C	Homo sapiens	67-72
28062682-11	2017	Conclusions: HLA-C*04:01 predisposes to nevirapine-induced SJS/TEN in sub-Saharan Africans, but not to other hypersensitivity phenotypes.	Nevirapine	40-50	major histocompatibility complex, class I, C	Homo sapiens	13-18
28122963-5	2017	By repairing the deletion, we resurrected 11 alleles of KIR2DP1F , the functional antecedent of KIR2DP1 We demonstrate how K44-KIR2DP1F with lysine 44 recognized C1+HLA-C, whereas T44-KIR2DP1F recognized C2+HLA-C.	Lysine	141-147	major histocompatibility complex, class I, C	Homo sapiens	165-170
28122963-5	2017	By repairing the deletion, we resurrected 11 alleles of KIR2DP1F , the functional antecedent of KIR2DP1 We demonstrate how K44-KIR2DP1F with lysine 44 recognized C1+HLA-C, whereas T44-KIR2DP1F recognized C2+HLA-C.	Lysine	141-147	major histocompatibility complex, class I, C	Homo sapiens	207-212
27942960-3	2016	Sprague-Dawley rats possessing ~99% alpha-MHC were treated with propylthiouracil to result in 100% beta-MHC.	Propylthiouracil	64-80	major histocompatibility complex, class I, C	Homo sapiens	104-107
28401156-7	2017	Molecular docking simulation demonstrated that the epitope could bind to the binding groove of MHC II and MHC I molecules by several hydrogen bonds.	Hydrogen	133-141	major histocompatibility complex, class I, C	Homo sapiens	95-98
28401156-7	2017	Molecular docking simulation demonstrated that the epitope could bind to the binding groove of MHC II and MHC I molecules by several hydrogen bonds.	Hydrogen	133-141	major histocompatibility complex, class I, C	Homo sapiens	106-109
28772259-2	2017	A percentage of the treated patients experience a potentially life-threatening hypersensitivity reaction, which was shown to be associated with the presence of the class I MHC allele, HLA-B*57:01; hence genotyping for HLA-B*57:01 prior to starting abacavir is nowadays recommended in international HIV treatment guidelines.	abacavir	248-256	major histocompatibility complex, class I, C	Homo sapiens	172-175
27942960-8	2016	The ATP study demonstrated that, in beta-MHC containing fibers, K 1 (ATP association constant) was greater (1.7x), k 2 and k -2 (cross-bridge detachment and its reversal rate constants) were smaller (x0.6).	Adenosine Triphosphate	4-7	major histocompatibility complex, class I, C	Homo sapiens	41-44
27942960-8	2016	The ATP study demonstrated that, in beta-MHC containing fibers, K 1 (ATP association constant) was greater (1.7x), k 2 and k -2 (cross-bridge detachment and its reversal rate constants) were smaller (x0.6).	Adenosine Triphosphate	69-72	major histocompatibility complex, class I, C	Homo sapiens	41-44
27554620-10	2016	There was a trend of a higher carrier rate of HLA-C*06:02 in the phenobarbital-induced SCARs when compared with those in the tolerant controls (29.63% vs. 11.11%, p = 0.059, OR 3.31, 95% CI 0.88-13.31).	Phenobarbital	65-78	major histocompatibility complex, class I, C	Homo sapiens	46-51
27566374-4	2016	RESULTS: In Young, Middle and Old age groups, by SDS-PAGE MHCI comprised ~1/3 and MHCII ~2/3 of total MHC.	Sodium Dodecyl Sulfate	49-52	major histocompatibility complex, class I, C	Homo sapiens	58-61
26842420-1	2016	Single muscle fiber sodium dodecyl sulfate polyacrylamide gel-electrophoresis (SDS-PAGE) is a sensitive technique for determining skeletal muscle myosin heavy chain (MHC) composition of human biopsy samples.	Sodium Dodecyl Sulfate	20-42	major histocompatibility complex, class I, C	Homo sapiens	166-169
27590508-4	2016	Transcriptomic profiles and function pathway analysis identified differentially expressed gene signatures for JLPR cells and JLPS cells, which differential expression levels of five genes (ATF5, CD79B, MHC, Myosin, and SAP18) in ascorbate-resistant cells were related to phosphoinositide 3 kinase, cdc42, DNA methylation and transcriptional repression, polyamine regulation, and integrin-linked kinase signaling pathways.	Ascorbic Acid	229-238	major histocompatibility complex, class I, C	Homo sapiens	202-205
26842420-1	2016	Single muscle fiber sodium dodecyl sulfate polyacrylamide gel-electrophoresis (SDS-PAGE) is a sensitive technique for determining skeletal muscle myosin heavy chain (MHC) composition of human biopsy samples.	polyacrylamide	43-57	major histocompatibility complex, class I, C	Homo sapiens	166-169
26842420-1	2016	Single muscle fiber sodium dodecyl sulfate polyacrylamide gel-electrophoresis (SDS-PAGE) is a sensitive technique for determining skeletal muscle myosin heavy chain (MHC) composition of human biopsy samples.	Sodium Dodecyl Sulfate	79-82	major histocompatibility complex, class I, C	Homo sapiens	166-169
26633653-4	2015	However, the mZac1-enhanced AP-1 transcriptional activity was suppressed by curcumin, indicating the anti-inflammatory property of this botanical agent and is exhibited by blocking the AP-1-mediated cross-talk between PSORS1 and PSORS4.	Curcumin	76-84	major histocompatibility complex, class I, C	Homo sapiens	218-224
25918017-6	2016	HLA-C*01:02, which is closely linked to HLA-B*59:01, had a weaker but notable association with methazolamide-induced SJS/TEN compared with the tolerant controls (OR=12.1; P=0.016) and general population (OR=15.5; P=2.0 x 10(-3)).	Methazolamide	95-108	major histocompatibility complex, class I, C	Homo sapiens	0-5
27076335-4	2016	To overcome this problem, we develop an ensemble prediction-based Web server, which we call MetaMHCpan, consisting of two parts: MetaMHCIpan and MetaMHCIIpan, for predicting peptides which can bind MHC-I and MHC-II, respectively.	metamhcpan	92-102	major histocompatibility complex, class I, C	Homo sapiens	133-136
27076335-4	2016	To overcome this problem, we develop an ensemble prediction-based Web server, which we call MetaMHCpan, consisting of two parts: MetaMHCIpan and MetaMHCIIpan, for predicting peptides which can bind MHC-I and MHC-II, respectively.	metamhciipan	145-157	major histocompatibility complex, class I, C	Homo sapiens	96-99
26241463-5	2015	Myosin heavy chain (MHC) cross-linking, another marker of protein oxidation, was greater in MAP with 80% oxygen than 0% and 20% oxygen.	Oxygen	105-111	major histocompatibility complex, class I, C	Homo sapiens	0-18
26241463-5	2015	Myosin heavy chain (MHC) cross-linking, another marker of protein oxidation, was greater in MAP with 80% oxygen than 0% and 20% oxygen.	Oxygen	105-111	major histocompatibility complex, class I, C	Homo sapiens	20-23
26241463-5	2015	Myosin heavy chain (MHC) cross-linking, another marker of protein oxidation, was greater in MAP with 80% oxygen than 0% and 20% oxygen.	Oxygen	128-134	major histocompatibility complex, class I, C	Homo sapiens	0-18
26241463-5	2015	Myosin heavy chain (MHC) cross-linking, another marker of protein oxidation, was greater in MAP with 80% oxygen than 0% and 20% oxygen.	Oxygen	128-134	major histocompatibility complex, class I, C	Homo sapiens	20-23
26086150-10	2015	CONCLUSION: Evidence of associations between co-trimoxazole-induced SJS/TEN and HLA alleles including HLA-B*15:02, HLA-C*06:02, and HLA-C*08:01 were found in the study population.	Trimethoprim, Sulfamethoxazole Drug Combination	45-59	major histocompatibility complex, class I, C	Homo sapiens	115-120
26342069-6	2015	TnTF72L increased the rate of XB distortion dynamics by 49% in alpha-MHC fibers but had no effect in beta-MHC fibers; these observations suggest that TnTF72L augmented XB detachment kinetics in alpha-MHC, but not beta-MHC, fibers.	tntf72l	0-7	major histocompatibility complex, class I, C	Homo sapiens	69-72
26342069-7	2015	TnTF72L increased the negative impact of strained XBs on the force-bearing XBs by 39% in alpha-MHC fibers but had no effect in beta-MHC fibers.	CHEMBL4082603	50-53	major histocompatibility complex, class I, C	Homo sapiens	95-98
26086150-7	2015	RESULTS: The frequencies of three alleles of HLA, namely HLA-B*15:02, HLA-C*06:02, and HLA-C*08:01, were significantly higher in the co-trimoxazole-induced SJS/TEN group compared with controls.	trimoxazole	136-147	major histocompatibility complex, class I, C	Homo sapiens	70-75
26613595-6	2015	A secondary effect was located at the leucine at amino-acid position 116 in the epitope-binding site of HLA-C (P = 1.69 x 10(-14)), completely tagging the HLA-C*15:02 allele.	Leucine	38-45	major histocompatibility complex, class I, C	Homo sapiens	104-109
26613595-6	2015	A secondary effect was located at the leucine at amino-acid position 116 in the epitope-binding site of HLA-C (P = 1.69 x 10(-14)), completely tagging the HLA-C*15:02 allele.	Leucine	38-45	major histocompatibility complex, class I, C	Homo sapiens	155-160
26735294-4	2015	We examined unadjusted MHC-related differences in warfarin eligibility and warfarin receipt among warfarin-eligible patients, using logistic regression for any MHC and for specific MHCs (adjusting for sociodemographic and clinical characteristics).	Warfarin	50-58	major histocompatibility complex, class I, C	Homo sapiens	23-26
26735294-4	2015	We examined unadjusted MHC-related differences in warfarin eligibility and warfarin receipt among warfarin-eligible patients, using logistic regression for any MHC and for specific MHCs (adjusting for sociodemographic and clinical characteristics).	Warfarin	75-83	major histocompatibility complex, class I, C	Homo sapiens	23-26
26735294-4	2015	We examined unadjusted MHC-related differences in warfarin eligibility and warfarin receipt among warfarin-eligible patients, using logistic regression for any MHC and for specific MHCs (adjusting for sociodemographic and clinical characteristics).	Warfarin	75-83	major histocompatibility complex, class I, C	Homo sapiens	23-26
26735294-7	2015	Warfarin-eligible patients with MHC were less likely to receive warfarin than those without MHC (adjusted odds ratio [AOR], 0.90; 95% CI, 0.87-0.94).	Warfarin	0-8	major histocompatibility complex, class I, C	Homo sapiens	32-35
26735294-7	2015	Warfarin-eligible patients with MHC were less likely to receive warfarin than those without MHC (adjusted odds ratio [AOR], 0.90; 95% CI, 0.87-0.94).	Warfarin	0-8	major histocompatibility complex, class I, C	Homo sapiens	92-95
26735294-7	2015	Warfarin-eligible patients with MHC were less likely to receive warfarin than those without MHC (adjusted odds ratio [AOR], 0.90; 95% CI, 0.87-0.94).	Warfarin	64-72	major histocompatibility complex, class I, C	Homo sapiens	32-35
26735294-8	2015	The association between MHC and warfarin receipt among warfarin-eligible patients varied by specific MHC.	Warfarin	32-40	major histocompatibility complex, class I, C	Homo sapiens	24-27
26735294-8	2015	The association between MHC and warfarin receipt among warfarin-eligible patients varied by specific MHC.	Warfarin	32-40	major histocompatibility complex, class I, C	Homo sapiens	101-104
26735294-8	2015	The association between MHC and warfarin receipt among warfarin-eligible patients varied by specific MHC.	Warfarin	55-63	major histocompatibility complex, class I, C	Homo sapiens	24-27
26239392-2	2015	HLA-C*14:02:13 differs from HLA-C*14:02:01 by a silent G to A substitution at nucleotide position 400 in exon 2, where lysine at position 66 remains unchanged.	Lysine	119-125	major histocompatibility complex, class I, C	Homo sapiens	0-5
26086150-7	2015	RESULTS: The frequencies of three alleles of HLA, namely HLA-B*15:02, HLA-C*06:02, and HLA-C*08:01, were significantly higher in the co-trimoxazole-induced SJS/TEN group compared with controls.	trimoxazole	136-147	major histocompatibility complex, class I, C	Homo sapiens	87-92
26086150-8	2015	The risks for co-trimoxazole-induced SJS/TEN in patients with the HLA-B*15:02, HLA-C*06:02, or HLA-C*08:01 allele were about 3-11-fold higher when compared with those who did not carry one of these alleles.	Trimethoprim, Sulfamethoxazole Drug Combination	14-28	major histocompatibility complex, class I, C	Homo sapiens	79-84
26086150-8	2015	The risks for co-trimoxazole-induced SJS/TEN in patients with the HLA-B*15:02, HLA-C*06:02, or HLA-C*08:01 allele were about 3-11-fold higher when compared with those who did not carry one of these alleles.	Trimethoprim, Sulfamethoxazole Drug Combination	14-28	major histocompatibility complex, class I, C	Homo sapiens	95-100
26086150-10	2015	CONCLUSION: Evidence of associations between co-trimoxazole-induced SJS/TEN and HLA alleles including HLA-B*15:02, HLA-C*06:02, and HLA-C*08:01 were found in the study population.	Trimethoprim, Sulfamethoxazole Drug Combination	45-59	major histocompatibility complex, class I, C	Homo sapiens	132-137
23835800-3	2014	RESULTS: By separation SDS-PAGE-Coomassie and Western blot, only conventional MHC are present.	Sodium Dodecyl Sulfate	23-26	major histocompatibility complex, class I, C	Homo sapiens	78-81
25297339-6	2015	Cryopreservation of MHC multimers was feasible for at least 6 months, when they were dissolved in buffer containing 5-16% glycerol (v/v) and 0.5% serum albumin (w/v).	Glycerol	122-130	major histocompatibility complex, class I, C	Homo sapiens	20-23
25311805-6	2014	Matrices were used to generate a large panel of HLA-C-specific peptide-binding data and update our pan-specific NetMHCpan predictor, whose predictive performance was considerably improved with respect to peptide binding to HLA-C.	netmhcpan	112-121	major histocompatibility complex, class I, C	Homo sapiens	223-228
25135637-2	2014	We have established and interrogated a database of around 70,000 naturally processed MHC-bound peptides and demonstrate that cysteine-containing peptides are presented on the surface of cells in an MHC allomorph-dependent manner and comprise on average 5-10% of the immunopeptidome.	Cysteine	125-133	major histocompatibility complex, class I, C	Homo sapiens	85-88
25135637-2	2014	We have established and interrogated a database of around 70,000 naturally processed MHC-bound peptides and demonstrate that cysteine-containing peptides are presented on the surface of cells in an MHC allomorph-dependent manner and comprise on average 5-10% of the immunopeptidome.	Cysteine	125-133	major histocompatibility complex, class I, C	Homo sapiens	198-201
24744588-16	2014	The same was observed for the HLA-C*07 allele with AR in 57%, 27% and 18% in recipients being homozygous, heterozygous and lacking HLA-C*07 respectively (P = 0.003).	Argon	51-53	major histocompatibility complex, class I, C	Homo sapiens	30-35
24744588-16	2014	The same was observed for the HLA-C*07 allele with AR in 57%, 27% and 18% in recipients being homozygous, heterozygous and lacking HLA-C*07 respectively (P = 0.003).	Argon	51-53	major histocompatibility complex, class I, C	Homo sapiens	131-136
24600035-5	2014	A highly conserved residue Arg(97) in the CDR3alpha loop played a major role in recognition of peptide and MHC to form a stabilizing ball-and-socket interaction with the MHC and peptide, contributing to the selection of the public TCR clonotype.	Arginine	27-30	major histocompatibility complex, class I, C	Homo sapiens	107-110
24600035-5	2014	A highly conserved residue Arg(97) in the CDR3alpha loop played a major role in recognition of peptide and MHC to form a stabilizing ball-and-socket interaction with the MHC and peptide, contributing to the selection of the public TCR clonotype.	Arginine	27-30	major histocompatibility complex, class I, C	Homo sapiens	170-173
25911107-0	2015	Histone Deacetylase 3 (HDAC3)-dependent Reversible Lysine Acetylation of Cardiac Myosin Heavy Chain Isoforms Modulates Their Enzymatic and Motor Activity.	Lysine	51-57	major histocompatibility complex, class I, C	Homo sapiens	81-99
25911107-6	2015	Biomechanical studies revealed that lysine acetylation significantly decreased the Km for the actin-activated ATPase activity of MHC isoforms.	Lysine	36-42	major histocompatibility complex, class I, C	Homo sapiens	129-132
26053620-2	2015	We reported that clenbuterol (CB) induced masseter muscle hypertrophy and slow-to-fast myosin heavy chain (MHC) isoform transition through direct muscle beta2-adrenergic receptor stimulation.	Clenbuterol	17-28	major histocompatibility complex, class I, C	Homo sapiens	87-105
26053620-2	2015	We reported that clenbuterol (CB) induced masseter muscle hypertrophy and slow-to-fast myosin heavy chain (MHC) isoform transition through direct muscle beta2-adrenergic receptor stimulation.	Clenbuterol	17-28	major histocompatibility complex, class I, C	Homo sapiens	107-110
26053620-6	2015	RESULTS AND CONCLUSION: Masseter muscle weight in the DEX-treated group was significantly lower than that in the Control group, as expected, but co-treatment with CB suppressed the DEX-induced masseter muscle atrophy, concomitantly with inhibition of fast-to-slow MHC isoforms transition.	Dextromethorphan	54-57	major histocompatibility complex, class I, C	Homo sapiens	264-267
25282040-4	2015	Addition of 1500ppm green tea extract was found to modify MHC as evaluated by SDS-PAGE combining both protein staining and specific thiol staining, indicating that protein modifications generated through reactions of green tea phenolic compounds with protein thiols, disrupted the meat emulsion properties leading to reduced water holding capacity and textural stability.	Sodium Dodecyl Sulfate	78-81	major histocompatibility complex, class I, C	Homo sapiens	58-61
25282040-4	2015	Addition of 1500ppm green tea extract was found to modify MHC as evaluated by SDS-PAGE combining both protein staining and specific thiol staining, indicating that protein modifications generated through reactions of green tea phenolic compounds with protein thiols, disrupted the meat emulsion properties leading to reduced water holding capacity and textural stability.	Sulfhydryl Compounds	132-137	major histocompatibility complex, class I, C	Homo sapiens	58-61
25282040-4	2015	Addition of 1500ppm green tea extract was found to modify MHC as evaluated by SDS-PAGE combining both protein staining and specific thiol staining, indicating that protein modifications generated through reactions of green tea phenolic compounds with protein thiols, disrupted the meat emulsion properties leading to reduced water holding capacity and textural stability.	Sulfhydryl Compounds	259-265	major histocompatibility complex, class I, C	Homo sapiens	58-61
25348595-2	2014	Sodium dithionite sensitive azobenzene-containing (Abc) peptides were applied for the temporary stabilization of recombinant MHC complexes, which can then be employed to generate libraries of MHC tetramers after exchange with a novel epitope.	Dithionite	0-17	major histocompatibility complex, class I, C	Homo sapiens	125-128
25348595-2	2014	Sodium dithionite sensitive azobenzene-containing (Abc) peptides were applied for the temporary stabilization of recombinant MHC complexes, which can then be employed to generate libraries of MHC tetramers after exchange with a novel epitope.	Dithionite	0-17	major histocompatibility complex, class I, C	Homo sapiens	192-195
25348595-2	2014	Sodium dithionite sensitive azobenzene-containing (Abc) peptides were applied for the temporary stabilization of recombinant MHC complexes, which can then be employed to generate libraries of MHC tetramers after exchange with a novel epitope.	azobenzene	28-38	major histocompatibility complex, class I, C	Homo sapiens	125-128
25348595-2	2014	Sodium dithionite sensitive azobenzene-containing (Abc) peptides were applied for the temporary stabilization of recombinant MHC complexes, which can then be employed to generate libraries of MHC tetramers after exchange with a novel epitope.	azobenzene	28-38	major histocompatibility complex, class I, C	Homo sapiens	192-195
25294906-0	2014	MHC class I loss is a frequent mechanism of immune escape in papillary thyroid cancer that is reversed by interferon and selumetinib treatment in vitro.	AZD 6244	121-132	major histocompatibility complex, class I, C	Homo sapiens	0-3
24860572-10	2014	In the present "Hypothesis & Theory," we reviewed the current knowledge on HLA-C mismatches and alloreactivity.	Adenosine Monophosphate	28-31	major histocompatibility complex, class I, C	Homo sapiens	79-84
23835800-3	2014	RESULTS: By separation SDS-PAGE-Coomassie and Western blot, only conventional MHC are present.	coomassie	32-41	major histocompatibility complex, class I, C	Homo sapiens	78-81
23901134-1	2013	OBJECTIVE: The MHC exerts the greatest contribution to RA susceptibility, where certain HLA-DRB1 alleles confer the greatest risk.	Radium	55-57	major histocompatibility complex, class I, C	Homo sapiens	15-18
25495410-7	2014	RESULTS: The frequency of HLA-C*08:01 allele in PHT-induced MPE was higher than that in the PHT-tolerant group (pc=0.0179) or in the MM population (pc<0.0001).	Phenytoin	48-51	major histocompatibility complex, class I, C	Homo sapiens	26-31
25495410-7	2014	RESULTS: The frequency of HLA-C*08:01 allele in PHT-induced MPE was higher than that in the PHT-tolerant group (pc=0.0179) or in the MM population (pc<0.0001).	Phenytoin	92-95	major histocompatibility complex, class I, C	Homo sapiens	26-31
25495410-9	2014	CONCLUSION: Our data suggest the HLA-A*02:01:01/-B*35:01:01/-C*04:01:01 haplotype may be a biomarker for LTG-induced MPE and the HLA-C*08:01 allele for PHT-induced MPE.	Phenytoin	152-155	major histocompatibility complex, class I, C	Homo sapiens	129-134
24482817-10	2014	Physical proximity between CD1d, MHC and GM1 molecules was also detected in the plasma membrane.	G(M1) Ganglioside	41-44	major histocompatibility complex, class I, C	Homo sapiens	33-36
23845398-7	2013	Myosin heavy chain (MHC) isoforms protein and messenger RNA (mRNA) expression were determined with SDS-PAGE (sodium dodecyl sulfate polyacrylamide gel electrophoresis) and RT-PCR (real-time polymerase chain reaction), respectively; IGF-1 (insulin-like growth factor 1), MuRF-1 (muscle RING-finger protein-1), and MAFbx (muscle atrophy f-box) mRNA expression were determined with quantitative RT-PCR.	Sodium Dodecyl Sulfate	99-102	major histocompatibility complex, class I, C	Homo sapiens	0-18
23861374-8	2013	In contrast, MHC-D2 mice showed increased survival rate after DOX treatment, and this was associated with a six-fold increase in myocardial glucose metabolism and improved cardiac function.	Doxorubicin	62-65	major histocompatibility complex, class I, C	Homo sapiens	13-16
23861374-9	2013	Myocardial activity and expression of AMPK, GLUT1, and Akt were also elevated in MHC-D2 and WT mice following DOX treatment.	Doxorubicin	110-113	major histocompatibility complex, class I, C	Homo sapiens	81-84
23756162-1	2013	HLA-DO (H2-O in mice) is an intracellular non-classical MHC class II molecule (MHCII).	hla-do	0-6	major histocompatibility complex, class I, C	Homo sapiens	56-59
23756162-1	2013	HLA-DO (H2-O in mice) is an intracellular non-classical MHC class II molecule (MHCII).	Water	8-12	major histocompatibility complex, class I, C	Homo sapiens	56-59
23845398-7	2013	Myosin heavy chain (MHC) isoforms protein and messenger RNA (mRNA) expression were determined with SDS-PAGE (sodium dodecyl sulfate polyacrylamide gel electrophoresis) and RT-PCR (real-time polymerase chain reaction), respectively; IGF-1 (insulin-like growth factor 1), MuRF-1 (muscle RING-finger protein-1), and MAFbx (muscle atrophy f-box) mRNA expression were determined with quantitative RT-PCR.	Sodium Dodecyl Sulfate	99-102	major histocompatibility complex, class I, C	Homo sapiens	20-23
23845398-7	2013	Myosin heavy chain (MHC) isoforms protein and messenger RNA (mRNA) expression were determined with SDS-PAGE (sodium dodecyl sulfate polyacrylamide gel electrophoresis) and RT-PCR (real-time polymerase chain reaction), respectively; IGF-1 (insulin-like growth factor 1), MuRF-1 (muscle RING-finger protein-1), and MAFbx (muscle atrophy f-box) mRNA expression were determined with quantitative RT-PCR.	Sodium Dodecyl Sulfate	109-131	major histocompatibility complex, class I, C	Homo sapiens	0-18
23732814-3	2013	Therefore, we generated mice with cardiac-specific, tamoxifen (TAM)-inducible overexpression of a human HO-1 (hHO-1) transgene (myosin heavy chain (MHC)-HO-1 mice) by breeding mice with cardiac-specific expression of a TAM-inducible Cre recombinase (MHC-Cre mice), with mice containing an hHO-1 transgene preceded by a floxed-stop signal.	Tamoxifen	63-66	major histocompatibility complex, class I, C	Homo sapiens	250-253
23732814-4	2013	MHC-HO-1 mice overexpress HO-1 mRNA and the enzymatically active protein following TAM administration (40 mg/kg body weight on 2 consecutive days).	Tamoxifen	83-86	major histocompatibility complex, class I, C	Homo sapiens	0-3
23732814-3	2013	Therefore, we generated mice with cardiac-specific, tamoxifen (TAM)-inducible overexpression of a human HO-1 (hHO-1) transgene (myosin heavy chain (MHC)-HO-1 mice) by breeding mice with cardiac-specific expression of a TAM-inducible Cre recombinase (MHC-Cre mice), with mice containing an hHO-1 transgene preceded by a floxed-stop signal.	Tamoxifen	52-61	major histocompatibility complex, class I, C	Homo sapiens	128-146
23732814-3	2013	Therefore, we generated mice with cardiac-specific, tamoxifen (TAM)-inducible overexpression of a human HO-1 (hHO-1) transgene (myosin heavy chain (MHC)-HO-1 mice) by breeding mice with cardiac-specific expression of a TAM-inducible Cre recombinase (MHC-Cre mice), with mice containing an hHO-1 transgene preceded by a floxed-stop signal.	Tamoxifen	52-61	major histocompatibility complex, class I, C	Homo sapiens	148-151
23732814-5	2013	In MHC-Cre controls, TAM administration leads to severe, acute cardiac toxicity, cardiomyocyte necrosis, and 80% mortality by day 3.	Tamoxifen	21-24	major histocompatibility complex, class I, C	Homo sapiens	3-6
23732814-3	2013	Therefore, we generated mice with cardiac-specific, tamoxifen (TAM)-inducible overexpression of a human HO-1 (hHO-1) transgene (myosin heavy chain (MHC)-HO-1 mice) by breeding mice with cardiac-specific expression of a TAM-inducible Cre recombinase (MHC-Cre mice), with mice containing an hHO-1 transgene preceded by a floxed-stop signal.	Tamoxifen	63-66	major histocompatibility complex, class I, C	Homo sapiens	128-146
23732814-3	2013	Therefore, we generated mice with cardiac-specific, tamoxifen (TAM)-inducible overexpression of a human HO-1 (hHO-1) transgene (myosin heavy chain (MHC)-HO-1 mice) by breeding mice with cardiac-specific expression of a TAM-inducible Cre recombinase (MHC-Cre mice), with mice containing an hHO-1 transgene preceded by a floxed-stop signal.	Tamoxifen	63-66	major histocompatibility complex, class I, C	Homo sapiens	148-151
23732814-7	2013	In MHC-HO-1 mice, HO-1 overexpression ameliorates the depression of cardiac function and high mortality rate observed in MHC-Cre mice following TAM administration and attenuates cardiomyocyte necrosis and neutrophil infiltration.	Tamoxifen	144-147	major histocompatibility complex, class I, C	Homo sapiens	3-6
23849069-4	2013	HLA-C*03:190 was identical to HLA-C*03:02:01 with the exception of a nucleotide change at codon 131 in exon 3 (CGC TGC), and resulted in the amino acid change from Arginine to Cysteine.	Arginine	164-172	major histocompatibility complex, class I, C	Homo sapiens	0-5
23849069-4	2013	HLA-C*03:190 was identical to HLA-C*03:02:01 with the exception of a nucleotide change at codon 131 in exon 3 (CGC TGC), and resulted in the amino acid change from Arginine to Cysteine.	Arginine	164-172	major histocompatibility complex, class I, C	Homo sapiens	30-35
23849069-4	2013	HLA-C*03:190 was identical to HLA-C*03:02:01 with the exception of a nucleotide change at codon 131 in exon 3 (CGC TGC), and resulted in the amino acid change from Arginine to Cysteine.	Cysteine	176-184	major histocompatibility complex, class I, C	Homo sapiens	0-5
23849069-4	2013	HLA-C*03:190 was identical to HLA-C*03:02:01 with the exception of a nucleotide change at codon 131 in exon 3 (CGC TGC), and resulted in the amino acid change from Arginine to Cysteine.	Cysteine	176-184	major histocompatibility complex, class I, C	Homo sapiens	30-35
23463416-2	2013	The improved technique of SDS-PAGE and 2DE were used to separate porcine MHC isoforms.	Sodium Dodecyl Sulfate	26-29	major histocompatibility complex, class I, C	Homo sapiens	73-76
23611695-3	2013	The MICA-129 methionine (Met) allele, particularly Met/Met homozygosity, was strongly associated with both cutaneous psoriasis (PsC) and psoriatic arthritis (PsA) independently of HLA-B and HLA-C in Toronto patients, and was also associated with PsA in St. John"s patients, but with no additional effect of Met/Met homozygosity.	Methionine	13-23	major histocompatibility complex, class I, C	Homo sapiens	190-195
23463416-4	2013	Up to 45% w/v of glycerol, 8% w/v of acrylamide content, and 25 h of electrophoretic time at 70 V allowed a clear separation of MHC isoforms.	Glycerol	17-25	major histocompatibility complex, class I, C	Homo sapiens	128-131
23463416-4	2013	Up to 45% w/v of glycerol, 8% w/v of acrylamide content, and 25 h of electrophoretic time at 70 V allowed a clear separation of MHC isoforms.	Acrylamide	37-47	major histocompatibility complex, class I, C	Homo sapiens	128-131
23463416-5	2013	Major MHC isoforms such as slow, 2a, 2x, and 2b were clearly separated by SDS-PAGE.	Sodium Dodecyl Sulfate	74-77	major histocompatibility complex, class I, C	Homo sapiens	6-9
23463416-7	2013	Therefore, four MHC isoforms such as slow/I, 2a, 2x, and 2b could be identified by the improved SDS-PAGE technique, 2DE and MS.	Sodium Dodecyl Sulfate	96-99	major histocompatibility complex, class I, C	Homo sapiens	16-19
23396903-0	2012	Vitamin C Up-regulates Expression of CD80, CD86 and MHC Class II on Dendritic Cell Line, DC-1 Via the Activation of p38 MAPK.	Ascorbic Acid	0-9	major histocompatibility complex, class I, C	Homo sapiens	52-55
23902989-3	2013	Expression of slow-twitch MHC isoforms was significantly increased in BO-rats with/without RAPA treatment, compared with controls, but the magnitude of the increase was much smaller in RAPA-treated BO-rats.	Sirolimus	91-95	major histocompatibility complex, class I, C	Homo sapiens	26-29
23902989-3	2013	Expression of slow-twitch MHC isoforms was significantly increased in BO-rats with/without RAPA treatment, compared with controls, but the magnitude of the increase was much smaller in RAPA-treated BO-rats.	Sirolimus	185-189	major histocompatibility complex, class I, C	Homo sapiens	26-29
23396903-4	2012	In the presence of vitamin C, the expression of CD80, CD86, and MHC molecules was increased, but it was decreased by the pre-treatment of SB203580, p38 MAPK-specific inhibitor.	Ascorbic Acid	19-28	major histocompatibility complex, class I, C	Homo sapiens	64-67
23396903-4	2012	In the presence of vitamin C, the expression of CD80, CD86, and MHC molecules was increased, but it was decreased by the pre-treatment of SB203580, p38 MAPK-specific inhibitor.	SB 203580	138-146	major histocompatibility complex, class I, C	Homo sapiens	64-67
23396903-6	2012	Taken together, these results suggest that vitamin C could enhance the activity of dendritic cells via the up-regulation of the expression of CD80, CD86, and MHC molecules and the activation of p38 MAPK is related to this process.	Ascorbic Acid	43-52	major histocompatibility complex, class I, C	Homo sapiens	158-161
22832093-3	2012	At low phosphate concentrations, phosphate is removed by coprecipitation of phosphate during the transformation of MHC to calcite.	Phosphates	7-16	major histocompatibility complex, class I, C	Homo sapiens	115-118
22990573-6	2012	We have also found that in the U group, type 2 MHC in the vastus lateralis muscle is positively correlated with basal fT:C ratio (r = 0.63, p = 0.01).	ft	118-120	major histocompatibility complex, class I, C	Homo sapiens	47-50
22832093-1	2012	The sorption behavior and mechanism of phosphate on monohydrocalcite (CaCO(3) H(2)O: MHC) were examined using batch sorption experiments as a function of phosphate concentrations, ionic strengths, temperatures, and reaction times.	Phosphates	39-48	major histocompatibility complex, class I, C	Homo sapiens	85-88
22832093-3	2012	At low phosphate concentrations, phosphate is removed by coprecipitation of phosphate during the transformation of MHC to calcite.	Phosphates	33-42	major histocompatibility complex, class I, C	Homo sapiens	115-118
22832093-3	2012	At low phosphate concentrations, phosphate is removed by coprecipitation of phosphate during the transformation of MHC to calcite.	Phosphates	33-42	major histocompatibility complex, class I, C	Homo sapiens	115-118
22832093-6	2012	The adsorption of phosphate on MHC depends strongly on ionic strength, but slightly on temperature.	Phosphates	18-27	major histocompatibility complex, class I, C	Homo sapiens	31-34
22832093-7	2012	The maximum adsorption capacities of MHC obtained from the regression of the experimental data to the Langmuir equation are higher than those reported for stable calcium carbonate (calcite or aragonite) in any conditions.	Calcium Carbonate	162-179	major histocompatibility complex, class I, C	Homo sapiens	37-40
22832093-13	2012	Therefore, the higher solubility of MHC facilitates the formation of the calcium phosphates more than with calcite and aragonite.	Calcium Phosphates	73-91	major histocompatibility complex, class I, C	Homo sapiens	36-39
22841358-9	2012	Relative expression of MHC proteins was determined by SDS-PAGE electrophoresis.	Sodium Dodecyl Sulfate	54-57	major histocompatibility complex, class I, C	Homo sapiens	23-26
22383964-9	2012	RESULT: The performance of TEPITOPEpan has been extensively evaluated using various data sets from different viewpoints: predicting MHC binding peptides, identifying HLA ligands and T-cell epitopes and recognizing binding cores.	tepitopepan	27-38	major histocompatibility complex, class I, C	Homo sapiens	132-135
22349184-10	2012	When assembled on PLL-5.7-PEG-coated microspheres, poly(I:C) was blocked from triggering class I MHC molecule expression on HFFs.	Polyethylene Glycols	26-29	major histocompatibility complex, class I, C	Homo sapiens	97-100
23041569-7	2012	One of these, KIR049-4, was an inhibitory KIR3DL that bound MHC-I tetramers and prevented activation, degranulation, and cytokine production by macaque NK cells after engagement with specific MHC-I molecules on the surface of target cells.	kir3dl	42-48	major histocompatibility complex, class I, C	Homo sapiens	60-63
23041569-7	2012	One of these, KIR049-4, was an inhibitory KIR3DL that bound MHC-I tetramers and prevented activation, degranulation, and cytokine production by macaque NK cells after engagement with specific MHC-I molecules on the surface of target cells.	kir3dl	42-48	major histocompatibility complex, class I, C	Homo sapiens	192-195
21859520-6	2012	However, alpha-SMA and MHC expression were affected by differentiation factors in strain culture, in particular, showing that treatment with retinoic acid significantly increased the expression of alpha-SMA (3.6-fold) and MHC (2-fold) as compared to strain alone.	Tretinoin	141-154	major histocompatibility complex, class I, C	Homo sapiens	23-26
21859520-6	2012	However, alpha-SMA and MHC expression were affected by differentiation factors in strain culture, in particular, showing that treatment with retinoic acid significantly increased the expression of alpha-SMA (3.6-fold) and MHC (2-fold) as compared to strain alone.	Tretinoin	141-154	major histocompatibility complex, class I, C	Homo sapiens	222-225
22346783-0	2011	Immunomodulatory Effects of Hypocrellin A on MHC-restricted Antigen Processing.	hypocrellin A	28-41	major histocompatibility complex, class I, C	Homo sapiens	45-48
22346783-3	2011	Hypocrellin A inhibited class II-MHC restricted presentation of exogenous antigen, but not class I MHC-restricted presentation of exogenous antigen, in dendritic cells.	hypocrellin A	0-13	major histocompatibility complex, class I, C	Homo sapiens	33-36
21707538-1	2011	The novel HLA-C allele HLA-C*07:147 contains one nucleotide substitution in exon 2 leading to an amino acid change in the alpha 1 domain from phenylalanine to leucine.	Phenylalanine	142-155	major histocompatibility complex, class I, C	Homo sapiens	10-15
21831970-5	2011	RESEARCH DESIGN AND METHODS: Associations of GADA and IA-2A with HLA-DRB1, HLA-DQB1, HLA-B, HLA-C, HLA-A, MICA, and 3,779 single nucleotide polymorphisms (SNPs) were analyzed in 2,531 childhood-onset case subjects (median time since diagnosis 5 years).	gada	45-49	major histocompatibility complex, class I, C	Homo sapiens	92-97
22242476-5	2011	RESULT: (1) MHC-II b was expressed in laryngeal muscles at mRNA levels, and not expressed at the protein level; (2) At both mRNA level and protein level, the expression of MHC-I was higher in the PCA muscles than in the LCA muscles while MHC-II level was higher in the LCA muscles than in the PCA muscles.	Lithocholic Acid	220-223	major histocompatibility complex, class I, C	Homo sapiens	12-15
22242476-5	2011	RESULT: (1) MHC-II b was expressed in laryngeal muscles at mRNA levels, and not expressed at the protein level; (2) At both mRNA level and protein level, the expression of MHC-I was higher in the PCA muscles than in the LCA muscles while MHC-II level was higher in the LCA muscles than in the PCA muscles.	Lithocholic Acid	220-223	major histocompatibility complex, class I, C	Homo sapiens	172-175
22242476-5	2011	RESULT: (1) MHC-II b was expressed in laryngeal muscles at mRNA levels, and not expressed at the protein level; (2) At both mRNA level and protein level, the expression of MHC-I was higher in the PCA muscles than in the LCA muscles while MHC-II level was higher in the LCA muscles than in the PCA muscles.	Lithocholic Acid	220-223	major histocompatibility complex, class I, C	Homo sapiens	172-175
22242476-5	2011	RESULT: (1) MHC-II b was expressed in laryngeal muscles at mRNA levels, and not expressed at the protein level; (2) At both mRNA level and protein level, the expression of MHC-I was higher in the PCA muscles than in the LCA muscles while MHC-II level was higher in the LCA muscles than in the PCA muscles.	Lithocholic Acid	269-272	major histocompatibility complex, class I, C	Homo sapiens	12-15
22242476-5	2011	RESULT: (1) MHC-II b was expressed in laryngeal muscles at mRNA levels, and not expressed at the protein level; (2) At both mRNA level and protein level, the expression of MHC-I was higher in the PCA muscles than in the LCA muscles while MHC-II level was higher in the LCA muscles than in the PCA muscles.	Lithocholic Acid	269-272	major histocompatibility complex, class I, C	Homo sapiens	172-175
22242476-5	2011	RESULT: (1) MHC-II b was expressed in laryngeal muscles at mRNA levels, and not expressed at the protein level; (2) At both mRNA level and protein level, the expression of MHC-I was higher in the PCA muscles than in the LCA muscles while MHC-II level was higher in the LCA muscles than in the PCA muscles.	Lithocholic Acid	269-272	major histocompatibility complex, class I, C	Homo sapiens	172-175
22242476-7	2011	PCA contained larger percentage of MHC-I fibers, while LCA contained more MHC-II fibers.	Lithocholic Acid	55-58	major histocompatibility complex, class I, C	Homo sapiens	74-77
21641731-5	2011	In LL muscle, MHC expression at the end of fattening was greater in the GH group than in the CT group.	ct	93-95	major histocompatibility complex, class I, C	Homo sapiens	14-17
21563272-8	2011	MHC and ICAM-1 molecules anchored on the bilayer diffused freely and stimulated T cell calcium flux and adhesion, respectively.	Calcium	87-94	major histocompatibility complex, class I, C	Homo sapiens	0-3
21707538-1	2011	The novel HLA-C allele HLA-C*07:147 contains one nucleotide substitution in exon 2 leading to an amino acid change in the alpha 1 domain from phenylalanine to leucine.	Phenylalanine	142-155	major histocompatibility complex, class I, C	Homo sapiens	23-28
21707538-1	2011	The novel HLA-C allele HLA-C*07:147 contains one nucleotide substitution in exon 2 leading to an amino acid change in the alpha 1 domain from phenylalanine to leucine.	Leucine	159-166	major histocompatibility complex, class I, C	Homo sapiens	10-15
21707538-1	2011	The novel HLA-C allele HLA-C*07:147 contains one nucleotide substitution in exon 2 leading to an amino acid change in the alpha 1 domain from phenylalanine to leucine.	Leucine	159-166	major histocompatibility complex, class I, C	Homo sapiens	23-28
21902447-6	2011	Among those receiving warfarin and monitored in VHA, highly supratherapeutic INRs were more common in the MHC group; for example, 27.3% versus 1.6% had any INR >5.0 (P <.001).	Warfarin	22-30	major histocompatibility complex, class I, C	Homo sapiens	106-109
21795600-2	2011	The first TCRs used in cancer gene therapy, DMF4 and DMF5, recognize two structurally distinct peptide epitopes of the melanoma-associated MART-1/Melan-A protein, both presented by the class I MHC protein HLA-A*0201.	dmf5	53-57	major histocompatibility complex, class I, C	Homo sapiens	193-196
21628073-5	2011	Previous studies demonstrated that PS inhibits the expression of MHC and co-stimulatory molecules, the secretion of IL-12p70, and the ability to activate T cells by human monocyte derived DCs.	Phosphatidylserines	35-37	major histocompatibility complex, class I, C	Homo sapiens	65-68
21795600-2	2011	The first TCRs used in cancer gene therapy, DMF4 and DMF5, recognize two structurally distinct peptide epitopes of the melanoma-associated MART-1/Melan-A protein, both presented by the class I MHC protein HLA-A*0201.	dmf4	44-48	major histocompatibility complex, class I, C	Homo sapiens	193-196
21541786-1	2011	Alternative lysine and methionine residues at position 44 in the D1 domain determine the specificities of human lineage III killer cell immunoglobulin-like receptors (KIR) for the C1 and C2 epitopes of HLA-C.	Lysine	12-18	major histocompatibility complex, class I, C	Homo sapiens	202-207
21541786-1	2011	Alternative lysine and methionine residues at position 44 in the D1 domain determine the specificities of human lineage III killer cell immunoglobulin-like receptors (KIR) for the C1 and C2 epitopes of HLA-C.	Methionine	23-33	major histocompatibility complex, class I, C	Homo sapiens	202-207
21795600-5	2011	Although DMF4 binds the two with a different orientation, altering its position over the peptide/MHC, DMF5 binds them both identically.	dmf4	9-13	major histocompatibility complex, class I, C	Homo sapiens	97-100
21795600-5	2011	Although DMF4 binds the two with a different orientation, altering its position over the peptide/MHC, DMF5 binds them both identically.	dmf5	102-106	major histocompatibility complex, class I, C	Homo sapiens	97-100
21253892-6	2011	The peptide/MHC/TCR interface was found to hold significant number of solvent molecules, more specifically the peptide has been found to have approximately seventeen hydrogen bonds with water molecules.	Hydrogen	166-174	major histocompatibility complex, class I, C	Homo sapiens	12-15
21253892-6	2011	The peptide/MHC/TCR interface was found to hold significant number of solvent molecules, more specifically the peptide has been found to have approximately seventeen hydrogen bonds with water molecules.	Water	186-191	major histocompatibility complex, class I, C	Homo sapiens	12-15
21644237-2	2011	METHODS: Polymerase chain reaction-sequence specific oligonucleotide (PCR-SSO) typing by Luminex was performed to genotype the HLA-C alleles in unrelated healthy individuals in the three populations.	Oligonucleotides	53-68	major histocompatibility complex, class I, C	Homo sapiens	127-132
21354601-10	2011	Three patterns of MHC-restricted reactivity (sulfamethoxazole-responsive, sulfamethoxazole metabolite-responsive, and cross-reactive) were observed with clones from patients without cystic fibrosis.	Sulfamethoxazole	45-61	major histocompatibility complex, class I, C	Homo sapiens	18-21
21354601-10	2011	Three patterns of MHC-restricted reactivity (sulfamethoxazole-responsive, sulfamethoxazole metabolite-responsive, and cross-reactive) were observed with clones from patients without cystic fibrosis.	Sulfamethoxazole	74-90	major histocompatibility complex, class I, C	Homo sapiens	18-21
21177250-0	2011	HDAC3-dependent reversible lysine acetylation of cardiac myosin heavy chain isoforms modulates their enzymatic and motor activity.	Lysine	27-33	major histocompatibility complex, class I, C	Homo sapiens	57-75
21453269-3	2011	The revelation that the autoimmune response specific for patients with RA is to particular protein antigens bearing the post-translational modification "citrulline" has therefore revolutionized diagnostics and has helped explain why patients carrying particular MHC alleles are predisposed to the disease.	Citrulline	153-163	major histocompatibility complex, class I, C	Homo sapiens	262-265
20810908-2	2010	Fiber myosin heavy chain (MHC) isoform content was assayed by SDS-PAGE.	Sodium Dodecyl Sulfate	62-65	major histocompatibility complex, class I, C	Homo sapiens	26-29
20691611-10	2010	Chronic stimulation of epithelium by antibodies to MHC and resulting increased levels of defensins induce growth factor production and epithelial proliferation contributing to the development of chronic rejection after LTx.	Leukotriene C4	219-222	major histocompatibility complex, class I, C	Homo sapiens	51-54
20849552-3	2010	In this study, we used a novel MHC-defined rhesus macaque model to examine the impact of MHC matching on the stability of costimulation blockade-/sirolimus-mediated chimerism, and to probe possible mechanisms of bone marrow rejection after nonmyeloablative transplant.	Sirolimus	146-155	major histocompatibility complex, class I, C	Homo sapiens	89-92
20739527-6	2010	These results illustrate that HLA-C-restricted CTL responses are capable of driving viral immune escape within Gag, but in contrast to what was previously described for HLA-B-restricted Gag escape mutants, the common Cw*03-Gag-303V variant selected resulted in no detectable benefit to the host.	Glycosaminoglycans	111-114	major histocompatibility complex, class I, C	Homo sapiens	30-35
20036705-8	2010	The genotype 2DL2+/HLA-C lys(80)+ was also more common in controls (IBD: p = 0.005; UC: p = 0.01; CD: p = NS); as well as 2DL1+/HLA-C Asn(80)+ (IBD: p = 0.026; UC: p = NS;CD: p = NS).	Lysine	25-28	major histocompatibility complex, class I, C	Homo sapiens	19-24
20226094-1	2010	BACKGROUND: Myosin performs ATP free energy transduction into mechanical work in the motor domain of the myosin heavy chain (MHC).	Adenosine Triphosphate	28-31	major histocompatibility complex, class I, C	Homo sapiens	105-123
20226094-1	2010	BACKGROUND: Myosin performs ATP free energy transduction into mechanical work in the motor domain of the myosin heavy chain (MHC).	Adenosine Triphosphate	28-31	major histocompatibility complex, class I, C	Homo sapiens	125-128
20399684-5	2010	Weak agonist MHC-peptide induced CD80-dependent TCR MCs that dissociated in the center of the IS without recruiting TSG101.	mcs	52-55	major histocompatibility complex, class I, C	Homo sapiens	13-16
20060953-6	2010	Myosin heavy chain (MHC) protein isoforms were quantified by silver stained SDS PAGE.	Sodium Dodecyl Sulfate	76-79	major histocompatibility complex, class I, C	Homo sapiens	0-18
20036705-8	2010	The genotype 2DL2+/HLA-C lys(80)+ was also more common in controls (IBD: p = 0.005; UC: p = 0.01; CD: p = NS); as well as 2DL1+/HLA-C Asn(80)+ (IBD: p = 0.026; UC: p = NS;CD: p = NS).	Lysine	25-28	major histocompatibility complex, class I, C	Homo sapiens	128-133
19773579-12	2009	Dexamethasone treatment lowered MHC and increased USP19.	Dexamethasone	0-13	major histocompatibility complex, class I, C	Homo sapiens	32-35
20054086-0	2010	A rationale for SDS-PAGE of MHC isoforms as a gold standard for determining contractile phenotype.	Sodium Dodecyl Sulfate	16-19	major histocompatibility complex, class I, C	Homo sapiens	28-31
19883388-2	2010	The myosin heavy chain (MHC) isoform distribution of the samples was determined by densitometry of MHC bands separated by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE).	Sodium Dodecyl Sulfate	122-144	major histocompatibility complex, class I, C	Homo sapiens	4-22
19883388-2	2010	The myosin heavy chain (MHC) isoform distribution of the samples was determined by densitometry of MHC bands separated by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE).	Sodium Dodecyl Sulfate	122-144	major histocompatibility complex, class I, C	Homo sapiens	24-27
19883388-2	2010	The myosin heavy chain (MHC) isoform distribution of the samples was determined by densitometry of MHC bands separated by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE).	polyacrylamide	145-159	major histocompatibility complex, class I, C	Homo sapiens	4-22
19883388-2	2010	The myosin heavy chain (MHC) isoform distribution of the samples was determined by densitometry of MHC bands separated by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE).	polyacrylamide	145-159	major histocompatibility complex, class I, C	Homo sapiens	24-27
19883388-2	2010	The myosin heavy chain (MHC) isoform distribution of the samples was determined by densitometry of MHC bands separated by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE).	Sodium Dodecyl Sulfate	181-184	major histocompatibility complex, class I, C	Homo sapiens	4-22
19883388-2	2010	The myosin heavy chain (MHC) isoform distribution of the samples was determined by densitometry of MHC bands separated by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE).	Sodium Dodecyl Sulfate	181-184	major histocompatibility complex, class I, C	Homo sapiens	24-27
19773579-13	2009	Depletion of USP19 reversed the dexamethasone suppression of MHC.	Dexamethasone	32-45	major histocompatibility complex, class I, C	Homo sapiens	61-64
19789338-6	2009	Crystal structure analysis of MHC/peptide complexes revealed that the conformation of the modified p2Gp3P-peptide was similar to the wild-type peptide, and indicated that this mimotope was stabilized through interactions between peptide residue p3P and the tyrosine residue Y159 that is conserved among most known MHC-I molecules throughout mammalian species.	Tyrosine	257-265	major histocompatibility complex, class I, C	Homo sapiens	30-33
19502511-11	2009	There was a ZH duration x DOF interaction (P < 0.01) for the expression of MHC-IIa and -IIx.	zh	12-14	major histocompatibility complex, class I, C	Homo sapiens	78-81
19502511-11	2009	There was a ZH duration x DOF interaction (P < 0.01) for the expression of MHC-IIa and -IIx.	dof	26-29	major histocompatibility complex, class I, C	Homo sapiens	78-81
19502511-12	2009	Expression of MHC-IIa was decreased in every ZH treatment within the 177 and 198 DOF groups (P < 0.02).	zh	45-47	major histocompatibility complex, class I, C	Homo sapiens	14-17
19502511-12	2009	Expression of MHC-IIa was decreased in every ZH treatment within the 177 and 198 DOF groups (P < 0.02).	dof	81-84	major histocompatibility complex, class I, C	Homo sapiens	14-17
19502511-13	2009	Expression of MHC-IIx was increased in the 20-d ZH group in the 157 DOF group (P = 0.03), and the 40-d ZH group in the 177 (P = 0.10) and 198 (P = 0.03) DOF groups.	zh	48-50	major histocompatibility complex, class I, C	Homo sapiens	14-17
19502511-13	2009	Expression of MHC-IIx was increased in the 20-d ZH group in the 157 DOF group (P = 0.03), and the 40-d ZH group in the 177 (P = 0.10) and 198 (P = 0.03) DOF groups.	dof	68-71	major histocompatibility complex, class I, C	Homo sapiens	14-17
19502511-13	2009	Expression of MHC-IIx was increased in the 20-d ZH group in the 157 DOF group (P = 0.03), and the 40-d ZH group in the 177 (P = 0.10) and 198 (P = 0.03) DOF groups.	zh	103-105	major histocompatibility complex, class I, C	Homo sapiens	14-17
19502511-13	2009	Expression of MHC-IIx was increased in the 20-d ZH group in the 157 DOF group (P = 0.03), and the 40-d ZH group in the 177 (P = 0.10) and 198 (P = 0.03) DOF groups.	dof	153-156	major histocompatibility complex, class I, C	Homo sapiens	14-17
19502511-15	2009	Collectively, the data indicate that ZH may influence net protein turnover by decreasing MHC-IIa mRNA transcription and possibly increasing MHC-IIx.	zh	37-39	major histocompatibility complex, class I, C	Homo sapiens	89-92
19502511-15	2009	Collectively, the data indicate that ZH may influence net protein turnover by decreasing MHC-IIa mRNA transcription and possibly increasing MHC-IIx.	zh	37-39	major histocompatibility complex, class I, C	Homo sapiens	140-143
19369448-6	2009	During MHC transitions with muscle unloading, histone H3 at the type I MHC becomes de-acetylated in correspondence with down-regulation of that gene, while upregulation of the fast type IIx and IIb MHCs occurs in conjunction with enhanced H3ac in those MHCs.	h3ac	239-243	major histocompatibility complex, class I, C	Homo sapiens	7-10
19251841-4	2009	Either hypoxia (1 h) or treatment with DT-3, a PKG inhibitor, increased associations of Elk-1 with myosin heavy chain (MHC) gene and serum response factor (SRF), which was paralleled by a decrease in association of myocardin with MHC gene and SRF.	Detrothyronine	39-43	major histocompatibility complex, class I, C	Homo sapiens	99-117
19251841-4	2009	Either hypoxia (1 h) or treatment with DT-3, a PKG inhibitor, increased associations of Elk-1 with myosin heavy chain (MHC) gene and serum response factor (SRF), which was paralleled by a decrease in association of myocardin with MHC gene and SRF.	Detrothyronine	39-43	major histocompatibility complex, class I, C	Homo sapiens	119-122
19251841-4	2009	Either hypoxia (1 h) or treatment with DT-3, a PKG inhibitor, increased associations of Elk-1 with myosin heavy chain (MHC) gene and serum response factor (SRF), which was paralleled by a decrease in association of myocardin with MHC gene and SRF.	Detrothyronine	39-43	major histocompatibility complex, class I, C	Homo sapiens	230-233
18978449-13	2008	Mixed MHC isoform distribution was confirmed by SDS-PAGE, which also indicated that the IIa and IIx isoforms were roughly equally present across the muscles.	Sodium Dodecyl Sulfate	48-51	major histocompatibility complex, class I, C	Homo sapiens	6-9
19095306-1	2009	Nitric oxide has been shown to induce immunosuppression by inhibiting class II MHC molecule expression and T-lymphocyte proliferation.	Nitric Oxide	0-12	major histocompatibility complex, class I, C	Homo sapiens	79-82
19319200-8	2009	Altogether, these data provide a mechanistic explanation on how Dex may stimulate non MHC restricted-anti-tumor effectors and induce tumor regression in vivo.	dex	64-67	major histocompatibility complex, class I, C	Homo sapiens	86-89
18981164-7	2008	Repertoires of T cell memory are discussed in the context of clonal diversity, where poly-Gly/Ala runs in the CDR3 of alpha- and beta-chains might provide high levels of TCR flexibility during Ag recognition while gene-encoded CDR1 and CDR2 contribute to the fine specificity of the TCR-peptide MHC interaction.	Alanine	94-97	major histocompatibility complex, class I, C	Homo sapiens	295-298
18787035-5	2008	Consistent with these results, SDS-PAGE analysis revealed significantly elevated expression of alpha myosin heavy chain (MHC) isoform in epicardial fibres (13 +/- 1%) versus endocardial fibres (3 +/- 1%).	Sodium Dodecyl Sulfate	31-34	major histocompatibility complex, class I, C	Homo sapiens	101-119
18787035-5	2008	Consistent with these results, SDS-PAGE analysis revealed significantly elevated expression of alpha myosin heavy chain (MHC) isoform in epicardial fibres (13 +/- 1%) versus endocardial fibres (3 +/- 1%).	Sodium Dodecyl Sulfate	31-34	major histocompatibility complex, class I, C	Homo sapiens	121-124
18297378-8	2008	The genotype 2DS1+/HLA-C lys(80)+ was more common in subjects with AS.	Lysine	25-28	major histocompatibility complex, class I, C	Homo sapiens	19-24
19171094-7	2008	After co-culture with uSMC, the morphology of the pMSC changed closely into that of the uSMC, and MHC was expressed in the pMSC.	usmc	22-26	major histocompatibility complex, class I, C	Homo sapiens	98-101
18521893-10	2008	Most notable was that the CTP contained specialized muscle fibers expressing some unusual MHC isoforms (i.e., slow-tonic, alpha-cardiac, neonatal, and embryonic).	Cytidine Triphosphate	26-29	major histocompatibility complex, class I, C	Homo sapiens	90-93
18523244-6	2008	In addition, we provide evidence that this signal is specifically inhibited by hypophosphorylation of the adjacent serine residue upon macrophage differentiation and that this allows high HLA-C expression in this cell type.	Serine	115-121	major histocompatibility complex, class I, C	Homo sapiens	188-193
17956861-4	2008	Pulse-labeling experiments with HLA-C transfectants and HLA homozygous cell lines demonstrated that KYRV alleles accumulate as free heavy chains because of both poor assembly and post-assembly instability.	kyrv	100-104	major histocompatibility complex, class I, C	Homo sapiens	32-37
18393506-8	2008	The majority of myosin heavy chain (MHC) was demonstrated to be cross-linked through intermolecular disulfide bonding 1 h after initiation of oxidation.	Disulfides	100-109	major histocompatibility complex, class I, C	Homo sapiens	16-34
18393506-8	2008	The majority of myosin heavy chain (MHC) was demonstrated to be cross-linked through intermolecular disulfide bonding 1 h after initiation of oxidation.	Disulfides	100-109	major histocompatibility complex, class I, C	Homo sapiens	36-39
18350151-5	2008	The catalytic activity of dipeptides such as Tyr-Arg was stereo-specific and could be enhanced by modifications addressing the conserved H-bond network near the P1 pocket of the MHC molecule.	Dipeptides	26-36	major histocompatibility complex, class I, C	Homo sapiens	178-181
17925381-6	2007	The effects of SV are reversed by inhibition of myosin heavy chain (MHC) ATPase (blebbistatin), MLCK (ML-7) or MEK (U0126), but not by inhibiting Rho-kinase with Y-27632.	blebbistatin	81-93	major histocompatibility complex, class I, C	Homo sapiens	68-71
18055619-3	2007	We found that gregarine infection was associated with a 10-fold average reduction in abundance of a approximately 155 kDa fragment of muscle myosin heavy chain (MHC; approximately 206 kDa intact size).	gregarine	14-23	major histocompatibility complex, class I, C	Homo sapiens	161-164
18162457-4	2007	The amount of proteins characteristic for cardiac cells (alpha-SA and MHC, VEGFR-2 and FVIII, SMA for the precursors of cardiomyocytes, endothelial and smooth muscle cells, respectively) inclines toward an increase in both alpha-SA and MHC.	alpha-sa	223-231	major histocompatibility complex, class I, C	Homo sapiens	70-73
17624386-9	2007	This limited impact of TNF-alpha on GR activity was not universal as TNF-alpha and DEX exerted an additive effect on the reduction in myosin heavy chain (MHC) protein expression caused by either agent alone.	Dexamethasone	83-86	major histocompatibility complex, class I, C	Homo sapiens	134-152
17475667-5	2007	Isoform differences located in the S1 head region of the MHC can alter actin binding and rates of ATP hydrolysis.	Adenosine Triphosphate	98-101	major histocompatibility complex, class I, C	Homo sapiens	57-60
17624386-9	2007	This limited impact of TNF-alpha on GR activity was not universal as TNF-alpha and DEX exerted an additive effect on the reduction in myosin heavy chain (MHC) protein expression caused by either agent alone.	Dexamethasone	83-86	major histocompatibility complex, class I, C	Homo sapiens	154-157
17014746-2	2006	The addition of reducing agents (beta-mercaptoethanol or dithiothreitol) to the top running buffer (TRB) radically improved separated MHC isoform resolution and the intensity of electrophoretic runs lasting longer than 5 h. In minigel systems, the MHC isoforms could be separated in as little as 5 h. The improved resolution of bands with the inclusion of reducing agents to the TRB facilitated the identification of clear boundaries for densitometric quantification of relative MHC isoform content, particularly for MHC IIa and MHC IIx.	Mercaptoethanol	33-53	major histocompatibility complex, class I, C	Homo sapiens	134-137
16709460-7	2007	MFCV was positively correlated with percentage of MHC I, power corresponding to LT and to VO2max (R2=0.84; 0.74; 0.53, respectively; P<0.05).	mfcv	0-4	major histocompatibility complex, class I, C	Homo sapiens	50-53
17225465-0	2006	Effects of mizoribine on MHC-restricted exogenous antigen presentation in dendritic cells.	mizoribine	11-21	major histocompatibility complex, class I, C	Homo sapiens	25-28
17187819-4	2007	We now report robust preparation of MHC tetramers with small molecule fluorophores, using a recombinant mutant of streptavidin incorporating a carboxy-terminal cysteine in each of the four identical subunits that is conjugated to maleimide derivatives of any of several small molecule fluorophores.	Cysteine	160-168	major histocompatibility complex, class I, C	Homo sapiens	36-39
17187819-4	2007	We now report robust preparation of MHC tetramers with small molecule fluorophores, using a recombinant mutant of streptavidin incorporating a carboxy-terminal cysteine in each of the four identical subunits that is conjugated to maleimide derivatives of any of several small molecule fluorophores.	maleimide	230-239	major histocompatibility complex, class I, C	Homo sapiens	36-39
16926382-6	2007	MFO was significantly correlated to muscle fiber type distribution, i.e., %MHC I (r = 0.62, P = 0.03), but was not different between trained (62 +/- 5%) and untrained subjects (72 +/- 2%).	mfo	0-3	major histocompatibility complex, class I, C	Homo sapiens	75-78
17288806-11	2006	KIR/HLA-C mismatch, homo-expression of HLA-Cw1 or Cw2, and co-expression of KIR2DL2 and KIR2DS2 may predict good prognosis for CBT.	N,N-BIS(4-CHLOROBENZYL)-1H-1,2,3,4-TETRAAZOL-5-AMINE	127-130	major histocompatibility complex, class I, C	Homo sapiens	4-9
16881064-0	2006	Effects of exercise and creatine on myosin heavy chain isoform composition in patients with Charcot-Marie-Tooth disease.	Creatine	24-32	major histocompatibility complex, class I, C	Homo sapiens	36-54
16881064-2	2006	Based on previous data, we hypothesized that resistance exercise and creatine would increase the percentage of type I MHC composition in the vastus lateralis muscle and that myosin isoform changes would correlate with improved chair rise-time in CMT subjects.	Creatine	69-77	major histocompatibility complex, class I, C	Homo sapiens	118-121
16881064-7	2006	Gel electrophoresis showed a significant decrease (approximately 30%) in MHC type I in CMT subjects given creatine supplementation when compared with placebo.	Creatine	106-114	major histocompatibility complex, class I, C	Homo sapiens	73-76
16881064-8	2006	There was a nonsignificant increase in both MHC type IIa (approximately 23%) and MHC type IIx (approximately 7%) in CMT subjects given creatine.	Creatine	135-143	major histocompatibility complex, class I, C	Homo sapiens	44-47
16881064-8	2006	There was a nonsignificant increase in both MHC type IIa (approximately 23%) and MHC type IIx (approximately 7%) in CMT subjects given creatine.	Creatine	135-143	major histocompatibility complex, class I, C	Homo sapiens	81-84
16881064-10	2006	The training-induced change in MHC IIa content was inversely correlated with chair rise-time in CMT subjects given creatine.	Creatine	115-123	major histocompatibility complex, class I, C	Homo sapiens	31-34
16881064-13	2006	Furthermore, the data are consistent with the hypothesis that creatine supplementation alters MHC composition in CMT patients undergoing resistance training and that MHC changes associated with creatine supplementation can improve muscle function.	Creatine	62-70	major histocompatibility complex, class I, C	Homo sapiens	94-97
16881064-13	2006	Furthermore, the data are consistent with the hypothesis that creatine supplementation alters MHC composition in CMT patients undergoing resistance training and that MHC changes associated with creatine supplementation can improve muscle function.	Creatine	194-202	major histocompatibility complex, class I, C	Homo sapiens	166-169
17014746-2	2006	The addition of reducing agents (beta-mercaptoethanol or dithiothreitol) to the top running buffer (TRB) radically improved separated MHC isoform resolution and the intensity of electrophoretic runs lasting longer than 5 h. In minigel systems, the MHC isoforms could be separated in as little as 5 h. The improved resolution of bands with the inclusion of reducing agents to the TRB facilitated the identification of clear boundaries for densitometric quantification of relative MHC isoform content, particularly for MHC IIa and MHC IIx.	Mercaptoethanol	33-53	major histocompatibility complex, class I, C	Homo sapiens	248-251
17014746-2	2006	The addition of reducing agents (beta-mercaptoethanol or dithiothreitol) to the top running buffer (TRB) radically improved separated MHC isoform resolution and the intensity of electrophoretic runs lasting longer than 5 h. In minigel systems, the MHC isoforms could be separated in as little as 5 h. The improved resolution of bands with the inclusion of reducing agents to the TRB facilitated the identification of clear boundaries for densitometric quantification of relative MHC isoform content, particularly for MHC IIa and MHC IIx.	Mercaptoethanol	33-53	major histocompatibility complex, class I, C	Homo sapiens	248-251
17014746-2	2006	The addition of reducing agents (beta-mercaptoethanol or dithiothreitol) to the top running buffer (TRB) radically improved separated MHC isoform resolution and the intensity of electrophoretic runs lasting longer than 5 h. In minigel systems, the MHC isoforms could be separated in as little as 5 h. The improved resolution of bands with the inclusion of reducing agents to the TRB facilitated the identification of clear boundaries for densitometric quantification of relative MHC isoform content, particularly for MHC IIa and MHC IIx.	Mercaptoethanol	33-53	major histocompatibility complex, class I, C	Homo sapiens	248-251
17014746-2	2006	The addition of reducing agents (beta-mercaptoethanol or dithiothreitol) to the top running buffer (TRB) radically improved separated MHC isoform resolution and the intensity of electrophoretic runs lasting longer than 5 h. In minigel systems, the MHC isoforms could be separated in as little as 5 h. The improved resolution of bands with the inclusion of reducing agents to the TRB facilitated the identification of clear boundaries for densitometric quantification of relative MHC isoform content, particularly for MHC IIa and MHC IIx.	Mercaptoethanol	33-53	major histocompatibility complex, class I, C	Homo sapiens	248-251
17014746-2	2006	The addition of reducing agents (beta-mercaptoethanol or dithiothreitol) to the top running buffer (TRB) radically improved separated MHC isoform resolution and the intensity of electrophoretic runs lasting longer than 5 h. In minigel systems, the MHC isoforms could be separated in as little as 5 h. The improved resolution of bands with the inclusion of reducing agents to the TRB facilitated the identification of clear boundaries for densitometric quantification of relative MHC isoform content, particularly for MHC IIa and MHC IIx.	Dithiothreitol	57-71	major histocompatibility complex, class I, C	Homo sapiens	134-137
17014746-2	2006	The addition of reducing agents (beta-mercaptoethanol or dithiothreitol) to the top running buffer (TRB) radically improved separated MHC isoform resolution and the intensity of electrophoretic runs lasting longer than 5 h. In minigel systems, the MHC isoforms could be separated in as little as 5 h. The improved resolution of bands with the inclusion of reducing agents to the TRB facilitated the identification of clear boundaries for densitometric quantification of relative MHC isoform content, particularly for MHC IIa and MHC IIx.	Dithiothreitol	57-71	major histocompatibility complex, class I, C	Homo sapiens	248-251
16951353-3	2006	In this study, we show that reversible MHC-peptide complexes (tetramers) can be prepared by conjugating MHC-peptide monomers with desthiobiotin (DTB; also called dethiobiotin) and multimerization by reaction with fluorescent streptavidin.	desthiobiotin	130-143	major histocompatibility complex, class I, C	Homo sapiens	39-42
16951353-3	2006	In this study, we show that reversible MHC-peptide complexes (tetramers) can be prepared by conjugating MHC-peptide monomers with desthiobiotin (DTB; also called dethiobiotin) and multimerization by reaction with fluorescent streptavidin.	desthiobiotin	130-143	major histocompatibility complex, class I, C	Homo sapiens	104-107
16951353-3	2006	In this study, we show that reversible MHC-peptide complexes (tetramers) can be prepared by conjugating MHC-peptide monomers with desthiobiotin (DTB; also called dethiobiotin) and multimerization by reaction with fluorescent streptavidin.	desthiobiotin	145-148	major histocompatibility complex, class I, C	Homo sapiens	39-42
16951353-3	2006	In this study, we show that reversible MHC-peptide complexes (tetramers) can be prepared by conjugating MHC-peptide monomers with desthiobiotin (DTB; also called dethiobiotin) and multimerization by reaction with fluorescent streptavidin.	desthiobiotin	145-148	major histocompatibility complex, class I, C	Homo sapiens	104-107
16951353-3	2006	In this study, we show that reversible MHC-peptide complexes (tetramers) can be prepared by conjugating MHC-peptide monomers with desthiobiotin (DTB; also called dethiobiotin) and multimerization by reaction with fluorescent streptavidin.	desthiobiotin	162-174	major histocompatibility complex, class I, C	Homo sapiens	39-42
16951353-3	2006	In this study, we show that reversible MHC-peptide complexes (tetramers) can be prepared by conjugating MHC-peptide monomers with desthiobiotin (DTB; also called dethiobiotin) and multimerization by reaction with fluorescent streptavidin.	desthiobiotin	162-174	major histocompatibility complex, class I, C	Homo sapiens	104-107
16766611-3	2006	Specificity characteristics improve as the time window for detection increases, saturating for time periods on the timescale of downregulation; thus, the calcium spike (30 s) has low specificity but a sensitivity to single-peptide MHC ligands, while the cytokine threshold (1 h) can distinguish ligands with a 30% variation in the complex lifetime.	Calcium	154-161	major histocompatibility complex, class I, C	Homo sapiens	231-234
17014746-2	2006	The addition of reducing agents (beta-mercaptoethanol or dithiothreitol) to the top running buffer (TRB) radically improved separated MHC isoform resolution and the intensity of electrophoretic runs lasting longer than 5 h. In minigel systems, the MHC isoforms could be separated in as little as 5 h. The improved resolution of bands with the inclusion of reducing agents to the TRB facilitated the identification of clear boundaries for densitometric quantification of relative MHC isoform content, particularly for MHC IIa and MHC IIx.	Dithiothreitol	57-71	major histocompatibility complex, class I, C	Homo sapiens	248-251
17014746-2	2006	The addition of reducing agents (beta-mercaptoethanol or dithiothreitol) to the top running buffer (TRB) radically improved separated MHC isoform resolution and the intensity of electrophoretic runs lasting longer than 5 h. In minigel systems, the MHC isoforms could be separated in as little as 5 h. The improved resolution of bands with the inclusion of reducing agents to the TRB facilitated the identification of clear boundaries for densitometric quantification of relative MHC isoform content, particularly for MHC IIa and MHC IIx.	Dithiothreitol	57-71	major histocompatibility complex, class I, C	Homo sapiens	248-251
17014746-2	2006	The addition of reducing agents (beta-mercaptoethanol or dithiothreitol) to the top running buffer (TRB) radically improved separated MHC isoform resolution and the intensity of electrophoretic runs lasting longer than 5 h. In minigel systems, the MHC isoforms could be separated in as little as 5 h. The improved resolution of bands with the inclusion of reducing agents to the TRB facilitated the identification of clear boundaries for densitometric quantification of relative MHC isoform content, particularly for MHC IIa and MHC IIx.	Dithiothreitol	57-71	major histocompatibility complex, class I, C	Homo sapiens	248-251
16777978-7	2006	More importantly, JNK activation induced by TNFalpha, C2-ceramide, and N-SMase is associated with reduced expression of the critical muscle transcription factor myogenin as well as the differentiation marker myosin heavy chain (MHC).	N-acetylsphingosine	54-65	major histocompatibility complex, class I, C	Homo sapiens	208-226
16777978-7	2006	More importantly, JNK activation induced by TNFalpha, C2-ceramide, and N-SMase is associated with reduced expression of the critical muscle transcription factor myogenin as well as the differentiation marker myosin heavy chain (MHC).	N-acetylsphingosine	54-65	major histocompatibility complex, class I, C	Homo sapiens	228-231
16720236-10	2006	MHC binding studies showed specific binding of the epsilon-[(111)In]DTPA-gp100:154m peptide to the JY cells at 4 degrees C. Interestingly, no specific binding was observed for the alpha-[(111)In]DTPA-gp100:154m peptide.	Pentetic Acid	68-72	major histocompatibility complex, class I, C	Homo sapiens	0-3
16823344-7	2006	MHC isoform composition was determined by SDS-PAGE.	Sodium Dodecyl Sulfate	42-45	major histocompatibility complex, class I, C	Homo sapiens	0-3
16860761-3	2006	Calcium signaling via TCR was blocked within 2 min by anti-MHCp treatment and 1 min by latrunculin-A treatment.	Calcium	0-7	major histocompatibility complex, class I, C	Homo sapiens	59-63
16815161-9	2006	T cells were stimulated by carbamazepine (metabolites) bound directly to MHC in the absence of processing.	Carbamazepine	27-40	major histocompatibility complex, class I, C	Homo sapiens	73-76
16815161-13	2006	CONCLUSION: These data show that carbamazepine and certain stable carbamazepine metabolites stimulate T cells rapidly via a direct interaction with MHC and specific T-cell receptors.	Carbamazepine	33-46	major histocompatibility complex, class I, C	Homo sapiens	148-151
16815161-13	2006	CONCLUSION: These data show that carbamazepine and certain stable carbamazepine metabolites stimulate T cells rapidly via a direct interaction with MHC and specific T-cell receptors.	Carbamazepine	66-79	major histocompatibility complex, class I, C	Homo sapiens	148-151
16644798-6	2006	Using a SDS-PAGE protocol that proved successful with mammalian muscle MHC isoforms, we were able to detect five MHC isoforms in Xenopus iliofibularis muscle.	Sodium Dodecyl Sulfate	8-11	major histocompatibility complex, class I, C	Homo sapiens	71-74
16644798-6	2006	Using a SDS-PAGE protocol that proved successful with mammalian muscle MHC isoforms, we were able to detect five MHC isoforms in Xenopus iliofibularis muscle.	Sodium Dodecyl Sulfate	8-11	major histocompatibility complex, class I, C	Homo sapiens	113-116
16774539-3	2006	In this study, HLA-C alleles were characterized by a PCR-SSOP (sequence-specific oligonucleotide probes) hybridization protocol in a sample of 97 Lebanese.	Oligonucleotides	81-96	major histocompatibility complex, class I, C	Homo sapiens	15-20
16720236-12	2006	CONCLUSION: When DTPA was conjugated to the epsilon NH2 group of the Lys(154) residue, MHC binding of the peptide was preserved and could still be recognized by cytotoxic T cells.	Pentetic Acid	17-21	major histocompatibility complex, class I, C	Homo sapiens	87-90
16720236-12	2006	CONCLUSION: When DTPA was conjugated to the epsilon NH2 group of the Lys(154) residue, MHC binding of the peptide was preserved and could still be recognized by cytotoxic T cells.	Lysine	69-72	major histocompatibility complex, class I, C	Homo sapiens	87-90
16388855-0	2006	Cholesterol and sphingolipids as lipid organizers of the immune cells" plasma membrane: their impact on the functions of MHC molecules, effector T-lymphocytes and T-cell death.	Cholesterol	0-11	major histocompatibility complex, class I, C	Homo sapiens	121-124
16388855-0	2006	Cholesterol and sphingolipids as lipid organizers of the immune cells" plasma membrane: their impact on the functions of MHC molecules, effector T-lymphocytes and T-cell death.	Sphingolipids	16-29	major histocompatibility complex, class I, C	Homo sapiens	121-124
16533350-4	2006	SDS-polyacrylamide electrophoresis revealed in single fibers that the number of fibers expressing myosin heavy chain (MHC) type I isoform decreased from 68.7% to 60.9% (P<0.05), MHC I/IIA isoform was unaltered, while MHC IIA fibers increased from 21.6% to 35.7% and the 4.8% MHC IIA/IIX disappeared with the training (both P<0.05).	Sodium Dodecyl Sulfate	0-3	major histocompatibility complex, class I, C	Homo sapiens	98-116
16339176-7	2006	MHC isoform distribution was shifted towards 2X fibres in BB.	boeravinone B	58-60	major histocompatibility complex, class I, C	Homo sapiens	0-3
16533350-4	2006	SDS-polyacrylamide electrophoresis revealed in single fibers that the number of fibers expressing myosin heavy chain (MHC) type I isoform decreased from 68.7% to 60.9% (P<0.05), MHC I/IIA isoform was unaltered, while MHC IIA fibers increased from 21.6% to 35.7% and the 4.8% MHC IIA/IIX disappeared with the training (both P<0.05).	Sodium Dodecyl Sulfate	0-3	major histocompatibility complex, class I, C	Homo sapiens	118-121
16185272-5	2005	This permits classifying all HLA-C alleles into two functional groups: asparagine (N80) or lysine (K80) carrying alleles.	Asparagine	71-81	major histocompatibility complex, class I, C	Homo sapiens	29-34
15891886-5	2005	We now show that treatment of tumor cells with the nonselective COX-1/COX-2 inhibitor indomethacin or the selective COX-2 inhibitor celecoxib leads to decreased expression of the MHC class I molecules Ld and Kd .	Indomethacin	86-98	major histocompatibility complex, class I, C	Homo sapiens	179-182
15891886-5	2005	We now show that treatment of tumor cells with the nonselective COX-1/COX-2 inhibitor indomethacin or the selective COX-2 inhibitor celecoxib leads to decreased expression of the MHC class I molecules Ld and Kd .	Celecoxib	132-141	major histocompatibility complex, class I, C	Homo sapiens	179-182
16185272-5	2005	This permits classifying all HLA-C alleles into two functional groups: asparagine (N80) or lysine (K80) carrying alleles.	Lysine	91-97	major histocompatibility complex, class I, C	Homo sapiens	29-34
16148127-7	2005	Structural analysis of peptides in which anchor residues were substituted with beta-amino acids revealed the basis for enhanced MHC binding and retention of immunogenicity observed for these analogs and paves the way for future vaccine design using beta-amino acids.	beta-amino acids	79-95	major histocompatibility complex, class I, C	Homo sapiens	128-131
16148127-7	2005	Structural analysis of peptides in which anchor residues were substituted with beta-amino acids revealed the basis for enhanced MHC binding and retention of immunogenicity observed for these analogs and paves the way for future vaccine design using beta-amino acids.	beta-amino acids	249-265	major histocompatibility complex, class I, C	Homo sapiens	128-131
16123136-7	2005	T cell antigen receptor recognition of MHC molecules independently of bound ligand has potential general implications in alloreactivity and identifies in the Hfe case a cognitive link supporting the concept that the immune system could be involved in the control of iron metabolism.	Iron	266-270	major histocompatibility complex, class I, C	Homo sapiens	39-42
16128698-8	2005	BR-SOL had a 19% decrease (P < 0.05) in MHC I fibres with a 22% increase in total hybrids.	Bromine	0-2	major histocompatibility complex, class I, C	Homo sapiens	43-46
15682450-5	2005	Finally, some types of carbohydrates are now known to be processed and presented to T cells by class II MHC.	Carbohydrates	23-36	major histocompatibility complex, class I, C	Homo sapiens	104-107
15731398-8	2005	MHC isoform composition was determined with SDS-PAGE.	Sodium Dodecyl Sulfate	44-47	major histocompatibility complex, class I, C	Homo sapiens	0-3
15895315-8	2005	MHC-IIx fibers decreased by 7 % in CTG (p < 0.05) and ETG had an 11 % increase in total hybrids (MHC-I/IIa + MHC-IIa/IIx) (p < 0.05).	ctg	35-38	major histocompatibility complex, class I, C	Homo sapiens	0-3
15895315-8	2005	MHC-IIx fibers decreased by 7 % in CTG (p < 0.05) and ETG had an 11 % increase in total hybrids (MHC-I/IIa + MHC-IIa/IIx) (p < 0.05).	etg	57-60	major histocompatibility complex, class I, C	Homo sapiens	100-103
15895315-8	2005	MHC-IIx fibers decreased by 7 % in CTG (p < 0.05) and ETG had an 11 % increase in total hybrids (MHC-I/IIa + MHC-IIa/IIx) (p < 0.05).	etg	57-60	major histocompatibility complex, class I, C	Homo sapiens	100-103
15877992-7	2005	Myosin heavy chain (MHC) composition was assessed using sodium dodecyl sulfate-polyacrylamide gel electrophoresis.	Sodium Dodecyl Sulfate	56-78	major histocompatibility complex, class I, C	Homo sapiens	0-18
15877992-7	2005	Myosin heavy chain (MHC) composition was assessed using sodium dodecyl sulfate-polyacrylamide gel electrophoresis.	polyacrylamide	79-93	major histocompatibility complex, class I, C	Homo sapiens	0-18
16127375-6	2005	Potential targets to prevent the toxic effects of bacterial superantigens include blocking the interaction of SEs with MHC or TCR, or other costimulatory molecules; inhibition of signal transduction pathways used by these superantigens; inhibition of cytokine and chemokine production; and inhibition of the downstream signaling pathways used by proinflammatory cytokines and chemokines.	Selenium	110-113	major histocompatibility complex, class I, C	Homo sapiens	119-122
15896208-3	2005	The new allele differs from Cw*020202 by one nucleotide substitution at nucleotide 61 (G-->A) of exon 2, which translates to a difference of one amino acid at residue 21 (His-->Arg) of the HLA-C heavy chain.	Histidine	174-177	major histocompatibility complex, class I, C	Homo sapiens	195-200
15943912-0	2005	Study of alanine-73 and aspartate-9 of HLA-C locus in Saudi psoriasis patients, using sequence-specific primers (PCR-SSP).	Aspartic Acid	24-33	major histocompatibility complex, class I, C	Homo sapiens	39-44
15943912-1	2005	Alanine at residue 73 (Ala-73) and aspartate at residue 9 (Asp-9) are characteristic to both Cw6 and Cw7 alleles of HLA-C gene and have been suggested as possible markers for psoriasis vulgaris (PsV).	Alanine	0-7	major histocompatibility complex, class I, C	Homo sapiens	116-121
15943912-1	2005	Alanine at residue 73 (Ala-73) and aspartate at residue 9 (Asp-9) are characteristic to both Cw6 and Cw7 alleles of HLA-C gene and have been suggested as possible markers for psoriasis vulgaris (PsV).	Alanine	0-3	major histocompatibility complex, class I, C	Homo sapiens	116-121
15943912-1	2005	Alanine at residue 73 (Ala-73) and aspartate at residue 9 (Asp-9) are characteristic to both Cw6 and Cw7 alleles of HLA-C gene and have been suggested as possible markers for psoriasis vulgaris (PsV).	Aspartic Acid	35-44	major histocompatibility complex, class I, C	Homo sapiens	116-121
15943912-1	2005	Alanine at residue 73 (Ala-73) and aspartate at residue 9 (Asp-9) are characteristic to both Cw6 and Cw7 alleles of HLA-C gene and have been suggested as possible markers for psoriasis vulgaris (PsV).	Aspartic Acid	59-62	major histocompatibility complex, class I, C	Homo sapiens	116-121
15943912-3	2005	In this study, an attempt has been made to examine the association between HLA-C (Ala-73 and Asp-9) and susceptibility to PsV among Saudi patients.	Alanine	82-85	major histocompatibility complex, class I, C	Homo sapiens	75-80
15943912-3	2005	In this study, an attempt has been made to examine the association between HLA-C (Ala-73 and Asp-9) and susceptibility to PsV among Saudi patients.	Aspartic Acid	93-96	major histocompatibility complex, class I, C	Homo sapiens	75-80
15837811-5	2005	Cysteine-to-valine substitution at peptide position 9, while optimizing peptide binding to the MHC, repositions the peptide main chain and generates subtly enhanced interactions between the analogue peptide and the TCR.	Cysteine	0-8	major histocompatibility complex, class I, C	Homo sapiens	95-98
15837811-5	2005	Cysteine-to-valine substitution at peptide position 9, while optimizing peptide binding to the MHC, repositions the peptide main chain and generates subtly enhanced interactions between the analogue peptide and the TCR.	Valine	12-18	major histocompatibility complex, class I, C	Homo sapiens	95-98
15361130-0	2004	Identification of new HLA-C alleles by polymerase chain reaction-sequence specific oligonucleotide typing: Cw*0314 and Cw*1511*.	Oligonucleotides	83-98	major histocompatibility complex, class I, C	Homo sapiens	22-27
15634919-4	2005	We found that substitutions at position K408 in tapasin affected the expression of MHC class I molecules at the cell surface, and down-regulated tapasin stabilization of TAP.	DIMETHYLCARBAMOYL CHLORIDE	40-44	major histocompatibility complex, class I, C	Homo sapiens	83-86
15621050-6	2005	MHC isoform composition was determined by one-dimensional SDS-gel electrophoresis.	Sodium Dodecyl Sulfate	58-61	major histocompatibility complex, class I, C	Homo sapiens	0-3
15621050-8	2005	Significant linear correlations were found between MHC isoform composition, ATP consumption and rate of force redevelopment.	Adenosine Triphosphate	76-79	major histocompatibility complex, class I, C	Homo sapiens	51-54
15306546-2	2004	The time to peak of stretch-induced delayed force increase (t(3)) was strongly correlated with MHC isoforms [t(3) given in ms for fiber types containing specified isoforms; means +/- SD with n in parentheses: MHCI 680 +/- 108 (13), MHCIIa 110.5 +/- 10.7 (23), MHCIIx(d) 46.2 +/- 5.2 (20), MHCIIb 23.5 +/- 3.3 (76)].	Nitrogen	29-30	major histocompatibility complex, class I, C	Homo sapiens	95-98
15495159-0	2004	MHC class I-associated presentation of exogenous peptides is not only enhanced but also prolonged by linking with a C-terminal Lys-Asp-Glu-Leu endoplasmic reticulum retrieval signal.	Lysine	127-130	major histocompatibility complex, class I, C	Homo sapiens	0-3
15495159-0	2004	MHC class I-associated presentation of exogenous peptides is not only enhanced but also prolonged by linking with a C-terminal Lys-Asp-Glu-Leu endoplasmic reticulum retrieval signal.	Aspartic Acid	131-134	major histocompatibility complex, class I, C	Homo sapiens	0-3
15495159-3	2004	In this study, we observed that exogenous peptides that were artificially fused with an endoplasmic reticulum (ER) retrieval signal, a C-terminal Lys-Asp-Glu-Leu sequence, could be efficiently presented by intracellular MHC class I molecules in a TAP- and proteasome-independent, but brefeldin A-sensitive manner.	Lysine	146-149	major histocompatibility complex, class I, C	Homo sapiens	220-223
15495159-3	2004	In this study, we observed that exogenous peptides that were artificially fused with an endoplasmic reticulum (ER) retrieval signal, a C-terminal Lys-Asp-Glu-Leu sequence, could be efficiently presented by intracellular MHC class I molecules in a TAP- and proteasome-independent, but brefeldin A-sensitive manner.	Aspartic Acid	150-153	major histocompatibility complex, class I, C	Homo sapiens	220-223
15495159-3	2004	In this study, we observed that exogenous peptides that were artificially fused with an endoplasmic reticulum (ER) retrieval signal, a C-terminal Lys-Asp-Glu-Leu sequence, could be efficiently presented by intracellular MHC class I molecules in a TAP- and proteasome-independent, but brefeldin A-sensitive manner.	Glutamic Acid	154-157	major histocompatibility complex, class I, C	Homo sapiens	220-223
15495159-3	2004	In this study, we observed that exogenous peptides that were artificially fused with an endoplasmic reticulum (ER) retrieval signal, a C-terminal Lys-Asp-Glu-Leu sequence, could be efficiently presented by intracellular MHC class I molecules in a TAP- and proteasome-independent, but brefeldin A-sensitive manner.	Leucine	158-161	major histocompatibility complex, class I, C	Homo sapiens	220-223
15495159-3	2004	In this study, we observed that exogenous peptides that were artificially fused with an endoplasmic reticulum (ER) retrieval signal, a C-terminal Lys-Asp-Glu-Leu sequence, could be efficiently presented by intracellular MHC class I molecules in a TAP- and proteasome-independent, but brefeldin A-sensitive manner.	Brefeldin A	284-295	major histocompatibility complex, class I, C	Homo sapiens	220-223
15634919-8	2005	Thus, the alanine substitution at position 408 in tapasin may interfere with the stable acquisition by MHC class I molecules of peptides that are sufficiently optimal to allow MHC class I release from tapasin.	Alanine	10-17	major histocompatibility complex, class I, C	Homo sapiens	103-106
15634919-8	2005	Thus, the alanine substitution at position 408 in tapasin may interfere with the stable acquisition by MHC class I molecules of peptides that are sufficiently optimal to allow MHC class I release from tapasin.	Alanine	10-17	major histocompatibility complex, class I, C	Homo sapiens	176-179
15340009-8	2004	F-actin staining further revealed that while the presence of unphosphorylated MHC was essential for the increase in F-actin in the cytoplasm in response to the increasing temporal gradient of cAMP in the front of a natural wave, the actual dephosphorylation event was essential for the associated increase in cortical F-actin.	Cyclic AMP	192-196	major histocompatibility complex, class I, C	Homo sapiens	78-81
15307188-9	2004	Our data suggest an additional role for SifA in interfering with MHC class II antigen-presentation.	sifa	40-44	major histocompatibility complex, class I, C	Homo sapiens	65-68
15282446-2	2004	Triiodothyronine, (T(3)), the physiologically active form of thyroid hormone, binds to nuclear receptor proteins and mediates the expression of several important cardiac genes, inducing transcription of the positively regulated genes including alpha-myosin heavy chain (MHC) and the sarcoplasmic reticulum calcium ATPase.	Triiodothyronine	0-16	major histocompatibility complex, class I, C	Homo sapiens	244-268
15282446-2	2004	Triiodothyronine, (T(3)), the physiologically active form of thyroid hormone, binds to nuclear receptor proteins and mediates the expression of several important cardiac genes, inducing transcription of the positively regulated genes including alpha-myosin heavy chain (MHC) and the sarcoplasmic reticulum calcium ATPase.	Triiodothyronine	0-16	major histocompatibility complex, class I, C	Homo sapiens	270-273
15282446-2	2004	Triiodothyronine, (T(3)), the physiologically active form of thyroid hormone, binds to nuclear receptor proteins and mediates the expression of several important cardiac genes, inducing transcription of the positively regulated genes including alpha-myosin heavy chain (MHC) and the sarcoplasmic reticulum calcium ATPase.	Triiodothyronine	19-23	major histocompatibility complex, class I, C	Homo sapiens	244-268
15282446-2	2004	Triiodothyronine, (T(3)), the physiologically active form of thyroid hormone, binds to nuclear receptor proteins and mediates the expression of several important cardiac genes, inducing transcription of the positively regulated genes including alpha-myosin heavy chain (MHC) and the sarcoplasmic reticulum calcium ATPase.	Triiodothyronine	19-23	major histocompatibility complex, class I, C	Homo sapiens	270-273
15144358-6	2004	Relative (%) myosin heavy-chain (MHC) expression increased for MHC IIa (pre=42.5+/-2.7, post=50.1+/-2.6), and decreased for MHC IIb (pre=21.8+/-2.8, post=15.4+/-2.4) for the CWT group.	CWT	174-177	major histocompatibility complex, class I, C	Homo sapiens	13-31
15186264-4	2004	Found in both humans and mice, CD1d-restricted NKT cells are a highly specialized cell type that, in contrast to conventional T cells, recognize lipid/glycolipid antigens presented by the non-classical MHC molecule CD1d.	Glycolipids	151-161	major histocompatibility complex, class I, C	Homo sapiens	202-205
15144358-6	2004	Relative (%) myosin heavy-chain (MHC) expression increased for MHC IIa (pre=42.5+/-2.7, post=50.1+/-2.6), and decreased for MHC IIb (pre=21.8+/-2.8, post=15.4+/-2.4) for the CWT group.	CWT	174-177	major histocompatibility complex, class I, C	Homo sapiens	33-36
12928367-4	2003	The results show that a panel of CD8+ CTL that are specific for the hapten DNP bound to two different peptides presented by HLA-A2 do the following: 1) show stringent MHC restriction, and 2) are largely affected by the same mutations on the HLA-A2 molecule that affected recognition by peptide-specific CTL.	2,4-Dinitrophenol	75-78	major histocompatibility complex, class I, C	Homo sapiens	167-170
15066441-0	2004	MHC-peptide binding is assisted by bound water molecules.	Water	41-46	major histocompatibility complex, class I, C	Homo sapiens	0-3
15066441-1	2004	Water plays an important role in determining the high affinity of epitopes to the class I MHC complex.	Water	0-5	major histocompatibility complex, class I, C	Homo sapiens	90-93
15066441-2	2004	To study the energy and dynamics of water interactions in the complex we performed molecular dynamics simulation of the class I MHC-HLA2 complex bound to the HIV reverse transcriptase epitope, ILKEPVHGV, and in the absence of the epitope.	Water	36-41	major histocompatibility complex, class I, C	Homo sapiens	128-131
15066441-4	2004	We studied the processes of water penetration in the interface between MHC and peptide, and identified 14 water molecules that stay bound for periods longer than 1ns in regions previously identified by crystallography.	Water	28-33	major histocompatibility complex, class I, C	Homo sapiens	71-74
15066441-4	2004	We studied the processes of water penetration in the interface between MHC and peptide, and identified 14 water molecules that stay bound for periods longer than 1ns in regions previously identified by crystallography.	Water	106-111	major histocompatibility complex, class I, C	Homo sapiens	71-74
15066441-5	2004	These water molecules in the interface perform definite "tasks" contributing to the binding energy: hydrogen bond bridges between MHC and peptide and filling empty spaces in the groove which enhance affinity without contributing to epitope specificity.	Water	6-11	major histocompatibility complex, class I, C	Homo sapiens	130-133
15066441-5	2004	These water molecules in the interface perform definite "tasks" contributing to the binding energy: hydrogen bond bridges between MHC and peptide and filling empty spaces in the groove which enhance affinity without contributing to epitope specificity.	Hydrogen	100-108	major histocompatibility complex, class I, C	Homo sapiens	130-133
15066441-6	2004	We calculate the binding energy for interfacial water molecules and find that there is an overall gain in free energy resulting from the formation of water clusters at the epitope-MHC interface.	Water	48-53	major histocompatibility complex, class I, C	Homo sapiens	180-183
15066441-6	2004	We calculate the binding energy for interfacial water molecules and find that there is an overall gain in free energy resulting from the formation of water clusters at the epitope-MHC interface.	Water	150-155	major histocompatibility complex, class I, C	Homo sapiens	180-183
15066441-8	2004	We conclude that water molecules at the interface play the role of active mediators in the MHC-peptide interaction, and might be responsible for the large binding affinity of the MHC complex to a large number of epitope sequences.	Water	17-22	major histocompatibility complex, class I, C	Homo sapiens	91-94
15066441-8	2004	We conclude that water molecules at the interface play the role of active mediators in the MHC-peptide interaction, and might be responsible for the large binding affinity of the MHC complex to a large number of epitope sequences.	Water	17-22	major histocompatibility complex, class I, C	Homo sapiens	179-182
14734778-0	2004	Metal-protein complex-mediated transport and delivery of Ni2+ to TCR/MHC contact sites in nickel-specific human T cell activation.	Nickel(2+)	57-61	major histocompatibility complex, class I, C	Homo sapiens	69-72
14734778-0	2004	Metal-protein complex-mediated transport and delivery of Ni2+ to TCR/MHC contact sites in nickel-specific human T cell activation.	Nickel	90-96	major histocompatibility complex, class I, C	Homo sapiens	69-72
14563688-2	2003	The expression of MHC-B, which contains an insert at the ATP binding pocket, has been linked to enhanced contractile kinetics.	Adenosine Triphosphate	57-60	major histocompatibility complex, class I, C	Homo sapiens	18-21
15084275-0	2004	T cells distinguish MHC-peptide complexes formed in separate vesicles and edited by H2-DM.	h2-dm	84-89	major histocompatibility complex, class I, C	Homo sapiens	20-23
12959962-2	2003	On the basis of potential age-related declines in aerobic enzyme activities and a shift in the expression of myosin heavy chain (MHC) isoforms, we hypothesized that maximal lactate steady-state (MLSS) exercise intensity would be altered as a function of age.	Lactic Acid	173-180	major histocompatibility complex, class I, C	Homo sapiens	109-127
12959962-2	2003	On the basis of potential age-related declines in aerobic enzyme activities and a shift in the expression of myosin heavy chain (MHC) isoforms, we hypothesized that maximal lactate steady-state (MLSS) exercise intensity would be altered as a function of age.	Lactic Acid	173-180	major histocompatibility complex, class I, C	Homo sapiens	129-132
12941846-4	2003	Here we report that coculture of immature DCs with tumor cells treated with the alkylating agents melphalan and chlorambucil leads to enhanced autologous and allogeneic T-cell activation, up-regulation of surface expression of MHC and costimulatory molecules, and increased interleukin (IL)-12 secretion.	Melphalan	98-107	major histocompatibility complex, class I, C	Homo sapiens	227-230
12941846-4	2003	Here we report that coculture of immature DCs with tumor cells treated with the alkylating agents melphalan and chlorambucil leads to enhanced autologous and allogeneic T-cell activation, up-regulation of surface expression of MHC and costimulatory molecules, and increased interleukin (IL)-12 secretion.	Chlorambucil	112-124	major histocompatibility complex, class I, C	Homo sapiens	227-230
12690105-1	2003	Recognition by CD8+ cytotoxic T lymphocytes (CTLs) of antigenic peptides bound to major histocompatibility class (MHC) I molecules on target cells leads to sustained calcium mobilization and CTL degranulation resulting in perforin-dependent killing.	Calcium	166-173	major histocompatibility complex, class I, C	Homo sapiens	114-117
12945896-1	2003	Glycopeptides that bind to MHC molecules on antigen presenting cells may elicit carbohydrate selective T cells.	Glycopeptides	0-13	major histocompatibility complex, class I, C	Homo sapiens	27-30
12945896-1	2003	Glycopeptides that bind to MHC molecules on antigen presenting cells may elicit carbohydrate selective T cells.	Carbohydrates	80-92	major histocompatibility complex, class I, C	Homo sapiens	27-30
12945896-6	2003	Our observation suggests an explanation for previous findings, which show that glycopeptides isolated from MHC molecules in nature usually carry small saccharides.	Glycopeptides	79-92	major histocompatibility complex, class I, C	Homo sapiens	107-110
12945896-6	2003	Our observation suggests an explanation for previous findings, which show that glycopeptides isolated from MHC molecules in nature usually carry small saccharides.	Carbohydrates	151-162	major histocompatibility complex, class I, C	Homo sapiens	107-110
12734360-5	2003	H4(b) is a consequence of a P3 threonine to isoleucine change in the MHC-bound peptide derived from epithelial membrane protein-3.	Threonine	31-40	major histocompatibility complex, class I, C	Homo sapiens	69-72
12736190-6	2003	MHC isoform composition was determined by SDS-PAGE silver staining, and mRNA levels of MHC isoforms were determined by RT-PCR.	Silver	51-57	major histocompatibility complex, class I, C	Homo sapiens	0-3
12784168-5	2003	MHC isoform was analyzed by SDS-PAGE using silver stain and MHC isoform mRNA by RT-PCR.	Sodium Dodecyl Sulfate	28-31	major histocompatibility complex, class I, C	Homo sapiens	0-3
12672369-0	2003	Chronic clenbuterol administration alters myosin heavy chain composition in standardbred mares.	Clenbuterol	8-19	major histocompatibility complex, class I, C	Homo sapiens	42-60
12672369-1	2003	The purpose of this study was to examine changes in myosin heavy chain (MHC) composition due to chronic clenbuterol administration with or without exercise in mares.	Clenbuterol	104-115	major histocompatibility complex, class I, C	Homo sapiens	52-70
12672369-1	2003	The purpose of this study was to examine changes in myosin heavy chain (MHC) composition due to chronic clenbuterol administration with or without exercise in mares.	Clenbuterol	104-115	major histocompatibility complex, class I, C	Homo sapiens	72-75
12672369-4	2003	MHC composition was determined via SDS gel electrophoresis and quantified using a scanning and densometric system.	Sodium Dodecyl Sulfate	35-38	major histocompatibility complex, class I, C	Homo sapiens	0-3
12672369-6	2003	MHC type IIA decreased (29.8+/-6.1 to 19.3+/-4.0%, CLENEX; and 36.8+/-12.4 to 26.4+/-7.9%, CLEN) and MHC type IIX increased (59.4+/-7.2 to 71.8+/-5.8%, CLENEX; and 50.5+/-12.5 to 62.0+/-9.3%, CLEN).	clenex	51-57	major histocompatibility complex, class I, C	Homo sapiens	0-3
12672369-6	2003	MHC type IIA decreased (29.8+/-6.1 to 19.3+/-4.0%, CLENEX; and 36.8+/-12.4 to 26.4+/-7.9%, CLEN) and MHC type IIX increased (59.4+/-7.2 to 71.8+/-5.8%, CLENEX; and 50.5+/-12.5 to 62.0+/-9.3%, CLEN).	clenex	152-158	major histocompatibility complex, class I, C	Homo sapiens	0-3
12672369-7	2003	Chronic clenbuterol administration with and without exercise resulted in a significant shift in MHC profile in Standardbred mares.	Clenbuterol	8-19	major histocompatibility complex, class I, C	Homo sapiens	96-99
12665986-7	2003	Conversely, CLFS induced changes in the MHC isoform pattern in the fast-to-slow direction with an approximately 20% decrease in the relative concentration of MHCIId/x (from 28% to 22%) and an approximately 10% increase in the relative concentration of MHCI (from 30% to 34%).	mhci	158-162	major histocompatibility complex, class I, C	Homo sapiens	40-43
12384546-7	2002	The analyzed Fabs not only recognize the cognate MHC-peptide complex in a recombinant soluble form but also the native complex as displayed on the surface of antigen-presenting cells and breast tumor cells.	FAB protocol	13-17	major histocompatibility complex, class I, C	Homo sapiens	49-52
12615513-11	2003	Intrathymic inoculation of fetal or paternal cells (like leukocyte, thymic dendritic cells, trophoblast cells) or paternal set of MHC molecules may cause central specific tolerance and may be a new possibility for immunotherapy in RSA patients.	rabbit sperm membrane autoantigen	231-234	major histocompatibility complex, class I, C	Homo sapiens	130-133
12402179-3	2002	SDS-PAGE of single muscle fibers revealed a higher proportion of MHC I in DIST compared to MID and REC (74.9 +/- 4.3 vs 54.4 +/- 2.8 vs 56.2 +/- 2.9 %, respectively; p < 0.05), less MHC IIa/IIx in DIST compared to MID and REC (0.0 +/- 0.0 vs 6.0 +/- 2.4 vs 15.9 +/- 4.2 %, respectively; p < 0.05), and more total hybrids (I/IIa+IIa/IIx+I/IIa/IIx) in REC than both run groups, DIST and MID (23.0 +/- 3.3 vs 6.2 +/- 1.1 vs 13.2 +/- 2.6 %, respectively; p < 0.05).	Sodium Dodecyl Sulfate	0-3	major histocompatibility complex, class I, C	Homo sapiens	65-68
12402179-3	2002	SDS-PAGE of single muscle fibers revealed a higher proportion of MHC I in DIST compared to MID and REC (74.9 +/- 4.3 vs 54.4 +/- 2.8 vs 56.2 +/- 2.9 %, respectively; p < 0.05), less MHC IIa/IIx in DIST compared to MID and REC (0.0 +/- 0.0 vs 6.0 +/- 2.4 vs 15.9 +/- 4.2 %, respectively; p < 0.05), and more total hybrids (I/IIa+IIa/IIx+I/IIa/IIx) in REC than both run groups, DIST and MID (23.0 +/- 3.3 vs 6.2 +/- 1.1 vs 13.2 +/- 2.6 %, respectively; p < 0.05).	Sodium Dodecyl Sulfate	0-3	major histocompatibility complex, class I, C	Homo sapiens	185-188
12121665-4	2002	The MHC clusters and ICAM-1 holes were mobile and transient and correlated with active and sustained signaling, as shown by staining with antibodies against phosphotyrosine and activated Lck.	Phosphotyrosine	157-172	major histocompatibility complex, class I, C	Homo sapiens	4-7
12218171-4	2002	This was accomplished by using analogue peptides of hTRT whose relative affinity for the MHC was increased by a targeted (-->Tyr) substitution in position one.	Tyrosine	128-131	major histocompatibility complex, class I, C	Homo sapiens	89-92
12193088-2	2002	During development, the heart switches from glycolysis to fatty acid beta-oxidation in vivo, as demonstrated by the developmental switching of the major isoform of myosin heavy chain (MHC) from beta to alpha.	Fatty Acids	58-68	major histocompatibility complex, class I, C	Homo sapiens	164-182
12084926-2	2002	The four MHC pockets at p1, p4, p6, and p9 that usually bind peptide side chains are largely empty because of alanines in the peptide at these positions.	Alanine	110-118	major histocompatibility complex, class I, C	Homo sapiens	9-12
12036932-6	2002	The analyzed Fabs not only recognize the cognate MHC-peptide complex in a recombinant soluble form but also the native complex as displayed on the surface of antigen-presenting cells and hTERT-expressing tumor cells.	FAB protocol	13-17	major histocompatibility complex, class I, C	Homo sapiens	49-52
12445324-1	2002	HLA-C alleles were characterized by a polymerase chain reaction-sequence specific oligonucleotide probe (PCR-SSOP) hybridization protocol in a sample of 120 Iranians from Tehran.	Oligonucleotides	82-97	major histocompatibility complex, class I, C	Homo sapiens	0-5
12010576-7	2002	The prevalence of SS and SB interactions at the MHC-peptide interface is shown in this study.	Antimony	25-27	major histocompatibility complex, class I, C	Homo sapiens	48-51
12010576-9	2002	CONCLUSION: The prevalently dominant SB interactions at the interface suggest the importance of peptide backbone conformation during MHC-peptide binding.	Antimony	37-39	major histocompatibility complex, class I, C	Homo sapiens	133-136
11937532-9	2002	The difference in the extent of this selection between the two SP lineages may indicate a class difference in the nature of the TCR-MHC interaction, the role of coreceptors in the selection process, or both.	sp	63-65	major histocompatibility complex, class I, C	Homo sapiens	132-135
11740293-5	2001	Expression of MHC isoforms was determined by SDS-PAGE.	Sodium Dodecyl Sulfate	45-48	major histocompatibility complex, class I, C	Homo sapiens	14-17
11966446-9	2002	This article reviews the rapidly expanding applications of beta-amino acids in the design of bioactive peptide analogues ranging from receptor agonists and antagonists, MHC-binding peptides, antimicrobial peptides and peptidase inhibitors.	beta-amino acids	59-75	major histocompatibility complex, class I, C	Homo sapiens	169-172
12074715-5	2002	The HLA Cw*0105 differs from Cw*0102 at positions 361 and 368 in exon 3 leading to a Trp to Arg and Cys to Ser substitution, respectively.	Tryptophan	85-88	major histocompatibility complex, class I, C	Homo sapiens	4-10
12074715-5	2002	The HLA Cw*0105 differs from Cw*0102 at positions 361 and 368 in exon 3 leading to a Trp to Arg and Cys to Ser substitution, respectively.	Arginine	92-95	major histocompatibility complex, class I, C	Homo sapiens	4-10
12074715-5	2002	The HLA Cw*0105 differs from Cw*0102 at positions 361 and 368 in exon 3 leading to a Trp to Arg and Cys to Ser substitution, respectively.	Cysteine	100-103	major histocompatibility complex, class I, C	Homo sapiens	4-10
12074715-5	2002	The HLA Cw*0105 differs from Cw*0102 at positions 361 and 368 in exon 3 leading to a Trp to Arg and Cys to Ser substitution, respectively.	Serine	107-110	major histocompatibility complex, class I, C	Homo sapiens	4-10
11836659-5	2002	Human leukocyte antigen (HLA)-Cw typing was performed by the polymerase chain reaction-sequence specific oligonucleotide probes (PCR-SSOP) method in 65 patients and in 177 healthy donors.	Oligonucleotides	105-120	major histocompatibility complex, class I, C	Homo sapiens	6-32
11777974-0	2002	NK cell inhibitory receptor Ly-49C residues involved in MHC class I binding.	ly-49c	28-34	major histocompatibility complex, class I, C	Homo sapiens	56-59
11777974-8	2002	The three Ly-49C mutations that affected MHC binding correspond to Ly-49A residues that are in contact or close to H-2D(d) in the co-crystal, demonstrating that MHC class I binding by Ly-49C is dependent on residues in the same area as that used by Ly-49A for ligand contacts.	Lysine	10-12	major histocompatibility complex, class I, C	Homo sapiens	41-44
11777974-8	2002	The three Ly-49C mutations that affected MHC binding correspond to Ly-49A residues that are in contact or close to H-2D(d) in the co-crystal, demonstrating that MHC class I binding by Ly-49C is dependent on residues in the same area as that used by Ly-49A for ligand contacts.	Lysine	10-12	major histocompatibility complex, class I, C	Homo sapiens	161-164
11777974-8	2002	The three Ly-49C mutations that affected MHC binding correspond to Ly-49A residues that are in contact or close to H-2D(d) in the co-crystal, demonstrating that MHC class I binding by Ly-49C is dependent on residues in the same area as that used by Ly-49A for ligand contacts.	ly-49c	10-16	major histocompatibility complex, class I, C	Homo sapiens	41-44
11777974-8	2002	The three Ly-49C mutations that affected MHC binding correspond to Ly-49A residues that are in contact or close to H-2D(d) in the co-crystal, demonstrating that MHC class I binding by Ly-49C is dependent on residues in the same area as that used by Ly-49A for ligand contacts.	ly-49c	10-16	major histocompatibility complex, class I, C	Homo sapiens	161-164
11777974-8	2002	The three Ly-49C mutations that affected MHC binding correspond to Ly-49A residues that are in contact or close to H-2D(d) in the co-crystal, demonstrating that MHC class I binding by Ly-49C is dependent on residues in the same area as that used by Ly-49A for ligand contacts.	Lysine	67-69	major histocompatibility complex, class I, C	Homo sapiens	41-44
11777974-8	2002	The three Ly-49C mutations that affected MHC binding correspond to Ly-49A residues that are in contact or close to H-2D(d) in the co-crystal, demonstrating that MHC class I binding by Ly-49C is dependent on residues in the same area as that used by Ly-49A for ligand contacts.	Lysine	67-69	major histocompatibility complex, class I, C	Homo sapiens	161-164
11714757-4	2001	Unlike clustering of HLA-C at the immune synapse, intercellular transfer of HLA-C is dependent on NK cell ATP, but not target cell ATP.	Adenosine Triphosphate	106-109	major histocompatibility complex, class I, C	Homo sapiens	76-81
11700035-5	2001	The interaction of BP with IFN-gamma inhibited the cytokine"s detection by immunoassay and impaired its activity, as assessed in three different assays: upregulation of MHC molecules on monocytes plus induction of nitric oxide synthesis and expression of monocyte chemoattractant protein-1 mRNA by epithelial cells.	Penicillin G	19-21	major histocompatibility complex, class I, C	Homo sapiens	169-172
11359825-6	2001	Blocking of CS.T3(378-395)-specific CD4+ T cell proliferation by anti-MHC class II mAb showed that recognition of promiscuous T cell epitopes is largely in association with MHC class II molecules.	Cesium	12-14	major histocompatibility complex, class I, C	Homo sapiens	70-73
11595517-4	2001	The MHC composition of the isolated fibres was determined by sodium dodecyl sulfate glycerol gel electrophoresis and Western blotting.	sodium dodecyl sulfate glycerol	61-92	major histocompatibility complex, class I, C	Homo sapiens	4-7
11562757-5	2001	Here, we show that carcinoma cells upregulate expression of CD54 and MHC molecules following in vitro exposure to srhCD40L but do not upregulate CD80 or CD86.	srhcd40l	114-122	major histocompatibility complex, class I, C	Homo sapiens	69-72
11581551-0	2001	Effects of oral creatine and resistance training on myosin heavy chain expression.	Creatine	16-24	major histocompatibility complex, class I, C	Homo sapiens	52-70
11581551-1	2001	PURPOSE: This study examined 12 wk of creatine (Cr) supplementation and heavy resistance training on muscle strength and myosin heavy chain (MHC) isoform mRNA and protein expression.	Creatine	38-46	major histocompatibility complex, class I, C	Homo sapiens	121-139
11581551-1	2001	PURPOSE: This study examined 12 wk of creatine (Cr) supplementation and heavy resistance training on muscle strength and myosin heavy chain (MHC) isoform mRNA and protein expression.	Creatine	38-46	major histocompatibility complex, class I, C	Homo sapiens	141-144
11581551-1	2001	PURPOSE: This study examined 12 wk of creatine (Cr) supplementation and heavy resistance training on muscle strength and myosin heavy chain (MHC) isoform mRNA and protein expression.	Creatine	48-50	major histocompatibility complex, class I, C	Homo sapiens	121-139
11581551-10	2001	CONCLUSION: Long-term Cr supplementation increases muscle strength and size, possibly as a result of increased MHC synthesis.	Creatine	22-24	major histocompatibility complex, class I, C	Homo sapiens	111-114
11470286-2	2001	Fluorescein-labelled peptides were used to determine MHC/peptide complex association and dissociation constants as well as the equilibrium binding constant (KD).	Fluorescein	0-11	major histocompatibility complex, class I, C	Homo sapiens	53-56
11359825-6	2001	Blocking of CS.T3(378-395)-specific CD4+ T cell proliferation by anti-MHC class II mAb showed that recognition of promiscuous T cell epitopes is largely in association with MHC class II molecules.	Cesium	12-14	major histocompatibility complex, class I, C	Homo sapiens	173-176
11172020-4	2001	Zn(2+)-dependent multimerization of KIR may be critical for formation of the clusters of KIR and HLA-C molecules, the "natural killer (NK) cell immune synapse," observed at the site of contact between the NK cell and target cell.	Zinc	0-2	major histocompatibility complex, class I, C	Homo sapiens	97-102
11401296-1	2001	We have developed a new method that provides enhanced resolution of myosin heavy chain (MHC) isoforms by sodium dodecyl sulfate--polyacrylamide gel electrophoresis (SDS-PAGE).	Sodium Dodecyl Sulfate	105-127	major histocompatibility complex, class I, C	Homo sapiens	88-91
11401296-1	2001	We have developed a new method that provides enhanced resolution of myosin heavy chain (MHC) isoforms by sodium dodecyl sulfate--polyacrylamide gel electrophoresis (SDS-PAGE).	polyacrylamide	129-143	major histocompatibility complex, class I, C	Homo sapiens	88-91
11401296-1	2001	We have developed a new method that provides enhanced resolution of myosin heavy chain (MHC) isoforms by sodium dodecyl sulfate--polyacrylamide gel electrophoresis (SDS-PAGE).	Sodium Dodecyl Sulfate	165-168	major histocompatibility complex, class I, C	Homo sapiens	88-91
11401296-7	2001	Alternative splicing of the rat alpha-MHC gene is known to generate two isoform species differing by inclusion (or exclusion) of a single glutamine residue, whose relative levels of expression correspond nicely with the amounts of each band identified in this study.	Glutamine	138-147	major histocompatibility complex, class I, C	Homo sapiens	38-41
11181631-3	2001	Because the myosin heavy chain (MHC) is the site of ATP hydrolysis and actin binding, we focus on the mechanical and energetic properties of different MHC isoforms.	Adenosine Triphosphate	52-55	major histocompatibility complex, class I, C	Homo sapiens	12-30
11181631-3	2001	Because the myosin heavy chain (MHC) is the site of ATP hydrolysis and actin binding, we focus on the mechanical and energetic properties of different MHC isoforms.	Adenosine Triphosphate	52-55	major histocompatibility complex, class I, C	Homo sapiens	32-35
11207317-0	2001	Immunosensitization of melanoma tumor cells to non-MHC Fas-mediated killing by MART-1-specific CTL cultures.	ammonium ferrous sulfate	55-58	major histocompatibility complex, class I, C	Homo sapiens	51-54
11207317-5	2001	In this study, we examined whether cis-diaminedichloroplatinum (II) cisplatin (CDDP) sensitizes MART-1/HLA A2.1(+) melanoma and melanoma variant tumor cells to non-MHC-restricted, Fas ligand (FasL)-mediated killing by CTL.	Cisplatin	68-77	major histocompatibility complex, class I, C	Homo sapiens	164-167
11207317-5	2001	In this study, we examined whether cis-diaminedichloroplatinum (II) cisplatin (CDDP) sensitizes MART-1/HLA A2.1(+) melanoma and melanoma variant tumor cells to non-MHC-restricted, Fas ligand (FasL)-mediated killing by CTL.	Cisplatin	79-83	major histocompatibility complex, class I, C	Homo sapiens	164-167
11292246-4	2001	Using an in vitro reaggregate thymic organ culture system which allows comparison of the abilities of various cell types to induce maturation of CD4+8+ precursors, we provide evidence that both MHC-peptide complexes and specialised accessory molecules must be provided by thymic epithelium for efficient mediation of positive selection.	cd4+8+	145-151	major histocompatibility complex, class I, C	Homo sapiens	194-197
11099312-8	2000	Hence, in these two TCR the Arg-Asp motif is clearly involved in contacting Ni-MHC complexes, and close cooperation between alpha and ss chain is required.	Arginine	28-31	major histocompatibility complex, class I, C	Homo sapiens	79-82
11161598-0	2001	Survival of intrastriatal xenografts of ventral mesencephalic dopamine neurons from MHC-deficient mice to adult rats.	Dopamine	62-70	major histocompatibility complex, class I, C	Homo sapiens	84-87
11133928-2	2001	This was done in the context of examining parallel findings concerning the role that thyroid hormone (T(3), 3,5,3"-triiodothyronine) plays in MHC expression.	Triiodothyronine	102-106	major histocompatibility complex, class I, C	Homo sapiens	142-145
11133928-2	2001	This was done in the context of examining parallel findings concerning the role that thyroid hormone (T(3), 3,5,3"-triiodothyronine) plays in MHC expression.	Triiodothyronine	108-131	major histocompatibility complex, class I, C	Homo sapiens	142-145
11099312-8	2000	Hence, in these two TCR the Arg-Asp motif is clearly involved in contacting Ni-MHC complexes, and close cooperation between alpha and ss chain is required.	Aspartic Acid	32-35	major histocompatibility complex, class I, C	Homo sapiens	79-82
11070166-1	2000	The structure of the A6 alphabetaTCR/HTLV-1 Tax-peptide/MHC I complex with proline 6 of Tax substituted with alanine (P6A), an antagonist, is nearly identical to the structure with wild-type Tax agonist.	Proline	75-82	major histocompatibility complex, class I, C	Homo sapiens	56-59
11160066-2	2001	We hypothesized that the reserve capacity for ATP consumption [1 -- (ratio of ATP(iso) to V(max) ATPase)] varies across VL muscle fibers expressing different MHC isoforms.	Adenosine Triphosphate	46-49	major histocompatibility complex, class I, C	Homo sapiens	158-161
11160066-2	2001	We hypothesized that the reserve capacity for ATP consumption [1 -- (ratio of ATP(iso) to V(max) ATPase)] varies across VL muscle fibers expressing different MHC isoforms.	Adenosine Triphosphate	78-81	major histocompatibility complex, class I, C	Homo sapiens	158-161
11160066-6	2001	The reserve capacity for ATP consumption was lower for fibers coexpressing MHC(2X) and MHC(2A) compared with fibers singularly expressing MHC(2A) and MHC(slow) (39 vs. 52 and 56%, respectively).	Adenosine Triphosphate	25-28	major histocompatibility complex, class I, C	Homo sapiens	75-78
11160066-6	2001	The reserve capacity for ATP consumption was lower for fibers coexpressing MHC(2X) and MHC(2A) compared with fibers singularly expressing MHC(2A) and MHC(slow) (39 vs. 52 and 56%, respectively).	Adenosine Triphosphate	25-28	major histocompatibility complex, class I, C	Homo sapiens	87-90
11160066-6	2001	The reserve capacity for ATP consumption was lower for fibers coexpressing MHC(2X) and MHC(2A) compared with fibers singularly expressing MHC(2A) and MHC(slow) (39 vs. 52 and 56%, respectively).	Adenosine Triphosphate	25-28	major histocompatibility complex, class I, C	Homo sapiens	87-90
11160066-6	2001	The reserve capacity for ATP consumption was lower for fibers coexpressing MHC(2X) and MHC(2A) compared with fibers singularly expressing MHC(2A) and MHC(slow) (39 vs. 52 and 56%, respectively).	Adenosine Triphosphate	25-28	major histocompatibility complex, class I, C	Homo sapiens	87-90
11029304-3	2000	Fibers expressing only the MHC I isoform could be appropriately identified on the basis of either the Ca(2+)- or Sr(2+)-activation characteristics or the MHC isoform composition.	strontium cation	113-119	major histocompatibility complex, class I, C	Homo sapiens	27-30
11029304-5	2000	A large proportion of fibers expressing both fast- and slow-twitch MHC isoforms displayed Ca(2+)- or Sr(2+)-activation properties that were not consistent with their MHC isoform composition; thus both fiber-typing methods were needed to fully characterize such fibers.	strontium cation	101-107	major histocompatibility complex, class I, C	Homo sapiens	67-70
11029304-6	2000	These data show that, in rat skeletal muscles, the extent of correlation between MHC isoform expression and Ca(2+)- or Sr(2+)-activation characteristics is fiber-type dependent.	strontium cation	119-125	major histocompatibility complex, class I, C	Homo sapiens	81-84
11070166-1	2000	The structure of the A6 alphabetaTCR/HTLV-1 Tax-peptide/MHC I complex with proline 6 of Tax substituted with alanine (P6A), an antagonist, is nearly identical to the structure with wild-type Tax agonist.	Alanine	109-116	major histocompatibility complex, class I, C	Homo sapiens	56-59
11070166-4	2000	We show that stepwise repair of a packing defect in the TCR/MHC interface using N-alkylated amino acids results in stepwise increases in TCR affinity and activity.	n-alkylated amino acids	80-103	major histocompatibility complex, class I, C	Homo sapiens	60-63
11343969-6	2000	Four of the suppressors identified to date reside in the MhC head, around the actin-binding site and near the lips of the pocket where ATP is hydrolyzed.	Adenosine Triphosphate	135-138	major histocompatibility complex, class I, C	Homo sapiens	57-60
10975839-0	2000	Beta 57-Asp plays an essential role in the unique SDS stability of HLA-DQA1*0102/DQB1*0602 alpha beta protein dimer, the class II MHC allele associated with protection from insulin-dependent diabetes mellitus.	beta 57-asp	0-11	major histocompatibility complex, class I, C	Homo sapiens	130-133
10975839-0	2000	Beta 57-Asp plays an essential role in the unique SDS stability of HLA-DQA1*0102/DQB1*0602 alpha beta protein dimer, the class II MHC allele associated with protection from insulin-dependent diabetes mellitus.	Sodium Dodecyl Sulfate	50-53	major histocompatibility complex, class I, C	Homo sapiens	130-133
10975839-1	2000	Studies of the stability of HLA-DQ have revealed a correlation between SDS stability of MHC class II alphabeta dimers and insulin-dependent diabetes mellitus (IDDM) susceptibility.	Sodium Dodecyl Sulfate	71-74	major histocompatibility complex, class I, C	Homo sapiens	88-91
10975839-2	2000	The MHC class II alphabeta dimer encoded by HLA-DQA1*0102/DQB1*0602 (DQ0602), which is a dominant protective allele in IDDM, exhibits the greatest SDS stability among HLA-DQ molecules in EBV-transformed B-lymphoblastoid cells and PBLs.	Sodium Dodecyl Sulfate	147-150	major histocompatibility complex, class I, C	Homo sapiens	4-7
10751194-3	2000	The in vivo rate of incorporation of 1-[(13)C]leucine into vastus lateralis MHC, actin, and mixed proteins was determined using a 14-h constant intravenous infusion of 1-[(13)C]leucine.	1-[(13)c]leucine	37-53	major histocompatibility complex, class I, C	Homo sapiens	76-79
10913316-0	2000	Class I MHC is stabilized against thermal denaturation by physiological concentrations of NaCl.	Sodium Chloride	90-94	major histocompatibility complex, class I, C	Homo sapiens	8-11
10913316-8	2000	While the degree of stabilization by 150 mM NaCl is greatest for low-affinity peptide/MHC complexes, the mechanism of stabilization is independent of peptide sequence.	Sodium Chloride	44-48	major histocompatibility complex, class I, C	Homo sapiens	86-89
10933163-3	2000	In the present study, we investigated in vitro whether CsA could alter the antigenicity of activated porcine aortic endothelial cells (PAECs) by reducing class I and class II MHC antigen expression.	Cyclosporine	55-58	major histocompatibility complex, class I, C	Homo sapiens	175-178
10933163-4	2000	METHODS: The effect of CsA on MHC antigen expression during tumor necrosis factor (TNF)-alpha- or lymphocyte-mediated PAEC activation was evaluated in vitro by flow cytometry and correlated to the ability of porcine ECs to promote human T lymphocyte proliferation.	Cyclosporine	23-26	major histocompatibility complex, class I, C	Homo sapiens	30-33
10933163-5	2000	The effect of CsA on class II MHC antigen mRNA expression was also analyzed and related to class II transcriptional activator (CIITA) mRNA expression.	Cyclosporine	14-17	major histocompatibility complex, class I, C	Homo sapiens	30-33
10933163-6	2000	RESULTS: Flow cytometry analysis showed that TNF-alpha-mediated induction of class II MHC antigen expression on PAECs was completely inhibited by CsA, whereas expression of class I MHC was reduced by 50%.	Cyclosporine	146-149	major histocompatibility complex, class I, C	Homo sapiens	86-89
10933163-10	2000	Pretreatment of PAECs with CsA for 4 hr before coculture with human peripheral blood leukocytes efficiently blocked the induction on PAECs of E-selectin and class II MHC antigens and inhibited overexpression of class I antigens.	Cyclosporine	27-30	major histocompatibility complex, class I, C	Homo sapiens	166-169
10933163-13	2000	CONCLUSION: Our study indicates that CsA could play a role in preventing porcine MHC antigens being directly presented to human T lymphocytes by xenogeneic ECs.	Cyclosporine	37-40	major histocompatibility complex, class I, C	Homo sapiens	81-84
10882406-2	2000	Here we show, for the MHC molecule HLA-A2, that this ability may be facilitated by a flexible water network that forms an interface between the MHC molecule and the peptide.	Water	94-99	major histocompatibility complex, class I, C	Homo sapiens	22-25
10882406-2	2000	Here we show, for the MHC molecule HLA-A2, that this ability may be facilitated by a flexible water network that forms an interface between the MHC molecule and the peptide.	Water	94-99	major histocompatibility complex, class I, C	Homo sapiens	144-147
10882406-6	2000	Conversely, for complexes of HLA-A2 with the more hydrophobic peptides, the water molecules are more rigidly bound at the MHC-peptide interface and a number of well-defined water-binding sites exist.	Water	76-81	major histocompatibility complex, class I, C	Homo sapiens	122-125
11009104-0	2000	A disulfide-linked natural killer cell receptor dimer has higher affinity for HLA-C than wild-type monomer.	Disulfides	2-11	major histocompatibility complex, class I, C	Homo sapiens	78-83
11256749-6	2000	The allotype specificity of KIR2DL2 for HLA-Cw3 is the result of a single hydrogen bond from Lys44 of the KIR to Asn80 of HLA-C as all other HLA-C residues that contact KIR are conserved.	Hydrogen	74-82	major histocompatibility complex, class I, C	Homo sapiens	40-45
10831129-3	2000	These EVT express HLA-G, HLA-E and HLA-C, an unusual combination of two non-classical and one classical MHC class I molecules.	EVT	6-9	major histocompatibility complex, class I, C	Homo sapiens	35-40
11249650-4	2000	In this review, we will discuss such crystal structures, as well as structures of glycopeptides and alternative T-cell antigens presented by MHC molecules.	Glycopeptides	82-95	major histocompatibility complex, class I, C	Homo sapiens	141-144
11256749-6	2000	The allotype specificity of KIR2DL2 for HLA-Cw3 is the result of a single hydrogen bond from Lys44 of the KIR to Asn80 of HLA-C as all other HLA-C residues that contact KIR are conserved.	Hydrogen	74-82	major histocompatibility complex, class I, C	Homo sapiens	122-127
10526246-4	1999	METHODS: MHC isoform composition in biopsies obtained from the vastus lateralis muscle was determined using SDS-PAGE.	Sodium Dodecyl Sulfate	108-111	major histocompatibility complex, class I, C	Homo sapiens	9-12
10631936-1	1999	The class I major histocompatibility complex (MHC class I) presents 8-10 residue peptides to cytotoxic T lymphocytes.	Peptides	81-89	major histocompatibility complex, class I, C	Homo sapiens	46-49
10656665-0	1999	Experimental evidence for the presence of a water network at the peptide-MHC interface.	Water	44-49	major histocompatibility complex, class I, C	Homo sapiens	73-76
10526246-12	1999	Maximal oxygen uptake (VO(2)max) per kg body weight (BW) (litres/min per kg) correlated significantly with the amount of MHC I (r=0.60) and MHC IIX (r=-0.72) but not with the amount of MHC IIA (r=0.35).	Oxygen	8-14	major histocompatibility complex, class I, C	Homo sapiens	121-124
10526246-12	1999	Maximal oxygen uptake (VO(2)max) per kg body weight (BW) (litres/min per kg) correlated significantly with the amount of MHC I (r=0.60) and MHC IIX (r=-0.72) but not with the amount of MHC IIA (r=0.35).	Oxygen	8-14	major histocompatibility complex, class I, C	Homo sapiens	140-143
10526246-12	1999	Maximal oxygen uptake (VO(2)max) per kg body weight (BW) (litres/min per kg) correlated significantly with the amount of MHC I (r=0.60) and MHC IIX (r=-0.72) but not with the amount of MHC IIA (r=0.35).	Oxygen	8-14	major histocompatibility complex, class I, C	Homo sapiens	140-143
10468663-9	1999	Single fibre studies have demonstrated a relationship between ATP phosphorylation potential and MHC isoform complement.	Adenosine Triphosphate	62-65	major histocompatibility complex, class I, C	Homo sapiens	96-99
10499066-8	1999	The adductor muscles--TA, LCA, and IA--have a higher percentage of type IIB MHC and a lower percentage of type I when compared with the abductor--PCA.	Lithocholic Acid	26-29	major histocompatibility complex, class I, C	Homo sapiens	76-79
10499066-9	1999	The rank file order for type IIB MHC composition (TA > LCA > or = IA > PCA) is the same in all specimens.	Lithocholic Acid	58-61	major histocompatibility complex, class I, C	Homo sapiens	33-36
10330269-0	1999	Binding of random copolymers of three amino acids to class II MHC molecules.	copolymers	18-28	major histocompatibility complex, class I, C	Homo sapiens	62-65
10426279-10	1999	While the MHC-peptide complexes formed with the native peptide are stable, complexes formed with the Ala-substituted peptide had a functional t1/2 of less than 4 hr at neutral pH.	Alanine	101-104	major histocompatibility complex, class I, C	Homo sapiens	10-13
10494800-2	1999	The myosin heavy chain (MHC) contains the actin- and ATP-binding sites and represents the molecular motor of muscle contraction.	Adenosine Triphosphate	53-56	major histocompatibility complex, class I, C	Homo sapiens	4-22
10494800-2	1999	The myosin heavy chain (MHC) contains the actin- and ATP-binding sites and represents the molecular motor of muscle contraction.	Adenosine Triphosphate	53-56	major histocompatibility complex, class I, C	Homo sapiens	24-27
10330269-3	1999	In the present study the binding of copolymers composed of three of the four amino acids found in poly(Y,E,A,K) to purified class II MHC molecules was examined.	copolymers	36-46	major histocompatibility complex, class I, C	Homo sapiens	133-136
10202015-0	1999	MHC-restricted, glycopeptide-specific T cells show specificity for both carbohydrate and peptide residues.	Carbohydrates	72-84	major histocompatibility complex, class I, C	Homo sapiens	0-3
10199819-9	1999	These findings suggest that, even though the bulk of the thyroid hormone responsiveness of the gene is contained within the first 215 bp of the beta-MHC promoter sequence, the exact mechanism of triiodothyronine (T3) action remains to be elucidated.	Triiodothyronine	195-211	major histocompatibility complex, class I, C	Homo sapiens	149-152
10199819-9	1999	These findings suggest that, even though the bulk of the thyroid hormone responsiveness of the gene is contained within the first 215 bp of the beta-MHC promoter sequence, the exact mechanism of triiodothyronine (T3) action remains to be elucidated.	Triiodothyronine	213-215	major histocompatibility complex, class I, C	Homo sapiens	149-152
10573776-9	1999	Almost 100% of the MHC mRNA in the dome, mid bladder body, and base contains a 7-amino acid insert near the ATP-binding region, whereas the MHC in the urethral smooth muscle is only 81% inserted.	7-amino acid	79-91	major histocompatibility complex, class I, C	Homo sapiens	19-22
10217154-3	1999	1993, 75, 2337-2340) previously established a sodium dodecyl sulfate - polyacrylamide gel electrophoresis (SDS-PAGE) protocol for separating all four rat skeletal muscle myosin heavy chain (MHC) isoforms (MHC I, IIa, IIx, IIb); however, when applied to human muscle, the type II MHC isoforms (Ila, IIx) are not clearly distinguished.	Sodium Dodecyl Sulfate	46-68	major histocompatibility complex, class I, C	Homo sapiens	190-193
10217154-3	1999	1993, 75, 2337-2340) previously established a sodium dodecyl sulfate - polyacrylamide gel electrophoresis (SDS-PAGE) protocol for separating all four rat skeletal muscle myosin heavy chain (MHC) isoforms (MHC I, IIa, IIx, IIb); however, when applied to human muscle, the type II MHC isoforms (Ila, IIx) are not clearly distinguished.	polyacrylamide	71-85	major histocompatibility complex, class I, C	Homo sapiens	190-193
10217154-3	1999	1993, 75, 2337-2340) previously established a sodium dodecyl sulfate - polyacrylamide gel electrophoresis (SDS-PAGE) protocol for separating all four rat skeletal muscle myosin heavy chain (MHC) isoforms (MHC I, IIa, IIx, IIb); however, when applied to human muscle, the type II MHC isoforms (Ila, IIx) are not clearly distinguished.	Sodium Dodecyl Sulfate	107-110	major histocompatibility complex, class I, C	Homo sapiens	190-193
10217154-4	1999	In this brief paper we describe a modification of the SDS-PAGE protocol which yields distinct and consistent separation of all three adult human MHC isoforms (MHC I, IIa, IIx) in a minigel system.	Sodium Dodecyl Sulfate	54-57	major histocompatibility complex, class I, C	Homo sapiens	145-148
10217154-4	1999	In this brief paper we describe a modification of the SDS-PAGE protocol which yields distinct and consistent separation of all three adult human MHC isoforms (MHC I, IIa, IIx) in a minigel system.	Sodium Dodecyl Sulfate	54-57	major histocompatibility complex, class I, C	Homo sapiens	159-162
10217154-6	1999	Results provide a valuable SDS-PAGE minigel technique for separating MHC isoforms in human muscle without the difficult task of casting gradient gels.	Sodium Dodecyl Sulfate	27-30	major histocompatibility complex, class I, C	Homo sapiens	69-72
9916711-6	1999	The TCR signaling efficacy was dramatically reduced during peptide/MHC engagement in the zeta mutants containing the displaced disulfide bond.	Disulfides	127-136	major histocompatibility complex, class I, C	Homo sapiens	67-70
10573776-9	1999	Almost 100% of the MHC mRNA in the dome, mid bladder body, and base contains a 7-amino acid insert near the ATP-binding region, whereas the MHC in the urethral smooth muscle is only 81% inserted.	Adenosine Triphosphate	108-111	major histocompatibility complex, class I, C	Homo sapiens	19-22
9843753-1	1998	Using sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), we have developed a simple method to isolate myosin heavy chain (MHC) and actin from small (60-80 mg) human skeletal muscle samples for the determination of their fractional synthesis rates.	Sodium Dodecyl Sulfate	6-28	major histocompatibility complex, class I, C	Homo sapiens	121-139
9843753-1	1998	Using sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), we have developed a simple method to isolate myosin heavy chain (MHC) and actin from small (60-80 mg) human skeletal muscle samples for the determination of their fractional synthesis rates.	Sodium Dodecyl Sulfate	65-68	major histocompatibility complex, class I, C	Homo sapiens	121-139
9843753-1	1998	Using sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), we have developed a simple method to isolate myosin heavy chain (MHC) and actin from small (60-80 mg) human skeletal muscle samples for the determination of their fractional synthesis rates.	Sodium Dodecyl Sulfate	65-68	major histocompatibility complex, class I, C	Homo sapiens	141-144
9843753-2	1998	The amounts of MHC and actin isolated are adequate for the quantification of [13C]leucine abundance by gas chromatography-combustion-isotope ratio mass spectrometry (GC-C-IRMS).	13c	78-81	major histocompatibility complex, class I, C	Homo sapiens	15-18
9843753-2	1998	The amounts of MHC and actin isolated are adequate for the quantification of [13C]leucine abundance by gas chromatography-combustion-isotope ratio mass spectrometry (GC-C-IRMS).	Leucine	82-89	major histocompatibility complex, class I, C	Homo sapiens	15-18
9925306-4	1998	A number of contacts shorter than the conventional van der Waals distance have been disclosed between CH hydrogens and aromatic side-chain groups in the MHC/peptide complexes.	Hydrogen	105-114	major histocompatibility complex, class I, C	Homo sapiens	153-156
9809978-5	1998	In this report, we show that five of five MHC class I+ tumor cell lines grown in medium containing Adriamycin developed into variants that expressed higher levels of MHC class I than did their corresponding parental cell lines.	Doxorubicin	99-109	major histocompatibility complex, class I, C	Homo sapiens	42-45
9809978-5	1998	In this report, we show that five of five MHC class I+ tumor cell lines grown in medium containing Adriamycin developed into variants that expressed higher levels of MHC class I than did their corresponding parental cell lines.	Doxorubicin	99-109	major histocompatibility complex, class I, C	Homo sapiens	166-169
9809978-9	1998	When the drug-selected variants were cocultured with the same CTLs to eliminate tumor cells expressing higher levels of MHC-I (MHC-Ihi), the CTL-resistant tumor cells exhibited a drug sensitivity profile similar to that of the parental cell lines that were not exposed to Adriamycin.	Doxorubicin	272-282	major histocompatibility complex, class I, C	Homo sapiens	120-123
9809978-9	1998	When the drug-selected variants were cocultured with the same CTLs to eliminate tumor cells expressing higher levels of MHC-I (MHC-Ihi), the CTL-resistant tumor cells exhibited a drug sensitivity profile similar to that of the parental cell lines that were not exposed to Adriamycin.	Doxorubicin	272-282	major histocompatibility complex, class I, C	Homo sapiens	127-130
9742454-2	1998	To date, the amino-acid sequence of the MHC of calcium-regulated myosins is known only for two closely related species of scallops.	Calcium	47-54	major histocompatibility complex, class I, C	Homo sapiens	40-43
9788828-0	1998	Improved exercise tolerance after losartan and enalapril in heart failure: correlation with changes in skeletal muscle myosin heavy chain composition.	Losartan	34-42	major histocompatibility complex, class I, C	Homo sapiens	119-137
9788828-0	1998	Improved exercise tolerance after losartan and enalapril in heart failure: correlation with changes in skeletal muscle myosin heavy chain composition.	Enalapril	47-56	major histocompatibility complex, class I, C	Homo sapiens	119-137
9730972-7	1998	A nucleotide binding site, which is located at residues 660-674, controls binding of AMPD1 to MHC in response to changes in intracellular ATP concentration.	Adenosine Triphosphate	138-141	major histocompatibility complex, class I, C	Homo sapiens	94-97
9730972-8	1998	Deletion analyses demonstrate that the amino-terminal 65 residues of AMPD1 play a critical role in modulating the sensitivity to ATP-induced inhibition of MHC binding.	Adenosine Triphosphate	129-132	major histocompatibility complex, class I, C	Homo sapiens	155-158
9730972-9	1998	Alternative splicing of the AMPD1 gene product, which alters the sequence of residues 8-12, produces two AMPD1 isoforms that exhibit different MHC binding properties in the presence of ATP.	Adenosine Triphosphate	185-188	major histocompatibility complex, class I, C	Homo sapiens	143-146
10397471-1	1998	This paper examines the monohydrated complex of cisplatin (MHC) with respect to kinetics and cytotoxicity.	Cisplatin	48-57	major histocompatibility complex, class I, C	Homo sapiens	59-62
10397471-8	1998	In culture media with low chloride ion concentrations, the stability of MHC was related to changes in pH.	Chlorides	26-34	major histocompatibility complex, class I, C	Homo sapiens	72-75
10397471-9	1998	At a pH of between 6.0 and 7.2, MHC was rapidly converted to cisplatin.	Cisplatin	61-70	major histocompatibility complex, class I, C	Homo sapiens	32-35
10397471-11	1998	These findings might have clinical significance given that MHC circulates in the blood stream of patients receiving cisplatin infusions and that solid tumours often have environments that are extremely acidotic.	Cisplatin	116-125	major histocompatibility complex, class I, C	Homo sapiens	59-62
9742454-7	1998	The deduced amino-acid sequence shows the squid MHC to be 72-73% identical and 86-87% similar to the calcium-regulated scallop MHCs cloned previously.	Calcium	101-108	major histocompatibility complex, class I, C	Homo sapiens	48-51
9710860-3	1998	The MHC composition of muscle homogenates was determined by electrophoresis techniques (SDS-PAGE).	Sodium Dodecyl Sulfate	88-91	major histocompatibility complex, class I, C	Homo sapiens	4-7
9670929-3	1998	One soluble KIR2D, derived from an inhibitory receptor with a long cytoplasmic tail (KIR2DL1), bound to HLA-C allotypes containing asparagine 77 and lysine 80 in the heavy chain, as expected, since these allotypes inhibit lysis by NK cells expressing KIR2DL1.	Asparagine	131-141	major histocompatibility complex, class I, C	Homo sapiens	104-109
9740224-0	1998	MHC-dependent and -independent activation of human nickel-specific CD8+ cytotoxic T cells from allergic donors.	Nickel	51-57	major histocompatibility complex, class I, C	Homo sapiens	0-3
9670929-3	1998	One soluble KIR2D, derived from an inhibitory receptor with a long cytoplasmic tail (KIR2DL1), bound to HLA-C allotypes containing asparagine 77 and lysine 80 in the heavy chain, as expected, since these allotypes inhibit lysis by NK cells expressing KIR2DL1.	Lysine	149-155	major histocompatibility complex, class I, C	Homo sapiens	104-109
9611151-2	1998	These analyses were performed in the context of slow-twitch type I myosin heavy-chain (MHC) expression, a 3,5,3"-triiodothyronine (T3)-regulated gene that displays varying responsiveness to T3 in the above tissues.	Triiodothyronine	106-129	major histocompatibility complex, class I, C	Homo sapiens	87-90
9611151-2	1998	These analyses were performed in the context of slow-twitch type I myosin heavy-chain (MHC) expression, a 3,5,3"-triiodothyronine (T3)-regulated gene that displays varying responsiveness to T3 in the above tissues.	Triiodothyronine	131-133	major histocompatibility complex, class I, C	Homo sapiens	87-90
9459510-4	1998	Cw*1203 (Ser-Asn) and Cw*12042 (Asn-Lys) constitute the second known example of HLA-C alleles only differing at the KIR-related dimorphism of residues 77-80.	Serine	9-12	major histocompatibility complex, class I, C	Homo sapiens	80-85
9670929-4	1998	Surprisingly, another KIR2D (KIR2DL2), which inhibits NK lysis of cells expressing HLA-C molecules with serine 77 and asparagine 80, bound to HLA-C allotypes carrying either amino acid motif.	Serine	104-110	major histocompatibility complex, class I, C	Homo sapiens	83-88
9670929-4	1998	Surprisingly, another KIR2D (KIR2DL2), which inhibits NK lysis of cells expressing HLA-C molecules with serine 77 and asparagine 80, bound to HLA-C allotypes carrying either amino acid motif.	Serine	104-110	major histocompatibility complex, class I, C	Homo sapiens	142-147
9670929-4	1998	Surprisingly, another KIR2D (KIR2DL2), which inhibits NK lysis of cells expressing HLA-C molecules with serine 77 and asparagine 80, bound to HLA-C allotypes carrying either amino acid motif.	Asparagine	118-128	major histocompatibility complex, class I, C	Homo sapiens	83-88
9670929-4	1998	Surprisingly, another KIR2D (KIR2DL2), which inhibits NK lysis of cells expressing HLA-C molecules with serine 77 and asparagine 80, bound to HLA-C allotypes carrying either amino acid motif.	Asparagine	118-128	major histocompatibility complex, class I, C	Homo sapiens	142-147
9761926-1	1998	Crystals of the human MHC-encoded molecule MICA, a homologue of MHC class I proteins, have been grown in hanging-drop vapor-diffusion trials using ammonium sulfate as a precipitating agent with recombinant protein expressed in a baculovirus-based system.	Ammonium Sulfate	147-163	major histocompatibility complex, class I, C	Homo sapiens	22-25
9518724-8	1998	Single fibre analysis using SDS-PAGE revealed that MHCs from immunohistochemically defined type 1, type 2 and type 3 fibres ran as three distinct isoform bands, while MHC of tonic fibres co-migrated with type 1 MHC.	Sodium Dodecyl Sulfate	28-31	major histocompatibility complex, class I, C	Homo sapiens	51-54
9575870-4	1998	Myosin was characterized with electrophoresis in nondenaturing conditions, SDS-glycerol PAGE, and Western blotting with monoclonal antibodies specific for slow and fast myosin heavy chain (MHC) isoforms.	Sodium Dodecyl Sulfate	75-78	major histocompatibility complex, class I, C	Homo sapiens	189-192
9523114-2	1998	Homologs of MHC molecules have diverse roles that include presentation of lipid antigens (by CD1), transport of immunoglobulins (by the neonatal Fc receptor), regulation of iron metabolism (by the hemochromatosis gene product, HFE), and deception of the host immune system (by viral homologs).	Iron	173-177	major histocompatibility complex, class I, C	Homo sapiens	12-15
9579585-0	1998	Three-step tumor targeting via biotin-avidin interaction as a versatile system to elicit T cell-mediated, non-MHC-restricted cytotoxic activity against neoplastic cells.	Biotin	31-37	major histocompatibility complex, class I, C	Homo sapiens	110-113
9530220-5	1998	The glycerol concentration in the separating gel is an important factor for successfully separating MHC-alpha and MHC-beta in myocardial samples from different species.	Glycerol	4-12	major histocompatibility complex, class I, C	Homo sapiens	100-103
9530220-5	1998	The glycerol concentration in the separating gel is an important factor for successfully separating MHC-alpha and MHC-beta in myocardial samples from different species.	Glycerol	4-12	major histocompatibility complex, class I, C	Homo sapiens	114-117
9521888-4	1998	Dual-immunofluorescence labeling for the smooth muscle contractile protein SM-myosin heavy chain (MHC) and for bromodeoxyuridine (BRDU) uptake revealed that prazosin treatment for 4 days stimulated a threefold increase in the density of proliferating fibroblasts surrounding transverse arteriolar trees.	Prazosin	157-165	major histocompatibility complex, class I, C	Homo sapiens	75-96
9521888-4	1998	Dual-immunofluorescence labeling for the smooth muscle contractile protein SM-myosin heavy chain (MHC) and for bromodeoxyuridine (BRDU) uptake revealed that prazosin treatment for 4 days stimulated a threefold increase in the density of proliferating fibroblasts surrounding transverse arteriolar trees.	Prazosin	157-165	major histocompatibility complex, class I, C	Homo sapiens	98-101
9459510-4	1998	Cw*1203 (Ser-Asn) and Cw*12042 (Asn-Lys) constitute the second known example of HLA-C alleles only differing at the KIR-related dimorphism of residues 77-80.	Asparagine	13-16	major histocompatibility complex, class I, C	Homo sapiens	80-85
9459510-4	1998	Cw*1203 (Ser-Asn) and Cw*12042 (Asn-Lys) constitute the second known example of HLA-C alleles only differing at the KIR-related dimorphism of residues 77-80.	Asparagine	32-35	major histocompatibility complex, class I, C	Homo sapiens	80-85
9459510-4	1998	Cw*1203 (Ser-Asn) and Cw*12042 (Asn-Lys) constitute the second known example of HLA-C alleles only differing at the KIR-related dimorphism of residues 77-80.	Lysine	36-39	major histocompatibility complex, class I, C	Homo sapiens	80-85
9237101-1	1997	Copolymer 1 (Cop 1), a synthetic copolymer of amino acids, effective in suppression of experimental allergic encephalomyelitis (EAE) and myelin basic protein (MBP), was shown to bind extensively and promiscuously to the class II MHC molecules on antigen-presenting cells (APC) without prior processing.	copolymer	0-9	major histocompatibility complex, class I, C	Homo sapiens	229-232
9400626-13	1997	These findings demonstrate the human T cell response to DNP-modified autologous melanoma cells is mediated by hapten-modified, MHC-associated peptides.	dnp	56-59	major histocompatibility complex, class I, C	Homo sapiens	127-130
9398727-7	1997	Fiber type distribution was assessed on the basis of myosin heavy chain (MHC) isoform composition determined by electrophoresis on polyacrylamide gels.	polyacrylamide	131-145	major histocompatibility complex, class I, C	Homo sapiens	73-76
9352354-2	1997	Two polymorphisms occur in this pocket in the human class II MHC beta chain at position 85 and 86. beta 85 is usually Val, occasionally Ala, whereas beta 86 can be Gly or Val.	Valine	118-121	major histocompatibility complex, class I, C	Homo sapiens	61-64
9352354-2	1997	Two polymorphisms occur in this pocket in the human class II MHC beta chain at position 85 and 86. beta 85 is usually Val, occasionally Ala, whereas beta 86 can be Gly or Val.	Alanine	136-139	major histocompatibility complex, class I, C	Homo sapiens	61-64
9352354-2	1997	Two polymorphisms occur in this pocket in the human class II MHC beta chain at position 85 and 86. beta 85 is usually Val, occasionally Ala, whereas beta 86 can be Gly or Val.	Glycine	164-167	major histocompatibility complex, class I, C	Homo sapiens	61-64
9352354-2	1997	Two polymorphisms occur in this pocket in the human class II MHC beta chain at position 85 and 86. beta 85 is usually Val, occasionally Ala, whereas beta 86 can be Gly or Val.	Valine	171-174	major histocompatibility complex, class I, C	Homo sapiens	61-64
9348531-1	1997	Myosin II heavy chain (MHC) specific protein kinase C (MHC-PKC), isolated from Dictyostelium discoideum, regulates myosin II assembly and localization in response to the chemoattractant cyclic AMP.	Cyclic AMP	186-196	major histocompatibility complex, class I, C	Homo sapiens	23-26
9348531-1	1997	Myosin II heavy chain (MHC) specific protein kinase C (MHC-PKC), isolated from Dictyostelium discoideum, regulates myosin II assembly and localization in response to the chemoattractant cyclic AMP.	Cyclic AMP	186-196	major histocompatibility complex, class I, C	Homo sapiens	55-58
9348531-6	1997	Furthermore, we found that the cytosolic MHC-PKC, which is inactive, formed a complex with Dd14-3-3 in the cytosol in a cyclic AMP-dependent manner, whereas the membrane-bound active MHC-PKC was not found in a complex with Dd14-3-3.	Cyclic AMP	120-130	major histocompatibility complex, class I, C	Homo sapiens	41-44
9310837-2	1997	In these simulations, a loosely structured network of water molecules is present in the binding groove between the peptide and the MHC molecule, and may be important in completing the peptide-MHC interface.	Water	54-59	major histocompatibility complex, class I, C	Homo sapiens	131-134
9310837-2	1997	In these simulations, a loosely structured network of water molecules is present in the binding groove between the peptide and the MHC molecule, and may be important in completing the peptide-MHC interface.	Water	54-59	major histocompatibility complex, class I, C	Homo sapiens	192-195
9242718-2	1997	Subsequently, the isoforms of the myosin heavy chain (MHC) were analysed by sodium dodecyl sulphate (SDS) gel electrophoresis.	Sodium Dodecyl Sulfate	76-99	major histocompatibility complex, class I, C	Homo sapiens	34-52
9242718-2	1997	Subsequently, the isoforms of the myosin heavy chain (MHC) were analysed by sodium dodecyl sulphate (SDS) gel electrophoresis.	Sodium Dodecyl Sulfate	76-99	major histocompatibility complex, class I, C	Homo sapiens	54-57
9242718-2	1997	Subsequently, the isoforms of the myosin heavy chain (MHC) were analysed by sodium dodecyl sulphate (SDS) gel electrophoresis.	Sodium Dodecyl Sulfate	101-104	major histocompatibility complex, class I, C	Homo sapiens	34-52
9242718-2	1997	Subsequently, the isoforms of the myosin heavy chain (MHC) were analysed by sodium dodecyl sulphate (SDS) gel electrophoresis.	Sodium Dodecyl Sulfate	101-104	major histocompatibility complex, class I, C	Homo sapiens	54-57
9271317-2	1997	The synthetic random copolymer of the amino acids, L-Glu, L-Lys, L-Ala and L-Tyr, termed GLAT, with promiscuous binding to multiple MHC class II alleles, reduces the incidence, onset and severity of disease in the BIO.D2 --> BALB/c model of lethal GVHD.	copolymer	21-30	major histocompatibility complex, class I, C	Homo sapiens	132-135
9271317-2	1997	The synthetic random copolymer of the amino acids, L-Glu, L-Lys, L-Ala and L-Tyr, termed GLAT, with promiscuous binding to multiple MHC class II alleles, reduces the incidence, onset and severity of disease in the BIO.D2 --> BALB/c model of lethal GVHD.	Glutamic Acid	51-56	major histocompatibility complex, class I, C	Homo sapiens	132-135
9271317-2	1997	The synthetic random copolymer of the amino acids, L-Glu, L-Lys, L-Ala and L-Tyr, termed GLAT, with promiscuous binding to multiple MHC class II alleles, reduces the incidence, onset and severity of disease in the BIO.D2 --> BALB/c model of lethal GVHD.	Lysine	58-63	major histocompatibility complex, class I, C	Homo sapiens	132-135
9271317-2	1997	The synthetic random copolymer of the amino acids, L-Glu, L-Lys, L-Ala and L-Tyr, termed GLAT, with promiscuous binding to multiple MHC class II alleles, reduces the incidence, onset and severity of disease in the BIO.D2 --> BALB/c model of lethal GVHD.	polyalanine	65-70	major histocompatibility complex, class I, C	Homo sapiens	132-135
9271317-2	1997	The synthetic random copolymer of the amino acids, L-Glu, L-Lys, L-Ala and L-Tyr, termed GLAT, with promiscuous binding to multiple MHC class II alleles, reduces the incidence, onset and severity of disease in the BIO.D2 --> BALB/c model of lethal GVHD.	Tyrosine	75-80	major histocompatibility complex, class I, C	Homo sapiens	132-135
9202065-0	1997	Direct, MHC-dependent presentation of the drug sulfamethoxazole to human alphabeta T cell clones.	Sulfamethoxazole	47-63	major histocompatibility complex, class I, C	Homo sapiens	8-11
9202065-6	1997	The MHC restriction was evaluated, first, by inhibition using anti-class I and anti-class II mAb, and second, by the degree of sulfamethoxazole-induced stimulation by partially matched APC.	Sulfamethoxazole	127-143	major histocompatibility complex, class I, C	Homo sapiens	4-7
9202065-12	1997	Sulfamethoxazole can be presented in an unstable, but MHC-restricted fashion, which is independent of processing.	Sulfamethoxazole	0-16	major histocompatibility complex, class I, C	Homo sapiens	54-57
9202065-13	1997	These features are best explained by a direct, noncovalent binding of sulfamethoxazole to the MHC-peptide complex.	Sulfamethoxazole	70-86	major histocompatibility complex, class I, C	Homo sapiens	94-97
9193569-0	1997	1,25-Dihydroxyvitamin D3 reduces MHC antigen expression on pancreatic beta-cells in vitro.	Calcitriol	0-24	major histocompatibility complex, class I, C	Homo sapiens	33-36
9161883-2	1997	Specific reduction in class I MHC levels (range 60-76%) was induced by brief exposure to citrate buffer (pH 3.0).	Citric Acid	89-96	major histocompatibility complex, class I, C	Homo sapiens	30-33
9120277-9	1997	Thus, the presence of Leu at position 33 generates an anchor specific for the restricting MHC allele and helps define the peptide binding motif of this allele, HLA-DRB3*0101 (DR52a).	Leucine	22-25	major histocompatibility complex, class I, C	Homo sapiens	90-93
9075934-2	1997	Using site-directed mutagenesis, residues on HLA-C that determine the locus specificity (alphaVal-76), allotype group specificity (a dimorphism alphaAsn-80/Lys-80), and affinity of NKIR binding (a second pair of dimorphisms, alphaAla-73, Asp-90 or alphaThr-73, Ala-90) have been identified.	Lysine	156-159	major histocompatibility complex, class I, C	Homo sapiens	45-50
9075934-2	1997	Using site-directed mutagenesis, residues on HLA-C that determine the locus specificity (alphaVal-76), allotype group specificity (a dimorphism alphaAsn-80/Lys-80), and affinity of NKIR binding (a second pair of dimorphisms, alphaAla-73, Asp-90 or alphaThr-73, Ala-90) have been identified.	alphaala	225-233	major histocompatibility complex, class I, C	Homo sapiens	45-50
9075934-2	1997	Using site-directed mutagenesis, residues on HLA-C that determine the locus specificity (alphaVal-76), allotype group specificity (a dimorphism alphaAsn-80/Lys-80), and affinity of NKIR binding (a second pair of dimorphisms, alphaAla-73, Asp-90 or alphaThr-73, Ala-90) have been identified.	Aspartic Acid	238-241	major histocompatibility complex, class I, C	Homo sapiens	45-50
9075934-2	1997	Using site-directed mutagenesis, residues on HLA-C that determine the locus specificity (alphaVal-76), allotype group specificity (a dimorphism alphaAsn-80/Lys-80), and affinity of NKIR binding (a second pair of dimorphisms, alphaAla-73, Asp-90 or alphaThr-73, Ala-90) have been identified.	Alanine	230-233	major histocompatibility complex, class I, C	Homo sapiens	45-50
9135559-0	1997	Effects of 1 alpha,25-dihydroxyvitamin D3 and cytokines on the expression of MHC antigens, complement receptors and other antigens on human blood monocytes and U937 cells: role in cell differentiation, activation and phagocytosis.	Calcitriol	11-41	major histocompatibility complex, class I, C	Homo sapiens	77-80
9057103-2	1997	We investigated expression of MHC genes of spontaneously contracting neonatal cardiomyocytes experimentally arrested by permanent depolarization [potassium chloride (KCl)] as well as by electromechanical uncoupling [2,3 butanedione monoxime (BDM)].	Potassium Chloride	146-164	major histocompatibility complex, class I, C	Homo sapiens	30-33
9057103-2	1997	We investigated expression of MHC genes of spontaneously contracting neonatal cardiomyocytes experimentally arrested by permanent depolarization [potassium chloride (KCl)] as well as by electromechanical uncoupling [2,3 butanedione monoxime (BDM)].	Potassium Chloride	166-169	major histocompatibility complex, class I, C	Homo sapiens	30-33
9057103-2	1997	We investigated expression of MHC genes of spontaneously contracting neonatal cardiomyocytes experimentally arrested by permanent depolarization [potassium chloride (KCl)] as well as by electromechanical uncoupling [2,3 butanedione monoxime (BDM)].	diacetylmonoxime	216-240	major histocompatibility complex, class I, C	Homo sapiens	30-33
9057103-2	1997	We investigated expression of MHC genes of spontaneously contracting neonatal cardiomyocytes experimentally arrested by permanent depolarization [potassium chloride (KCl)] as well as by electromechanical uncoupling [2,3 butanedione monoxime (BDM)].	diacetylmonoxime	242-245	major histocompatibility complex, class I, C	Homo sapiens	30-33
9057103-5	1997	However, treatment with phenylephrine for the same period increased significantly beta-MHC expression to 55%.	Phenylephrine	24-37	major histocompatibility complex, class I, C	Homo sapiens	87-90
9224541-7	1997	MHC protein isoform differences were determined through sodium dodecyl-polyacrylamide gel electrophoresis (SDS-PAGE) followed by densitometric analysis.	sodium dodecyl-polyacrylamide	56-85	major histocompatibility complex, class I, C	Homo sapiens	0-3
9224541-7	1997	MHC protein isoform differences were determined through sodium dodecyl-polyacrylamide gel electrophoresis (SDS-PAGE) followed by densitometric analysis.	Sodium Dodecyl Sulfate	107-110	major histocompatibility complex, class I, C	Homo sapiens	0-3
9135559-11	1997	Our results demonstrate that calcitriol, alone or in combination with cytokines, modulates expression of MHC, CD11b, CD11c, CD14 and CD71 Ag on both monocytes and U937 cells, and impairs the phagocytic property of monocytes.	Calcitriol	29-39	major histocompatibility complex, class I, C	Homo sapiens	105-108
9013965-2	1997	Using synthetic peptides, we demonstrated recently that this was due to expression of subthreshold levels of appropriate MHC-peptide complexes.	Peptides	16-24	major histocompatibility complex, class I, C	Homo sapiens	121-124
9038850-3	1997	We determined to what extent the synthesis rate of mixed muscle protein in humans reflects that of myosin heavy chain (MHC), the main contractile protein responsible for the conversion of ATP to mechanical energy as muscle contraction.	Adenosine Triphosphate	188-191	major histocompatibility complex, class I, C	Homo sapiens	99-117
9038850-3	1997	We determined to what extent the synthesis rate of mixed muscle protein in humans reflects that of myosin heavy chain (MHC), the main contractile protein responsible for the conversion of ATP to mechanical energy as muscle contraction.	Adenosine Triphosphate	188-191	major histocompatibility complex, class I, C	Homo sapiens	119-122
9118981-5	1997	Myosin heavy chain (MHC) differences were determined through sodium dodecyl-polyacrylamide gel electrophoresis followed by densitometric analysis.	sodium dodecyl-polyacrylamide	61-90	major histocompatibility complex, class I, C	Homo sapiens	0-18
9118981-5	1997	Myosin heavy chain (MHC) differences were determined through sodium dodecyl-polyacrylamide gel electrophoresis followed by densitometric analysis.	sodium dodecyl-polyacrylamide	61-90	major histocompatibility complex, class I, C	Homo sapiens	20-23
9118981-14	1997	Subjects with higher compositions of type II MHC accumulated more lactate and displayed greater reductions in MF and MFCV during fatigue.	Lactic Acid	66-73	major histocompatibility complex, class I, C	Homo sapiens	45-48
9156650-2	1997	In addition, we have shown that both chloroquine and hydroxychloroquine can inhibit T cell responses in vitro to minor and major histocompatibility (MHC) antigens.	Chloroquine	37-48	major histocompatibility complex, class I, C	Homo sapiens	149-152
9156650-2	1997	In addition, we have shown that both chloroquine and hydroxychloroquine can inhibit T cell responses in vitro to minor and major histocompatibility (MHC) antigens.	Hydroxychloroquine	53-71	major histocompatibility complex, class I, C	Homo sapiens	149-152
9156650-3	1997	We review the rationale for the use of lysosomotropic amines, whose primary mechanism of action appears to be inhibition of MHC class II antigen presentation, as therapy for GVHD in humans.	Amines	54-60	major histocompatibility complex, class I, C	Homo sapiens	124-127
9156650-5	1997	The lysosomotropic amines, at low concentrations, in combination with the T cell-specific agent, cyclosporin A, synergistically suppresses the T cell response to MiHC and MHC in mouse and in human.	Amines	19-25	major histocompatibility complex, class I, C	Homo sapiens	171-174
9156650-5	1997	The lysosomotropic amines, at low concentrations, in combination with the T cell-specific agent, cyclosporin A, synergistically suppresses the T cell response to MiHC and MHC in mouse and in human.	Cyclosporine	97-110	major histocompatibility complex, class I, C	Homo sapiens	171-174
8970619-0	1996	Antioxidant lazaroid U-74006F improves renal function and reduces the expression of cytokines, inducible nitric oxide synthase, and MHC antigens in a syngeneic renal transplant model.	lazaroid u-74006f	12-29	major histocompatibility complex, class I, C	Homo sapiens	132-135
8781544-15	1996	In addition, data presented here provide the first documentation that phosphorylation and sulfation of tyrosine residues may retain the MHC-binding ability and T-cell stimulatory activity of class II epitopes.	Tyrosine	103-111	major histocompatibility complex, class I, C	Homo sapiens	136-139
9001571-7	1996	DNP-modified vaccine also induces T cells in the peripheral blood, which respond to DNP-modified autologous cells in a hapten-specific, MHC-restricted manner.	dnp	0-3	major histocompatibility complex, class I, C	Homo sapiens	136-139
9001571-7	1996	DNP-modified vaccine also induces T cells in the peripheral blood, which respond to DNP-modified autologous cells in a hapten-specific, MHC-restricted manner.	dnp	84-87	major histocompatibility complex, class I, C	Homo sapiens	136-139
9001571-8	1996	Moreover, a T cell line generated from these lymphocytes responded to only a single HPLC fraction of MHC-associated, DNP-modified tumor peptides.	dnp	117-120	major histocompatibility complex, class I, C	Homo sapiens	101-104
8953412-0	1996	Study of aspartate at residue 9 of HLA-C molecules in Japanese patients with psoriasis vulgaris.	Aspartic Acid	9-18	major histocompatibility complex, class I, C	Homo sapiens	35-40
8953412-1	1996	The frequency of aspartate at residue 9 (Asp-9) of HLA-C molecules was investigated among 75 Japanese patients with psoriasis vulgaris and 50 healthy controls.	Aspartic Acid	17-26	major histocompatibility complex, class I, C	Homo sapiens	51-56
8953412-1	1996	The frequency of aspartate at residue 9 (Asp-9) of HLA-C molecules was investigated among 75 Japanese patients with psoriasis vulgaris and 50 healthy controls.	Aspartic Acid	41-44	major histocompatibility complex, class I, C	Homo sapiens	51-56
8953412-2	1996	We developed a technique of polymerase chain reaction sequence-specific primer (PCR-SSP) amplification of genomic DNA for HLA-C alleles with a codon for Asp-9.	Aspartic Acid	153-156	major histocompatibility complex, class I, C	Homo sapiens	122-127
8953412-7	1996	Asp-9 is located on a beta sheet of alpha 1 domain of HLA-C molecule and influences the peptide binding of the C pocket of the groove together with Ala-73.	Aspartic Acid	0-3	major histocompatibility complex, class I, C	Homo sapiens	54-59
8953412-7	1996	Asp-9 is located on a beta sheet of alpha 1 domain of HLA-C molecule and influences the peptide binding of the C pocket of the groove together with Ala-73.	Alanine	148-151	major histocompatibility complex, class I, C	Homo sapiens	54-59
8909942-7	1996	The polymorphic regions of the class II MHC were identified by PCR in association with sequence-specific oligonucleotide probes.	Oligonucleotides	105-120	major histocompatibility complex, class I, C	Homo sapiens	40-43
8883300-10	1996	The guanine found in Cw*0403 is identical to all HLA-C alleles except HLA-Cw*0401, which has an adenine.	Guanine	4-11	major histocompatibility complex, class I, C	Homo sapiens	49-54
8621918-5	1996	Results of T cell stimulation studies were correlated with two well studied characteristics of the peptide/MHC complex, which are the affinity of peptide binding to MHC and the stability of the resulting complex upon PAGE in the presence of SDS.	Sodium Dodecyl Sulfate	241-244	major histocompatibility complex, class I, C	Homo sapiens	107-110
8691154-3	1996	Here, we show that a human killer inhibitory receptor specific for HLA-C also recruits PTP-1C after phosphorylation induced either by the pharmacological agent phenylarsine oxide or by conjugation with target cells.	oxophenylarsine	160-178	major histocompatibility complex, class I, C	Homo sapiens	67-72
8617950-5	1996	In contrast, HLA-C allotypes have four glycan structures, comprising those associated with HLA-A and -B and two additional glycans.	Polysaccharides	39-45	major histocompatibility complex, class I, C	Homo sapiens	13-18
8617950-5	1996	In contrast, HLA-C allotypes have four glycan structures, comprising those associated with HLA-A and -B and two additional glycans.	Polysaccharides	123-130	major histocompatibility complex, class I, C	Homo sapiens	13-18
8617950-6	1996	Identical oligosaccharides were present on different allotypes of a class I HLA locus, and in particular, HLA-C allotypes defining two inhibitory specificities for NK cells were shown to possess the same set of oligosaccharides.	Oligosaccharides	211-227	major histocompatibility complex, class I, C	Homo sapiens	106-111
8739245-7	1996	Furthermore, we present data showing that an endogenous anti-beta-MHC transcript is regulated by both pressure-overload- or thyroxine-induced cardiac hypertrophy.	Thyroxine	124-133	major histocompatibility complex, class I, C	Homo sapiens	66-69
8739245-9	1996	In vitro studies, where oligonucleotides complementary to beta-MHC have been introduced into cardiomyocytes, show that the mRNA levels of beta-MHC are decreased by 14-21% within 72 h after addition of the oligonucleotides.	Oligonucleotides	24-40	major histocompatibility complex, class I, C	Homo sapiens	143-146
8739245-9	1996	In vitro studies, where oligonucleotides complementary to beta-MHC have been introduced into cardiomyocytes, show that the mRNA levels of beta-MHC are decreased by 14-21% within 72 h after addition of the oligonucleotides.	Oligonucleotides	205-221	major histocompatibility complex, class I, C	Homo sapiens	63-66
8739245-9	1996	In vitro studies, where oligonucleotides complementary to beta-MHC have been introduced into cardiomyocytes, show that the mRNA levels of beta-MHC are decreased by 14-21% within 72 h after addition of the oligonucleotides.	Oligonucleotides	205-221	major histocompatibility complex, class I, C	Homo sapiens	143-146
8790939-3	1996	During differentiation, CL6 cells displayed the following general cardiac muscle properties: (1) alpha- and beta-cardiac myosin heavy chain (MHC) transcripts were first detected on day 10 after treatment with DMSO.	Dimethyl Sulfoxide	209-213	major histocompatibility complex, class I, C	Homo sapiens	141-144
8596693-3	1996	After 6 months of FES-training the number of fibres containing only MHC IIB was reduced to 2.6% (P < 0.05), the number of fibres containing only MHC IIA was increased to 44.3% (P < 0.05), and the number of fibres co-expressing MHC IIA and MHC IIB was 50.9% (ns).	fes	18-21	major histocompatibility complex, class I, C	Homo sapiens	68-71
8596693-9	1996	This study shows that FES-training of paralysed human skeletal muscle administrated over a prolonged period of time, can lead to a marked switch in MHC expression from about equal amounts of MHC IIA and MHC IIB to an almost total dominance of MHC IIA.	fes	22-25	major histocompatibility complex, class I, C	Homo sapiens	148-151
8596693-9	1996	This study shows that FES-training of paralysed human skeletal muscle administrated over a prolonged period of time, can lead to a marked switch in MHC expression from about equal amounts of MHC IIA and MHC IIB to an almost total dominance of MHC IIA.	fes	22-25	major histocompatibility complex, class I, C	Homo sapiens	191-194
8596693-9	1996	This study shows that FES-training of paralysed human skeletal muscle administrated over a prolonged period of time, can lead to a marked switch in MHC expression from about equal amounts of MHC IIA and MHC IIB to an almost total dominance of MHC IIA.	fes	22-25	major histocompatibility complex, class I, C	Homo sapiens	191-194
8596693-9	1996	This study shows that FES-training of paralysed human skeletal muscle administrated over a prolonged period of time, can lead to a marked switch in MHC expression from about equal amounts of MHC IIA and MHC IIB to an almost total dominance of MHC IIA.	fes	22-25	major histocompatibility complex, class I, C	Homo sapiens	191-194
8920244-2	1996	Our data suggest that MHC bound antigen analogs which antagonize the mature T-cell response, bind the T-cell receptor below a crucial affinity threshold required to stimulate the early biochemical events necessary for activation, such as phosphatidylinositol metabolism and the Ca2+ influx.	Phosphatidylinositols	238-258	major histocompatibility complex, class I, C	Homo sapiens	22-25
8690894-3	1996	The identity of the product was confirmed by Southern blotting and hybridization by a second HLA-C-specific oligonucleotide.	Oligonucleotides	108-123	major histocompatibility complex, class I, C	Homo sapiens	93-98
8568273-1	1996	Rats transgenic for the human MHC molecule HLA-B27 were used to study the effect of two alleles, cima and cimb, which are associated with peptide transport by the MHC-encoded Tap2 transporter, on the function of HLA-B27 as a restriction element for CTL recognition of the male H-Y minor H Ag and on the multisystem inflammatory disease characteristic of B27 transgenic rats.	cima	97-101	major histocompatibility complex, class I, C	Homo sapiens	163-166
8568273-1	1996	Rats transgenic for the human MHC molecule HLA-B27 were used to study the effect of two alleles, cima and cimb, which are associated with peptide transport by the MHC-encoded Tap2 transporter, on the function of HLA-B27 as a restriction element for CTL recognition of the male H-Y minor H Ag and on the multisystem inflammatory disease characteristic of B27 transgenic rats.	cimb	106-110	major histocompatibility complex, class I, C	Homo sapiens	163-166
8932525-1	1996	In this study, we have cloned a 1.0 kb myosin heavy chain (MHC) cDNA by screening an axolotl heart cDNA library with the monoclonal antibody MF20 against a light meromyosin (LMM) region of MHC.	meromyosin	162-172	major histocompatibility complex, class I, C	Homo sapiens	59-62
8543946-7	1995	Myosin heavy chain (MHC) and light chain (MLC) isoforms were resolved by 6% and 12% sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE), respectively, and quantified densitometrically.	Sodium Dodecyl Sulfate	84-107	major histocompatibility complex, class I, C	Homo sapiens	0-18
8543946-7	1995	Myosin heavy chain (MHC) and light chain (MLC) isoforms were resolved by 6% and 12% sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE), respectively, and quantified densitometrically.	polyacrylamide	108-122	major histocompatibility complex, class I, C	Homo sapiens	0-18
8543946-7	1995	Myosin heavy chain (MHC) and light chain (MLC) isoforms were resolved by 6% and 12% sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE), respectively, and quantified densitometrically.	Sodium Dodecyl Sulfate	144-147	major histocompatibility complex, class I, C	Homo sapiens	0-18
7665617-5	1995	MHC mRNA levels in messenger ribonucleoprotein complexes and translating polysomes were examined by sucrose gradient fractionation.	Sucrose	100-107	major histocompatibility complex, class I, C	Homo sapiens	0-3
8533830-2	1995	We describe a missense mutation of the beta-cardiac myosin heavy chain (MHC) gene, a G to T transversion (741 Gly-->Trp) identified by direct sequencing of exon 20 in four individuals affected with familial hypertrophic cardiomyopathy.	Tryptophan	119-122	major histocompatibility complex, class I, C	Homo sapiens	72-75
8522454-5	1995	Three of 26 clones recognized tissue-specific antigens in the context of donor MHC class I antigens lysing donor KCLs but not B-LCLs.	Potassium Chloride	113-117	major histocompatibility complex, class I, C	Homo sapiens	79-82
7629517-3	1995	The previously defined NK clones belonging to "group 1" recognize HLA-C*0401 (Cw4) and other HLA-C alleles sharing Asn at position 77 and Lys at position 80.	Asparagine	115-118	major histocompatibility complex, class I, C	Homo sapiens	93-98
7629517-4	1995	Conversely, the "group 2" NK clones recognize HLA-Cw*0302 (Cw3) and other HLA-C alleles characterized by Ser at position 77 and Asn at position 80.	Serine	105-108	major histocompatibility complex, class I, C	Homo sapiens	46-51
7565816-12	1995	Rationally designed synthetic peptides, either alone or in a stable complex with MHC, might be of value for controlling CTL activity.	Peptides	30-38	major histocompatibility complex, class I, C	Homo sapiens	81-84
7615460-5	1995	Although captopril treatment significantly reversed the elevations in mean arterial pressure, LV mass, and beta-MHC content in the AbCon group, it had very little effect on these variables in the Nx-D group.	Captopril	9-18	major histocompatibility complex, class I, C	Homo sapiens	112-115
7675770-1	1995	Microwave heating of formalin-fixed, paraffin embedded tissue sections in citrate buffer (MHC) has been shown recently to enhance the antigenicity of a number of formalin-sensitive epitopes.	Formaldehyde	21-29	major histocompatibility complex, class I, C	Homo sapiens	90-93
7675770-1	1995	Microwave heating of formalin-fixed, paraffin embedded tissue sections in citrate buffer (MHC) has been shown recently to enhance the antigenicity of a number of formalin-sensitive epitopes.	Paraffin	37-45	major histocompatibility complex, class I, C	Homo sapiens	90-93
7675770-1	1995	Microwave heating of formalin-fixed, paraffin embedded tissue sections in citrate buffer (MHC) has been shown recently to enhance the antigenicity of a number of formalin-sensitive epitopes.	Citric Acid	74-81	major histocompatibility complex, class I, C	Homo sapiens	90-93
7675770-1	1995	Microwave heating of formalin-fixed, paraffin embedded tissue sections in citrate buffer (MHC) has been shown recently to enhance the antigenicity of a number of formalin-sensitive epitopes.	Formaldehyde	162-170	major histocompatibility complex, class I, C	Homo sapiens	90-93
7675770-8	1995	We concluded that MHC facilitates the recognition of diagnostically important antigens in formalin-fixed, paraffin-embedded tissue and can be applied routinely without adverse affects.	Formaldehyde	90-98	major histocompatibility complex, class I, C	Homo sapiens	18-21
7675770-8	1995	We concluded that MHC facilitates the recognition of diagnostically important antigens in formalin-fixed, paraffin-embedded tissue and can be applied routinely without adverse affects.	Paraffin	106-114	major histocompatibility complex, class I, C	Homo sapiens	18-21
7643135-5	1995	Immunosuppression with Cyclosporin A prevented invasion of T-lymphocytes and allowed differentiation of implanted myoblasts into myofibres as well as down-regulation of MHC expression.	Cyclosporine	23-36	major histocompatibility complex, class I, C	Homo sapiens	169-172
7643135-13	1995	It is suggested that the start of immune reaction following Cyclosporin A withdrawal is initiated by remaining small amounts of donor MHC molecules, possibly related to the continuous proliferation of the cell-lined-derived donor myoblasts.	Cyclosporine	60-73	major histocompatibility complex, class I, C	Homo sapiens	134-137
7887887-0	1995	The cardiac myosin heavy chain Arg-403-->Gln mutation that causes hypertrophic cardiomyopathy does not affect the actin- or ATP-binding capacities of two size-limited recombinant myosin heavy chain fragments.	Arginine	31-34	major histocompatibility complex, class I, C	Homo sapiens	12-30
7887887-0	1995	The cardiac myosin heavy chain Arg-403-->Gln mutation that causes hypertrophic cardiomyopathy does not affect the actin- or ATP-binding capacities of two size-limited recombinant myosin heavy chain fragments.	Glutamine	44-47	major histocompatibility complex, class I, C	Homo sapiens	12-30
7887887-2	1995	We observed the presence of a mutated beta-MHC mRNA in a formalin-fixed paraffin-embedded myocardial tissue of a proband from family A, which Geisterfer-Lowrance et al.	Formaldehyde	57-65	major histocompatibility complex, class I, C	Homo sapiens	43-46
7887887-2	1995	We observed the presence of a mutated beta-MHC mRNA in a formalin-fixed paraffin-embedded myocardial tissue of a proband from family A, which Geisterfer-Lowrance et al.	Paraffin	72-80	major histocompatibility complex, class I, C	Homo sapiens	43-46
7864081-2	1995	Separation and detection of MHCs by sodium dodecyl sulfate-polyacrylamide gel electrophoresis were achieved to a degree such that MHC composition is consistent with previous reports on functional and mRNA data.	Sodium Dodecyl Sulfate	36-58	major histocompatibility complex, class I, C	Homo sapiens	28-31
7864081-2	1995	Separation and detection of MHCs by sodium dodecyl sulfate-polyacrylamide gel electrophoresis were achieved to a degree such that MHC composition is consistent with previous reports on functional and mRNA data.	polyacrylamide	59-73	major histocompatibility complex, class I, C	Homo sapiens	28-31
9346848-5	1995	While alpha-linked glycopeptides can bind to MHC without major alterations in the spatial arrangements and hydrogen bonding pattern of class II-peptide binding, the binding of beta-linked glycopeptides is considerably less favorable due to steric and columbic conflicts.	Glycopeptides	19-32	major histocompatibility complex, class I, C	Homo sapiens	45-48
7962778-1	1994	BACKGROUND: Psoriasis vulgaris was reported to be associated with a specific alanine residue at position 73 of HLA-C alleles in Japanese patients.	Alanine	77-84	major histocompatibility complex, class I, C	Homo sapiens	111-116
7962778-4	1994	RESULTS: All patients possessed in their HLA-C antigens an alanine residue at position 73 (p < 0.002).	Alanine	59-66	major histocompatibility complex, class I, C	Homo sapiens	41-46
7860358-3	1994	The genes encoding the 21OH enzyme are located in the class III segment of the MHC complex.	21oh	23-27	major histocompatibility complex, class I, C	Homo sapiens	79-82
9346848-0	1995	Computer design of T-cell agonist or antagonist glycopeptides: the effect of sugar identity and anomeric configuration on MHC binding.	Glycopeptides	48-61	major histocompatibility complex, class I, C	Homo sapiens	122-125
7868378-1	1994	Oligonucleotide typing for alleles of the MHC loci DRB1, DQA1, and DQB1 was performed in 160 patients suffering from EOPA, JCA (or JRA = juvenile rheumatoid arthritis).	Oligonucleotides	0-15	major histocompatibility complex, class I, C	Homo sapiens	42-45
7860358-6	1994	Also, we tested whether presence of autoantibodies against 21OH is associated with specific alleles in MHC.	21oh	59-63	major histocompatibility complex, class I, C	Homo sapiens	103-106
7860358-10	1994	The presence of autoantibodies against 21OH was not found to be directly determined by the MHC alleles; rather it was associated with the clinical form of the disease.	21oh	39-43	major histocompatibility complex, class I, C	Homo sapiens	91-94
7836942-9	1994	Even in biopsies that contained relatively large amounts of these last three fibre types, the amount of neonatal and/or alpha-cardiac MHC detected on SDS-PAGE was limited, suggesting that these MHCs are a minor component in the fibres in which they are expressed.	Sodium Dodecyl Sulfate	150-153	major histocompatibility complex, class I, C	Homo sapiens	134-137
7917991-0	1994	Alanine at position 73 of HLA-C is associated with psoriasis vulgaris in Finland.	Alanine	0-7	major histocompatibility complex, class I, C	Homo sapiens	26-31
7985807-4	1994	In addition, measurements of the ks of MHC in skeletal muscle of rats in vivo using radioisotope-tracer methodologies are described.	Potassium	33-35	major histocompatibility complex, class I, C	Homo sapiens	39-42
7917991-2	1994	This sequence codes for alanine at position 73 of the HLA-C molecule in the antigen binding cleft, and alanine may play a role in susceptibility to the disease.	Alanine	103-110	major histocompatibility complex, class I, C	Homo sapiens	54-59
7917991-2	1994	This sequence codes for alanine at position 73 of the HLA-C molecule in the antigen binding cleft, and alanine may play a role in susceptibility to the disease.	Alanine	24-31	major histocompatibility complex, class I, C	Homo sapiens	54-59
7812819-5	1994	The reduction of MHC-antigens expressiveness, which takes place due to serotonin, is intermediated by the classical 5-HT2 receptor.	Serotonin	71-80	major histocompatibility complex, class I, C	Homo sapiens	17-20
8045787-2	1994	Almost all of the class II region of the MHC has already been cloned in cosmids but a gap remained between the DMB and LMP2 genes.	dmb	111-114	major histocompatibility complex, class I, C	Homo sapiens	41-44
8214040-1	1993	The objectives of this study were to 1) examine the effect of hypo- and hyperthyroidism (triiodothyronine treatment) on the distribution of type IIA myosin heavy chain (MHC) in the soleus at the single fiber level and 2) correlate changes in the single fiber distribution of type IIA MHC with the maximal shortening velocity of whole skeletal muscle.	Triiodothyronine	89-105	major histocompatibility complex, class I, C	Homo sapiens	169-172
7514604-1	1994	Rhamnogalacturonan-mediated enhancement of MHC-unrestricted cytotoxicity was studied with freshly isolated CD56+CD3- natural killer (NK) cells, interleukin-2 (IL-2)-activated CD56+ lymphokine-activated killer (LAK) cells und IL-2/anti-CD3-activated T cells as effector cells using NK-sensitive and NK-insensitive tumor cells as targets.	rhamnogalacturonan	0-18	major histocompatibility complex, class I, C	Homo sapiens	43-46
8265660-6	1993	Transfection of cells with HLA-C alleles encoding Asn-77-Lys-80 (including HLA-Cw4, -Cw5, and -Cw6) inhibited the lysis of the targets by NK1-specific NK cells, whereas HLA-C alleles encoding Ser-77-Asn-80 (including HLA-Cw1, -Cw7, and -Cw13) protected the targets from NK2-specific NK cells.	Serine	192-195	major histocompatibility complex, class I, C	Homo sapiens	27-32
8265660-6	1993	Transfection of cells with HLA-C alleles encoding Asn-77-Lys-80 (including HLA-Cw4, -Cw5, and -Cw6) inhibited the lysis of the targets by NK1-specific NK cells, whereas HLA-C alleles encoding Ser-77-Asn-80 (including HLA-Cw1, -Cw7, and -Cw13) protected the targets from NK2-specific NK cells.	Serine	192-195	major histocompatibility complex, class I, C	Homo sapiens	75-80
8265660-6	1993	Transfection of cells with HLA-C alleles encoding Asn-77-Lys-80 (including HLA-Cw4, -Cw5, and -Cw6) inhibited the lysis of the targets by NK1-specific NK cells, whereas HLA-C alleles encoding Ser-77-Asn-80 (including HLA-Cw1, -Cw7, and -Cw13) protected the targets from NK2-specific NK cells.	Asparagine	50-53	major histocompatibility complex, class I, C	Homo sapiens	27-32
8265660-6	1993	Transfection of cells with HLA-C alleles encoding Asn-77-Lys-80 (including HLA-Cw4, -Cw5, and -Cw6) inhibited the lysis of the targets by NK1-specific NK cells, whereas HLA-C alleles encoding Ser-77-Asn-80 (including HLA-Cw1, -Cw7, and -Cw13) protected the targets from NK2-specific NK cells.	Asparagine	50-53	major histocompatibility complex, class I, C	Homo sapiens	75-80
8290568-8	1994	Biochemical analysis of one FHC mutant (Arg-249-->Gln) demonstrates that the structures formed by the mutant are solubilized at a lower ionic strength than those formed by wild-type MHC.	Arginine	40-43	major histocompatibility complex, class I, C	Homo sapiens	185-188
8290568-8	1994	Biochemical analysis of one FHC mutant (Arg-249-->Gln) demonstrates that the structures formed by the mutant are solubilized at a lower ionic strength than those formed by wild-type MHC.	Glutamine	53-56	major histocompatibility complex, class I, C	Homo sapiens	185-188
8253204-1	1993	At least four myosin heavy chain (MHC) isoforms were separated by SDS-PAGE in extracts of intrafusal fibers isolated by microdissection from human lumbrical muscles.	Sodium Dodecyl Sulfate	66-69	major histocompatibility complex, class I, C	Homo sapiens	34-37
8218246-4	1993	The presence of a C-terminal Lys in many of the peptides that are restricted to IEk suggests that this electrostatic interaction is widely used to bind peptides to this MHC molecule.	Lysine	29-32	major histocompatibility complex, class I, C	Homo sapiens	169-172
8106277-6	1993	The results indicate that (a) intracellular MHC molecules show higher peptide-binding capacity, (b) peptides that are about 18-25 amino acids long need only a core region of 11 amino acids for binding, (c) specific positions of the peptides are important for DR1 binding, (d) most of the naturally processed peptides show a proline at position 2 or 3 that may represent a stop signal for trimming, and (e) Ii peptides are very abundant in DR1 peptide pools derived from intracellular compartments.	Proline	324-331	major histocompatibility complex, class I, C	Homo sapiens	44-47
8360471-0	1993	Glycopeptides bind MHC molecules and elicit specific T cell responses.	Glycopeptides	0-13	major histocompatibility complex, class I, C	Homo sapiens	19-22
8344254-7	1993	Consistent with a role as chaperones, we find that glucose starvation induces complex formation between p100/110 and MHC-E3/19K.	Glucose	51-58	major histocompatibility complex, class I, C	Homo sapiens	117-120
8343162-2	1993	Sequencing analysis revealed an A to G transition at codon 778 leading to replacement of the Asp residue, which is adjacent to the interaction sites of myosin heavy chain (MHC) with actin and is a conserved amino acid residue in various MHC across species, to the Gly residue.	Aspartic Acid	93-96	major histocompatibility complex, class I, C	Homo sapiens	152-170
8343162-2	1993	Sequencing analysis revealed an A to G transition at codon 778 leading to replacement of the Asp residue, which is adjacent to the interaction sites of myosin heavy chain (MHC) with actin and is a conserved amino acid residue in various MHC across species, to the Gly residue.	Aspartic Acid	93-96	major histocompatibility complex, class I, C	Homo sapiens	172-175
8343162-2	1993	Sequencing analysis revealed an A to G transition at codon 778 leading to replacement of the Asp residue, which is adjacent to the interaction sites of myosin heavy chain (MHC) with actin and is a conserved amino acid residue in various MHC across species, to the Gly residue.	Aspartic Acid	93-96	major histocompatibility complex, class I, C	Homo sapiens	237-240
8343162-2	1993	Sequencing analysis revealed an A to G transition at codon 778 leading to replacement of the Asp residue, which is adjacent to the interaction sites of myosin heavy chain (MHC) with actin and is a conserved amino acid residue in various MHC across species, to the Gly residue.	Glycine	264-267	major histocompatibility complex, class I, C	Homo sapiens	152-170
8343162-2	1993	Sequencing analysis revealed an A to G transition at codon 778 leading to replacement of the Asp residue, which is adjacent to the interaction sites of myosin heavy chain (MHC) with actin and is a conserved amino acid residue in various MHC across species, to the Gly residue.	Glycine	264-267	major histocompatibility complex, class I, C	Homo sapiens	172-175
8343162-3	1993	Linkage study of the mutation and two dinucleotides repeat markers of the cardiac beta-MHC gene in three affected families showed that the mutation was on the same haplotype of the cardiac beta-MHC gene and linked to HCM.	Dinucleoside Phosphates	38-51	major histocompatibility complex, class I, C	Homo sapiens	87-90
8343162-3	1993	Linkage study of the mutation and two dinucleotides repeat markers of the cardiac beta-MHC gene in three affected families showed that the mutation was on the same haplotype of the cardiac beta-MHC gene and linked to HCM.	Dinucleoside Phosphates	38-51	major histocompatibility complex, class I, C	Homo sapiens	194-197
8352560-8	1993	The conjugate formation of activated T cells with tumour cells as well as the additional rhamnogalacturonan-mediated bridging must be based on the expression of receptors with acetyl mannose specificity, since enhancements of MHC-unrestricted T cell cytotoxicity and conjugate formation were inhibited in a dose-dependent manner when acetylated mannose was present in the assays.	rhamnogalacturonan	89-107	major histocompatibility complex, class I, C	Homo sapiens	226-229
8352560-8	1993	The conjugate formation of activated T cells with tumour cells as well as the additional rhamnogalacturonan-mediated bridging must be based on the expression of receptors with acetyl mannose specificity, since enhancements of MHC-unrestricted T cell cytotoxicity and conjugate formation were inhibited in a dose-dependent manner when acetylated mannose was present in the assays.	acetyl-mannose	176-190	major histocompatibility complex, class I, C	Homo sapiens	226-229
8330311-1	1993	The aim of this study was to clarify the role of the oligosaccharide side chains of MHC Class II antigens in allostimulation.	Oligosaccharides	53-68	major histocompatibility complex, class I, C	Homo sapiens	84-87
8330311-13	1993	Accordingly, in terms of the latter set of clones oligosaccharide side chains of MHC may not be required for allostimulation.	Oligosaccharides	50-65	major histocompatibility complex, class I, C	Homo sapiens	81-84
8324899-10	1993	Our data are in sharp contrast to the previously held view that women with RSA may be hyporesponsive to paternal MHC antigens.	rabbit sperm membrane autoantigen	75-78	major histocompatibility complex, class I, C	Homo sapiens	113-116
8509418-5	1993	Sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis of purified myosin revealed that the relative mobilities of the previously described intestinal MHC isoforms SM1 (204 kDa) and SM2 (200 kDa) were slower than the corresponding vascular SM1 and SM2 isoforms.	sodium dodecyl sulfate-polyacrylamide	0-37	major histocompatibility complex, class I, C	Homo sapiens	163-166
8509418-9	1993	Exchange of the intestinal myosin light chains onto the vascular MHC did not alter its activity in the in vitro motility assay, suggesting that the 7-amino acid MHC insert is responsible for the different enzymatic activities of vascular and intestinal myosins.	7-amino acid	148-160	major histocompatibility complex, class I, C	Homo sapiens	161-164
8320826-3	1993	Recently, in vitro medel of myocardial stretch on the silicone sheet has demonstrated the up regulation of the "cardiac fetal genes", including beta-MHC, skeletal alpha-actin, and atrial natriuretic factor (ANF), which is known to be a hallmark of the altered gene expression in the hypertrophic heart.	Silicones	54-62	major histocompatibility complex, class I, C	Homo sapiens	149-152
8320827-2	1993	Amino acid sequence comparison of the human cardiac alpha- and beta-MHC have demonstrated that there are, at least, 7 isoform-specific divergent regions, including important binding protein-related sites such as ATP, actin and myosin light chain.	Adenosine Triphosphate	212-215	major histocompatibility complex, class I, C	Homo sapiens	68-71
8493555-2	1993	Alloreactive NK cells specific for the NK-1 alloantigen could be reproducibly generated from individuals that were homozygous for HLA-C with asparagine at residue 77 and lysine at residue 80 [HLA-C(Asn77,Lys80)] by stimulation with target cells that were homozygous for HLA-C(Ser77,Asn80); the reciprocal stimulation yielded NK cells specific for the NK-2 alloantigen.	Asparagine	141-151	major histocompatibility complex, class I, C	Homo sapiens	130-135
8096405-0	1993	Combination treatment of 2-chlorodeoxyadenosine and type I interferon on hairy cell leukemia-like cells: cytotoxic effect and MHC-unrestricted killer cell regulation.	Cladribine	25-47	major histocompatibility complex, class I, C	Homo sapiens	126-129
8096501-1	1993	MHC-extended haplotypes were investigated in multiplex families of patients with hyperthyroid GD.	hyperthyroid gd	81-96	major histocompatibility complex, class I, C	Homo sapiens	0-3
8093457-4	1993	A poly-alanine peptide containing only four of the original residues was an effective MHC class II binder and in vivo immunogen, although lacking the ability to stimulate the hybridoma.	poly-alanine peptide	2-22	major histocompatibility complex, class I, C	Homo sapiens	86-89
8093457-7	1993	However, these two effects of glutamic acid were not complementary and were mediated by distinct mechanisms, as the change in the peptide altered the extent of binding to class II, but the change in the MHC molecule decreased recognition without inhibiting peptide binding.	Glutamic Acid	30-43	major histocompatibility complex, class I, C	Homo sapiens	203-206
8498577-1	1993	Two smooth muscle myosin heavy chains (MHC; SM1 and SM2) of approximately 204 and 200 kDa exist in smooth muscle cells and can be visualized on reducing sodium dodecyl sulfate (SDS)-polyacrylamide gels.	Sodium Dodecyl Sulfate	153-175	major histocompatibility complex, class I, C	Homo sapiens	39-42
8498577-1	1993	Two smooth muscle myosin heavy chains (MHC; SM1 and SM2) of approximately 204 and 200 kDa exist in smooth muscle cells and can be visualized on reducing sodium dodecyl sulfate (SDS)-polyacrylamide gels.	Sodium Dodecyl Sulfate	177-180	major histocompatibility complex, class I, C	Homo sapiens	39-42
8498577-1	1993	Two smooth muscle myosin heavy chains (MHC; SM1 and SM2) of approximately 204 and 200 kDa exist in smooth muscle cells and can be visualized on reducing sodium dodecyl sulfate (SDS)-polyacrylamide gels.	polyacrylamide	182-196	major histocompatibility complex, class I, C	Homo sapiens	39-42
8498577-4	1993	Electrophoresis of the LMM fragments on a reducing SDS-polyacrylamide gel resolves two subunits from the two MHC [LM1 from SM1 (approximately 100 kDa) and LM2 from SM2 (approximately 95 kDa), where LM1 and LM2 are LMM from SM1 and SM2, respectively].	polyacrylamide	55-69	major histocompatibility complex, class I, C	Homo sapiens	109-112
7684189-6	1993	In situ hybridization of biotin-labeled human smooth muscle MHC probe (UMYHSM fragment) to normal human metaphase chromosome independently showed that the human smooth muscle MHC gene (MYH11) is assigned to chromosome region 16q12.	Biotin	25-31	major histocompatibility complex, class I, C	Homo sapiens	60-63
7684189-6	1993	In situ hybridization of biotin-labeled human smooth muscle MHC probe (UMYHSM fragment) to normal human metaphase chromosome independently showed that the human smooth muscle MHC gene (MYH11) is assigned to chromosome region 16q12.	Biotin	25-31	major histocompatibility complex, class I, C	Homo sapiens	175-178
1782227-14	1991	To assess the effect of bile acids on MHC expression, human hepatocytes were incubated with bile acids.	Bile Acids and Salts	24-34	major histocompatibility complex, class I, C	Homo sapiens	38-41
1383381-12	1992	In particular, conserved motifs in the alpha 1 helix and the conserved glycine at the base of the B pocket (position 45) provide a combination of features that is uniquely found in HLA-C molecules.	Glycine	71-78	major histocompatibility complex, class I, C	Homo sapiens	181-186
1421576-5	1992	Okadaic acid, a protein phosphatase inhibitor, induced a delayed but massive cell shortening preceded by a large increase in MHC and LC20 phosphorylation.	Okadaic Acid	0-12	major histocompatibility complex, class I, C	Homo sapiens	125-128
1421576-6	1992	Staurosporine, a kinase inhibitor known to effect dissolution but not contraction of stress fibers, immediately caused an increase in MHC and LC20 phosphorylation followed within minutes by the dephosphorylation of LC20 to a level below that of untreated cells.	Staurosporine	0-13	major histocompatibility complex, class I, C	Homo sapiens	134-137
1616011-3	1992	In static cultures after 3-5 days, 10(-8) M Dex decreased total protein content 42-74%, total protein synthesis rates 38-56%, mean myofiber diameter 35%, myosin heavy chain (MHC) content 86%, MHC synthesis rate 44%, and fibronectin synthesis rate 29%.	Dexamethasone	44-47	major histocompatibility complex, class I, C	Homo sapiens	154-172
1616011-3	1992	In static cultures after 3-5 days, 10(-8) M Dex decreased total protein content 42-74%, total protein synthesis rates 38-56%, mean myofiber diameter 35%, myosin heavy chain (MHC) content 86%, MHC synthesis rate 44%, and fibronectin synthesis rate 29%.	Dexamethasone	44-47	major histocompatibility complex, class I, C	Homo sapiens	174-177
1616011-3	1992	In static cultures after 3-5 days, 10(-8) M Dex decreased total protein content 42-74%, total protein synthesis rates 38-56%, mean myofiber diameter 35%, myosin heavy chain (MHC) content 86%, MHC synthesis rate 44%, and fibronectin synthesis rate 29%.	Dexamethasone	44-47	major histocompatibility complex, class I, C	Homo sapiens	192-195
1616011-4	1992	Repetitive 10% stretch-relaxations of the cultured myofibers for 60 s every 5 min for 3-4 days prevented 52% of the Dex-induced decrease in protein content, 42% of the decrease in total protein synthesis rate, 77% of the decrease in MHC content, 42% of the decrease in MHC synthesis rate, and 67% of the decrease in fibronectin synthesis rate.	Dexamethasone	116-119	major histocompatibility complex, class I, C	Homo sapiens	233-236
1616011-4	1992	Repetitive 10% stretch-relaxations of the cultured myofibers for 60 s every 5 min for 3-4 days prevented 52% of the Dex-induced decrease in protein content, 42% of the decrease in total protein synthesis rate, 77% of the decrease in MHC content, 42% of the decrease in MHC synthesis rate, and 67% of the decrease in fibronectin synthesis rate.	Dexamethasone	116-119	major histocompatibility complex, class I, C	Homo sapiens	269-272
1371950-1	1992	Cyclosporin A (CsA) was tested for its modulatory effects on the mIgM-mediated signaling of G0*-associated increases in class II MHC expression, G1-related RNA synthesis, and S phase-related DNA synthesis in human B cells.	Cyclosporine	15-18	major histocompatibility complex, class I, C	Homo sapiens	129-132
1590733-3	1992	Amplification of exon 13 of the beta MHC from paraffin-embedded myocardium using the polymerase chain reaction (PCR) was performed and analysis of the amplified product for migration abnormalities using denaturing gradient gel electrophoresis (DGGE) and direct sequencing of the PCR product were used.	Paraffin	46-54	major histocompatibility complex, class I, C	Homo sapiens	37-40
1541903-5	1992	We have also demonstrated that the induction of MGCs by anti-class II MHC antibody and phorbol ester requires protein kinase C activity, because MGC formation was totally inhibited by the protein kinase C inhibitors staurosporine and H-7.	Staurosporine	216-229	major histocompatibility complex, class I, C	Homo sapiens	70-73
1541903-5	1992	We have also demonstrated that the induction of MGCs by anti-class II MHC antibody and phorbol ester requires protein kinase C activity, because MGC formation was totally inhibited by the protein kinase C inhibitors staurosporine and H-7.	1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine	234-237	major histocompatibility complex, class I, C	Homo sapiens	70-73
1541903-6	1992	In analyzing the signal induced by anti-class II MHC mAb"s we have demonstrated that cross-linking of the class II MHC antigens with intact mAb"s, or with F(ab")2 fragments of anti-class II MHC mAb"s and F(ab")2 fragments of rabbit antimouse (RAM) immunoglobulin G, produced an intracellular calcium rise.	Calcium	292-299	major histocompatibility complex, class I, C	Homo sapiens	49-52
1541903-6	1992	In analyzing the signal induced by anti-class II MHC mAb"s we have demonstrated that cross-linking of the class II MHC antigens with intact mAb"s, or with F(ab")2 fragments of anti-class II MHC mAb"s and F(ab")2 fragments of rabbit antimouse (RAM) immunoglobulin G, produced an intracellular calcium rise.	Calcium	292-299	major histocompatibility complex, class I, C	Homo sapiens	115-118
1541903-6	1992	In analyzing the signal induced by anti-class II MHC mAb"s we have demonstrated that cross-linking of the class II MHC antigens with intact mAb"s, or with F(ab")2 fragments of anti-class II MHC mAb"s and F(ab")2 fragments of rabbit antimouse (RAM) immunoglobulin G, produced an intracellular calcium rise.	Calcium	292-299	major histocompatibility complex, class I, C	Homo sapiens	115-118
1939265-4	1991	To study the expression patterns of these MHC genes in vitro we isolated and partially sequenced the cDNAs expressed in EBs such that specific oligonucleotides suitable for polymerase chain reaction analyses and appropriate riboprobes for in situ hybridizations could be made.	Oligonucleotides	143-159	major histocompatibility complex, class I, C	Homo sapiens	42-45
1750798-18	1991	For insulin dependent diabetes mellitus it has been shown that the MHC determined susceptibility to the disease is conferred by neutral residues (Val, Ser, Ala), at position 57 of the DQ beta chain, while Asp at this position correlates with resistance.	Valine	146-149	major histocompatibility complex, class I, C	Homo sapiens	67-70
1750798-18	1991	For insulin dependent diabetes mellitus it has been shown that the MHC determined susceptibility to the disease is conferred by neutral residues (Val, Ser, Ala), at position 57 of the DQ beta chain, while Asp at this position correlates with resistance.	Serine	151-154	major histocompatibility complex, class I, C	Homo sapiens	67-70
1750798-18	1991	For insulin dependent diabetes mellitus it has been shown that the MHC determined susceptibility to the disease is conferred by neutral residues (Val, Ser, Ala), at position 57 of the DQ beta chain, while Asp at this position correlates with resistance.	Alanine	156-159	major histocompatibility complex, class I, C	Homo sapiens	67-70
1750798-18	1991	For insulin dependent diabetes mellitus it has been shown that the MHC determined susceptibility to the disease is conferred by neutral residues (Val, Ser, Ala), at position 57 of the DQ beta chain, while Asp at this position correlates with resistance.	Aspartic Acid	205-208	major histocompatibility complex, class I, C	Homo sapiens	67-70
1569576-6	1992	The sequence of this neuronal MHC is compared with those of other non-muscle MHCs, to which it shows an overall similarity of structure, especially with respect to conserved regions within the head (ATP binding site, actin binding site, reactive thiols) and the presence of an alpha-helical coiled-coil tail that can be arranged as 28-residue repeating units plus four skip residues.	Adenosine Triphosphate	199-202	major histocompatibility complex, class I, C	Homo sapiens	30-33
1569576-6	1992	The sequence of this neuronal MHC is compared with those of other non-muscle MHCs, to which it shows an overall similarity of structure, especially with respect to conserved regions within the head (ATP binding site, actin binding site, reactive thiols) and the presence of an alpha-helical coiled-coil tail that can be arranged as 28-residue repeating units plus four skip residues.	Sulfhydryl Compounds	246-252	major histocompatibility complex, class I, C	Homo sapiens	30-33
1931813-5	1991	Accordingly, the interactions between the MHC molecule and the peptide antigen appear to be essentially mediated by hydrophobic interactions and hydrogen bonding, while electrostatic interactions between charged residues might be important in the association of TCR and MHC molecules.	Hydrogen	145-153	major histocompatibility complex, class I, C	Homo sapiens	42-45
2071937-1	1991	The association of specific HLA-C nucleotide sequences with psoriasis vulgaris was investigated in 75 Japanese patients by the polymerase chain reaction method, followed by slot-blot hybridization using two specific oligonucleotide probes.	Oligonucleotides	216-231	major histocompatibility complex, class I, C	Homo sapiens	28-33
2071937-5	1991	It is suggested that alanine at position 73 of HLA-C molecules can be a good marker for psoriasis vulgaris and that this residue may play an important role in determining susceptibility to this disease.	Alanine	21-28	major histocompatibility complex, class I, C	Homo sapiens	47-52
1782227-15	1991	Chenodeoxycholic acid (CDCA) (an endogenous bile acid) but not UDCA induced a dose-dependent MHC class I hyperexpression.	Chenodeoxycholic Acid	0-21	major histocompatibility complex, class I, C	Homo sapiens	93-96
1782227-15	1991	Chenodeoxycholic acid (CDCA) (an endogenous bile acid) but not UDCA induced a dose-dependent MHC class I hyperexpression.	Chenodeoxycholic Acid	23-27	major histocompatibility complex, class I, C	Homo sapiens	93-96
1782227-16	1991	UDCA suppressed the CDCA-induced MHC hyperexpression.	Chenodeoxycholic Acid	20-24	major histocompatibility complex, class I, C	Homo sapiens	33-36
1704395-6	1991	This epitope was recognized in association with at least one subtype of the widely distributed human class II MHC specificity DPw4, namely DPw4.2.	dpw4	126-130	major histocompatibility complex, class I, C	Homo sapiens	110-113
2049342-5	1991	The fluorescein hapten on each analogue was fully accessible to quenching by anti-fluorescein antibody after binding of the peptide to the MHC class II protein, indicating that these regions of the peptide are exposed in the MHC binding site.	Fluorescein	4-15	major histocompatibility complex, class I, C	Homo sapiens	139-142
2049342-5	1991	The fluorescein hapten on each analogue was fully accessible to quenching by anti-fluorescein antibody after binding of the peptide to the MHC class II protein, indicating that these regions of the peptide are exposed in the MHC binding site.	Fluorescein	4-15	major histocompatibility complex, class I, C	Homo sapiens	225-228
2049342-5	1991	The fluorescein hapten on each analogue was fully accessible to quenching by anti-fluorescein antibody after binding of the peptide to the MHC class II protein, indicating that these regions of the peptide are exposed in the MHC binding site.	Fluorescein	82-93	major histocompatibility complex, class I, C	Homo sapiens	139-142
2049342-5	1991	The fluorescein hapten on each analogue was fully accessible to quenching by anti-fluorescein antibody after binding of the peptide to the MHC class II protein, indicating that these regions of the peptide are exposed in the MHC binding site.	Fluorescein	82-93	major histocompatibility complex, class I, C	Homo sapiens	225-228
1704395-6	1991	This epitope was recognized in association with at least one subtype of the widely distributed human class II MHC specificity DPw4, namely DPw4.2.	dpw4	139-143	major histocompatibility complex, class I, C	Homo sapiens	110-113
2003383-6	1991	However, the results disclosed no methyl methacrylate-induced DNA synthesis, although methyl methacrylate-induced MHC locus II antigen and IL-2R activation marker expression were recorded; notably, this expression was less pronounced than that seen in PHA or PPD antigen driven lymphocyte response.	Methylmethacrylate	86-105	major histocompatibility complex, class I, C	Homo sapiens	114-117
1910688-11	1991	Recent experiments demonstrating that peptides with polyalanine, polyproline, or polyglycine bind well to MHC proteins have proven that the structural requirements for binding are quite minimal.	polyalanine	52-63	major histocompatibility complex, class I, C	Homo sapiens	106-109
1910688-11	1991	Recent experiments demonstrating that peptides with polyalanine, polyproline, or polyglycine bind well to MHC proteins have proven that the structural requirements for binding are quite minimal.	polyproline	65-76	major histocompatibility complex, class I, C	Homo sapiens	106-109
1910688-11	1991	Recent experiments demonstrating that peptides with polyalanine, polyproline, or polyglycine bind well to MHC proteins have proven that the structural requirements for binding are quite minimal.	polyglycine	81-92	major histocompatibility complex, class I, C	Homo sapiens	106-109
1838253-9	1991	Treatment of cells known to activate the protein kinase C (TPA) and inositol triphosphate pathways has increased the level of beta-MHC mRNA while that of alpha-MHC remained unchanged.	Tetradecanoylphorbol Acetate	59-62	major histocompatibility complex, class I, C	Homo sapiens	131-134
1838253-9	1991	Treatment of cells known to activate the protein kinase C (TPA) and inositol triphosphate pathways has increased the level of beta-MHC mRNA while that of alpha-MHC remained unchanged.	Inositol triphosphate	68-89	major histocompatibility complex, class I, C	Homo sapiens	131-134
2222530-1	1990	A method has been developed for the analysis of deuterium oxide solutions of tritiated alanine eight-component isotopic mixtures by using high resolution 3H and 1H NMR spectra at frequencies 266.8 and 500.13 MHc, respectively.	Deuterium Oxide	48-63	major histocompatibility complex, class I, C	Homo sapiens	208-211
1720960-7	1991	As analysed with lymphocyte activation markers, the hydroxyapatite-dependent expression of MHC locus II antigen was modest and differed significantly (P less than 0.05) from that in culture medium only on day 3.	Durapatite	52-66	major histocompatibility complex, class I, C	Homo sapiens	91-94
1676012-2	1991	HLA-DP, is encoded centromeric to DR-DQ and its alleles are in weak linkage disequilibrium with the rest of the MHC; thus a certain number of HLA matched pairs could be actually DP incompatible to study a possible correlation between HLA-DP matching and GvHD, 24 HLA identical BMT/donor-recipient sibling pairs (serologically tested for HLA Class I and DR antigens) were tested for DQ and DP genes using restriction fragment length polymorphism (RFLP) analysis.	dp	4-6	major histocompatibility complex, class I, C	Homo sapiens	112-115
2172380-1	1990	Engagement of the TCR (CD3-Ti) by Ag/MHC, CD3 mAb, or lectin mitogen stimulates the very early tyrosine phosphorylation of several cellular substrates including TCR-zeta.	Tyrosine	95-103	major histocompatibility complex, class I, C	Homo sapiens	37-40
2128549-7	1990	Indirect Id stimulation of group-1 cells by Id-I or Id-C, and group-2 cells by Id-I or EPI, was inhibited by anti-HLA-DR,DP(DQ) mAb or sodium azide, and exogenous IL-1 alone did not support this processed, MHC-mediated T-cell stimulation, but live adherent cells did.	dp	121-123	major histocompatibility complex, class I, C	Homo sapiens	206-209
2128549-7	1990	Indirect Id stimulation of group-1 cells by Id-I or Id-C, and group-2 cells by Id-I or EPI, was inhibited by anti-HLA-DR,DP(DQ) mAb or sodium azide, and exogenous IL-1 alone did not support this processed, MHC-mediated T-cell stimulation, but live adherent cells did.	Sodium Azide	135-147	major histocompatibility complex, class I, C	Homo sapiens	206-209
2166048-7	1990	However, our results show no PGA-induced lymphocyte DNA synthesis, but PGA-induced MHC locus II antigen and IL-2R activation marker expression was seen, greater than in negative controls, but less than that seen in PPD antigen driven lymphocyte response.	Polyglycolic Acid	71-74	major histocompatibility complex, class I, C	Homo sapiens	83-86
1694205-4	1990	A preliminary model of DPw4-restricted T cell determinants is elaborated based on a hypothesis of how the 2 alpha-helical peptides may bind to this MHC molecule.	dpw4	23-27	major histocompatibility complex, class I, C	Homo sapiens	148-151
1694205-5	1990	Results are further discussed in the context of the usefulness in identifying DPw4-restricted T cell epitopes for the production of synthetic vaccines because this MHC class II molecule is found with high frequency in the population.	dpw4	78-82	major histocompatibility complex, class I, C	Homo sapiens	164-167
2222530-1	1990	A method has been developed for the analysis of deuterium oxide solutions of tritiated alanine eight-component isotopic mixtures by using high resolution 3H and 1H NMR spectra at frequencies 266.8 and 500.13 MHc, respectively.	Alanine	87-94	major histocompatibility complex, class I, C	Homo sapiens	208-211
35373498-7	2022	Increased mitochondrial ROS was responsible for myotube atrophy by activating Muscle Ring Finger 1 (MuRF-1)-mediated myosin heavy chain (MHC) degradation.	Reactive Oxygen Species	24-27	major histocompatibility complex, class I, C	Homo sapiens	117-135
34728329-13	2022	Mice injected with MOTS-c neutralizing antibody showed a higher expression of MHC-fast than the control mice.	UNII-A5CV6JFB78	19-25	major histocompatibility complex, class I, C	Homo sapiens	78-81
34505756-8	2021	The amino acid residues isoleucine, tyrosine, and leucine at positions 95, 116 and 163 of HLA-C, respectively, were associated with CIN II/III susceptibility.	Isoleucine	24-34	major histocompatibility complex, class I, C	Homo sapiens	90-95
34505756-8	2021	The amino acid residues isoleucine, tyrosine, and leucine at positions 95, 116 and 163 of HLA-C, respectively, were associated with CIN II/III susceptibility.	Leucine	50-57	major histocompatibility complex, class I, C	Homo sapiens	90-95
34478713-4	2021	Utilising NAD+, the ecto-enzyme adenosine diphosphate (ADP) ribosyl transferase 2.2 (ART2.2) catalyzes the addition of ADP-ribosyl groups onto arginine residues of CD8alpha or beta chains and alters the interaction between the MHC and TCR complexes.	NAD	10-14	major histocompatibility complex, class I, C	Homo sapiens	227-230
34478713-4	2021	Utilising NAD+, the ecto-enzyme adenosine diphosphate (ADP) ribosyl transferase 2.2 (ART2.2) catalyzes the addition of ADP-ribosyl groups onto arginine residues of CD8alpha or beta chains and alters the interaction between the MHC and TCR complexes.	Adenosine	32-41	major histocompatibility complex, class I, C	Homo sapiens	227-230
34478713-6	2021	Here, we show that ADP-ribosylation of CD8 facilitates the binding of the liver-restricted non-classical MHC, H2-Q10, independent of the associated TCR or presented peptide, and propose that this highly regulated binding imposes an additional inhibitory leash on the activation of CD8-expressing cells in the presence of NAD+.	NAD	321-325	major histocompatibility complex, class I, C	Homo sapiens	105-108
34439266-1	2021	APVO436 is a recombinant T cell-engaging humanized bispecific antibody designed to redirect host T cell cytotoxicity in an MHC-independent manner to CD123-expressing blast cells from patients with hematologic malignancies and has exhibited single-agent anti-leukemia activity in murine xenograft models of acute myeloid leukemia (AML).	apvo436	0-7	major histocompatibility complex, class I, C	Homo sapiens	123-126
34072812-6	2021	SFN treatment also induced DNA demethylation in the promoter region of the MHC-SLA1 gene, resulting in the upregulation of Toll-like receptor 4 (TLR4), MHC-SLA1, and inflammatory cytokines" expression at 6 h of LPS stimulation.	sulforaphane	0-3	major histocompatibility complex, class I, C	Homo sapiens	75-78
34072812-6	2021	SFN treatment also induced DNA demethylation in the promoter region of the MHC-SLA1 gene, resulting in the upregulation of Toll-like receptor 4 (TLR4), MHC-SLA1, and inflammatory cytokines" expression at 6 h of LPS stimulation.	sulforaphane	0-3	major histocompatibility complex, class I, C	Homo sapiens	152-155
34124164-6	2021	We found that cisplatin treatment led to dramatically decreased cell viability; accumulated ROS level; down-regulated expressions of MyoD1 (myoblast determination protein 1), myogenin, and MHC (myosin heavy chain); and impaired myotube differentiation in myoblasts.	Cisplatin	14-23	major histocompatibility complex, class I, C	Homo sapiens	189-192
34124164-6	2021	We found that cisplatin treatment led to dramatically decreased cell viability; accumulated ROS level; down-regulated expressions of MyoD1 (myoblast determination protein 1), myogenin, and MHC (myosin heavy chain); and impaired myotube differentiation in myoblasts.	Cisplatin	14-23	major histocompatibility complex, class I, C	Homo sapiens	194-212
34124164-7	2021	Significantly, taurine supplementation protected myoblasts against cisplatin-induced cell viability decrease, promoted cellular ROS clearance, and, most importantly, preserved the expressions of MyoD1, myogenin, and MHC as well as myotube differentiation ability.	Taurine	15-22	major histocompatibility complex, class I, C	Homo sapiens	216-219
1968075-6	1990	Mouse and human target cells could be lysed in the presence of MTM both by MTM-stimulated CD8+ lymphocytes and by MHC class I-restricted CTL clones of defined Ag specificity.	3'-O-methylthiomethylthymidine	63-66	major histocompatibility complex, class I, C	Homo sapiens	114-117
2404992-2	1990	Dictyostelium hmm cells were created by insertional mutagenesis of the myosin heavy chain gene (De Lozanne, A., and J.	lozanne	99-106	major histocompatibility complex, class I, C	Homo sapiens	71-89
2305471-7	1990	When cloned cells were transferred in vivo into lethally irradiated (1025 cGy) recipients unable to reject allogeneic marrow, results utilizing splenic 125IUdR uptake indicated that these MHC-specific cytotoxic clones could suppress marrow proliferation.	125iudr	152-159	major histocompatibility complex, class I, C	Homo sapiens	188-191
33940160-4	2021	Using hemophilia A as a model, we sought to engineer antigen-specific Tregs to suppress antibody formation against the soluble therapeutic protein factor VIII in an MHC-independent fashion.	tregs	70-75	major histocompatibility complex, class I, C	Homo sapiens	165-168
34477462-6	2021	The Dox-treated MHC-hHsp27 mice showed improved survival and cardiac function (both MRI and echocardiography), in terms of contractility (%EF) and left ventricular inner diameter (LVID), compared to the Dox-treated Non-TG mice.	Doxorubicin	4-7	major histocompatibility complex, class I, C	Homo sapiens	16-19
34477462-8	2021	Furthermore, transactivation of p53 was found to be attenuated only in Dox-treated MHC-hHsp27 mice-derived cardiomyocytes in vitro, as low p53 was detected in the nuclei, not in mutant hHsp27 overexpressing cardiomyocytes.	Doxorubicin	71-74	major histocompatibility complex, class I, C	Homo sapiens	83-86
34686187-11	2021	We also demonstrated the in vitro and in vivo efficacies of pNK cells against cisplatin-resistant A2780cis ovarian cancer cells having a high programmed death-ligand 1(PD-L1) and low HLA-C expression.	Cisplatin	78-87	major histocompatibility complex, class I, C	Homo sapiens	183-188
35373498-7	2022	Increased mitochondrial ROS was responsible for myotube atrophy by activating Muscle Ring Finger 1 (MuRF-1)-mediated myosin heavy chain (MHC) degradation.	Reactive Oxygen Species	24-27	major histocompatibility complex, class I, C	Homo sapiens	137-140
35561310-4	2022	DLBCL MHC-presented peptides were identified via mass spectrometry following tazemetostat or decitabine treatments alone, or in combination with IFN-gamma.	tazemetostat	77-89	major histocompatibility complex, class I, C	Homo sapiens	6-9
35122707-11	2022	Molecular docking analysis indicated that MTZ binds more stably to the pocket of HLA-B*59:01 and HLA-B*55:02 than to that of non-risk alleles of HLA-B*40:01 and HLA-C*01:02.	Methazolamide	42-45	major histocompatibility complex, class I, C	Homo sapiens	161-166
35561310-4	2022	DLBCL MHC-presented peptides were identified via mass spectrometry following tazemetostat or decitabine treatments alone, or in combination with IFN-gamma.	Decitabine	93-103	major histocompatibility complex, class I, C	Homo sapiens	6-9
35561310-9	2022	Overall, our results show that EZH2 inhibition in combination with decitabine and IFN-gamma can expand the repertoire of MHC ligands presented on DLBCLs by revealing suppressed epitopes, thus allowing the systematic analysis and identification of new potential immunotherapy targets.	Decitabine	67-77	major histocompatibility complex, class I, C	Homo sapiens	121-124
35411556-10	2022	Moreover, we found that calcitriol could increase myosin heavy chain (MHC) protein translation and overall nascent protein synthesis in a cycloheximide-sensitive manner, indicating that calcitriol can directly bind and enhance ribosomal activity to boost muscle growth.	Calcitriol	24-34	major histocompatibility complex, class I, C	Homo sapiens	50-68
35602060-8	2022	The predictive analysis by NetMHCpan-4.1 server showed that human leukocyte antigen (HLA)-C*04:01 is a strong binder for the 9-mers peptide in HepG2.2.15 cells.	netmhcpan	27-36	major histocompatibility complex, class I, C	Homo sapiens	66-91
35411556-10	2022	Moreover, we found that calcitriol could increase myosin heavy chain (MHC) protein translation and overall nascent protein synthesis in a cycloheximide-sensitive manner, indicating that calcitriol can directly bind and enhance ribosomal activity to boost muscle growth.	Calcitriol	24-34	major histocompatibility complex, class I, C	Homo sapiens	70-73
35411556-10	2022	Moreover, we found that calcitriol could increase myosin heavy chain (MHC) protein translation and overall nascent protein synthesis in a cycloheximide-sensitive manner, indicating that calcitriol can directly bind and enhance ribosomal activity to boost muscle growth.	Cycloheximide	138-151	major histocompatibility complex, class I, C	Homo sapiens	50-68
35411556-10	2022	Moreover, we found that calcitriol could increase myosin heavy chain (MHC) protein translation and overall nascent protein synthesis in a cycloheximide-sensitive manner, indicating that calcitriol can directly bind and enhance ribosomal activity to boost muscle growth.	Cycloheximide	138-151	major histocompatibility complex, class I, C	Homo sapiens	70-73
35411556-10	2022	Moreover, we found that calcitriol could increase myosin heavy chain (MHC) protein translation and overall nascent protein synthesis in a cycloheximide-sensitive manner, indicating that calcitriol can directly bind and enhance ribosomal activity to boost muscle growth.	Calcitriol	186-196	major histocompatibility complex, class I, C	Homo sapiens	50-68
35411556-10	2022	Moreover, we found that calcitriol could increase myosin heavy chain (MHC) protein translation and overall nascent protein synthesis in a cycloheximide-sensitive manner, indicating that calcitriol can directly bind and enhance ribosomal activity to boost muscle growth.	Calcitriol	186-196	major histocompatibility complex, class I, C	Homo sapiens	70-73
35352505-7	2022	We observed significant interactions between HLA-C*06:02 and rs118179173 (snp31443520; p = 8.21 x 10-20 , OR = 0.22) and between HLA-C*06:02 and HLA-B:AA67 (p = 1.22 x 10-12 , OR = 0.45).	snp31443520	74-85	major histocompatibility complex, class I, C	Homo sapiens	45-50
35096006-9	2021	Six of the hub genes were nominally differentially expressed in studies of vitamin D effects on adult normal mucosa organoids: LCN2, HLA-C, AIF1L, PTPRU, PDE4B and IFI6.	Vitamin D	75-84	major histocompatibility complex, class I, C	Homo sapiens	133-138
35169303-0	2022	HLA-B*07:02 and HLA-C*07:02 are associated with trimethoprim-sulfamethoxazole respiratory failure.	Trimethoprim, Sulfamethoxazole Drug Combination	48-77	major histocompatibility complex, class I, C	Homo sapiens	16-21
35169303-7	2022	Our results suggests that HLA-B*07:02 and HLA-C*07:02 are necessary for a patient to develop respiratory failure due to TMP-SMX.	Trimethoprim, Sulfamethoxazole Drug Combination	120-127	major histocompatibility complex, class I, C	Homo sapiens	42-47
2480658-8	1989	The inability of stimulator cells expressing such "nude" MHC molecules to elicit T cell proliferation after chemical modification could be due to easier crosslinking of the allodeterminants by paraformaldehyde when the binding site is empty but could also mean that nude MHC molecules are not per se immunogenic and become so only after acquisition of a peptide.	paraform	193-209	major histocompatibility complex, class I, C	Homo sapiens	57-60
2477284-3	1989	Alterations in levels of specific myosin heavy chain (MHC) isoform mRNAs were measured using the slot blot procedure with radioactively labelled oligonucleotides as probes.	Oligonucleotides	145-161	major histocompatibility complex, class I, C	Homo sapiens	54-57
2478042-3	1989	Studies on the effect of ethanol on class I MHC antigens demonstrate that ethanol significantly enhances their cell surface expression in a variety of cell lines in vitro.	Ethanol	25-32	major histocompatibility complex, class I, C	Homo sapiens	44-47
2478042-3	1989	Studies on the effect of ethanol on class I MHC antigens demonstrate that ethanol significantly enhances their cell surface expression in a variety of cell lines in vitro.	Ethanol	74-81	major histocompatibility complex, class I, C	Homo sapiens	44-47
2478042-6	1989	Measurement of class I MHC antigens on peripheral blood lymphocytes in a population of acutely ethanol-intoxicated patients showed a highly significant increase relative to controls.	Ethanol	95-102	major histocompatibility complex, class I, C	Homo sapiens	23-26
2478042-7	1989	The possibility that the elevated levels of MHC antigens induced by ethanol may play a role in the evolution of ethanol-related disease is discussed.	Ethanol	68-75	major histocompatibility complex, class I, C	Homo sapiens	44-47
2478042-7	1989	The possibility that the elevated levels of MHC antigens induced by ethanol may play a role in the evolution of ethanol-related disease is discussed.	Ethanol	112-119	major histocompatibility complex, class I, C	Homo sapiens	44-47
2667211-9	1989	Cyclosporine treatment of blood-transfused recipients reduced the leukocyte infiltration and MHC induction to levels seen in untreated controls--i.e., the accelerated MHC induction caused by the transfusion was partially reversible by cyclosporine.	Cyclosporine	0-12	major histocompatibility complex, class I, C	Homo sapiens	93-96
2667211-9	1989	Cyclosporine treatment of blood-transfused recipients reduced the leukocyte infiltration and MHC induction to levels seen in untreated controls--i.e., the accelerated MHC induction caused by the transfusion was partially reversible by cyclosporine.	Cyclosporine	0-12	major histocompatibility complex, class I, C	Homo sapiens	167-170
2667211-9	1989	Cyclosporine treatment of blood-transfused recipients reduced the leukocyte infiltration and MHC induction to levels seen in untreated controls--i.e., the accelerated MHC induction caused by the transfusion was partially reversible by cyclosporine.	Cyclosporine	235-247	major histocompatibility complex, class I, C	Homo sapiens	167-170
2469725-1	1989	Cross-linking class I MHC molecules on human T cell clones by reacting them with various mAb directed at either monomorphic or polymorphic determinants on class I MHC molecules followed by cross-linking with GaMIg stimulated a rise in intracellular free calcium concentration ([Ca2+]i), and induced proliferation and IL-2 production.	gamig	208-213	major histocompatibility complex, class I, C	Homo sapiens	22-25
2469725-1	1989	Cross-linking class I MHC molecules on human T cell clones by reacting them with various mAb directed at either monomorphic or polymorphic determinants on class I MHC molecules followed by cross-linking with GaMIg stimulated a rise in intracellular free calcium concentration ([Ca2+]i), and induced proliferation and IL-2 production.	Calcium	254-261	major histocompatibility complex, class I, C	Homo sapiens	22-25
2469725-1	1989	Cross-linking class I MHC molecules on human T cell clones by reacting them with various mAb directed at either monomorphic or polymorphic determinants on class I MHC molecules followed by cross-linking with GaMIg stimulated a rise in intracellular free calcium concentration ([Ca2+]i), and induced proliferation and IL-2 production.	Calcium	254-261	major histocompatibility complex, class I, C	Homo sapiens	163-166
2469725-6	1989	Cross-linking class I MHC molecules on Jurkat cells induced a rise by [Ca2+]i and induced IL-2 production upon co-stimulation with PMA.	Tetradecanoylphorbol Acetate	131-134	major histocompatibility complex, class I, C	Homo sapiens	22-25
2547831-6	1989	By SDS-polyacrylamide gel electrophoresis 2X-MHC shows a lower mobility compared to 2B-MHC and appears to comigrate with 2A-MHC.	Sodium Dodecyl Sulfate	3-6	major histocompatibility complex, class I, C	Homo sapiens	45-48
2547831-6	1989	By SDS-polyacrylamide gel electrophoresis 2X-MHC shows a lower mobility compared to 2B-MHC and appears to comigrate with 2A-MHC.	polyacrylamide	7-21	major histocompatibility complex, class I, C	Homo sapiens	45-48
2469725-1	1989	Cross-linking class I MHC molecules on human T cell clones by reacting them with various mAb directed at either monomorphic or polymorphic determinants on class I MHC molecules followed by cross-linking with GaMIg stimulated a rise in intracellular free calcium concentration ([Ca2+]i), and induced proliferation and IL-2 production.	gamig	208-213	major histocompatibility complex, class I, C	Homo sapiens	163-166
2721112-13	1989	The demonstrated influence of amiodarone on both alpha- and beta-MHC mRNAs and interactions between amiodarone and thyroid status in regulating MHC gene expression may be relevant to its therapeutic effect in man.	Amiodarone	30-40	major histocompatibility complex, class I, C	Homo sapiens	144-147
2721112-13	1989	The demonstrated influence of amiodarone on both alpha- and beta-MHC mRNAs and interactions between amiodarone and thyroid status in regulating MHC gene expression may be relevant to its therapeutic effect in man.	Amiodarone	100-110	major histocompatibility complex, class I, C	Homo sapiens	144-147
2461903-4	1989	Two amino acid residues of HLA-A29.1, gln-144 and arg-151, were found in all 24 HLA-B and HLA-C alleles examined but were present in only one of 15 HLA-A alleles for which sequence data are available.	Glutamine	38-41	major histocompatibility complex, class I, C	Homo sapiens	90-95
2655227-5	1989	In contrast, cyclophosphamide (CyP) treatment led to acute (less than 4 weeks) destruction of both 1st- and 2nd-set allografts; breaking of tolerance was regularly seen when donor and host differed by two MHC haplotypes, but occurred infrequently in semiallogeneic combinations.	Cyclophosphamide	13-29	major histocompatibility complex, class I, C	Homo sapiens	205-208
2651768-10	1989	The most likely candidates are the immunosuppressive drugs, such as cyclosporine and prednisone, which decrease MHC antigen expression.	Cyclosporine	68-80	major histocompatibility complex, class I, C	Homo sapiens	112-115
2651768-10	1989	The most likely candidates are the immunosuppressive drugs, such as cyclosporine and prednisone, which decrease MHC antigen expression.	Prednisone	85-95	major histocompatibility complex, class I, C	Homo sapiens	112-115
2647926-3	1989	Our hypothesis was that changes in histocompatibility (MHC) expression induced by immunosuppressive therapy with cyclosporine plays an important role in directing an immune response to the arterial bed.	Cyclosporine	113-125	major histocompatibility complex, class I, C	Homo sapiens	55-58
3064644-0	1988	Evidence of increased class I MHC expression on human peripheral blood lymphocytes during acute ethanol intoxication.	Ethanol	96-103	major histocompatibility complex, class I, C	Homo sapiens	30-33
3067866-7	1988	Genes on chromosome 14 may also influence susceptibility to RA, probably by interaction with MHC genes and there are different Gm associations for DR4-positive and collagen-antibody-positive rheumatoid subgroups.	Radium	60-62	major histocompatibility complex, class I, C	Homo sapiens	93-96
2461903-4	1989	Two amino acid residues of HLA-A29.1, gln-144 and arg-151, were found in all 24 HLA-B and HLA-C alleles examined but were present in only one of 15 HLA-A alleles for which sequence data are available.	Arginine	50-53	major histocompatibility complex, class I, C	Homo sapiens	90-95
2461903-8	1989	These observations are consistent with the notion that gln-144 and arg-151 define a determinant common to HLA-B, HLA-C, and the HLA-Aw19 cross-reactive group and the binding site of the monoclonal antibody 4E.	Glutamine	55-58	major histocompatibility complex, class I, C	Homo sapiens	113-118
2461903-8	1989	These observations are consistent with the notion that gln-144 and arg-151 define a determinant common to HLA-B, HLA-C, and the HLA-Aw19 cross-reactive group and the binding site of the monoclonal antibody 4E.	Arginine	67-70	major histocompatibility complex, class I, C	Homo sapiens	113-118
2450913-2	1988	The initial studies demonstrated that cross-linking class I MHC molecules either by culturing highly purified T4 cells with immobilized mAb to class I MHC Ag or reacting the T4 cells with mAb to class I MHC Ag and then cross-linking the mAb with goat antimouse Ig (GaMIg) enhanced T4 cell proliferation induced by an immobilized mAb to CD3, OKT3.	gamig	265-270	major histocompatibility complex, class I, C	Homo sapiens	60-63
3061073-3	1988	CsA treatment prevented the induction of MHC antigen within allografts.	Cyclosporine	0-3	major histocompatibility complex, class I, C	Homo sapiens	41-44
3061073-4	1988	Whereas at day 4, both rejecting and CsA treated grafts showed donor class I MHC expression on duct epithelium and islet cells, only rejecting grafts displayed class I MHC induction on acinar cells.	Cyclosporine	37-40	major histocompatibility complex, class I, C	Homo sapiens	77-80
3061073-5	1988	Rejecting grafts showed strong induction of class II MHC antigen expression on duct epithelium from day 4 onward but this was completely prevented by CsA treatment.	Cyclosporine	150-153	major histocompatibility complex, class I, C	Homo sapiens	53-56
3061073-8	1988	These results show a favorable effect of CsA on rat fetal pancreas allografts with a reduction in MHC antigen expression within the graft and prolonged survival of insulin-rich endocrine tissue.	Cyclosporine	41-44	major histocompatibility complex, class I, C	Homo sapiens	98-101
3266762-0	1988	Effect of cortisol on the native and in vitro induced non-MHC restricted cytotoxicity of large granular lymphocytes.	Hydrocortisone	10-18	major histocompatibility complex, class I, C	Homo sapiens	58-61
2790930-3	1989	The temporal appearance and magnitude of a PGI developing in either LLca-syngeneic or semi-syngeneic hosts, but not the allogeneic strains, suggested that the mechanism(s) involved in PGI development like the GVHR, was restricted by the MHC.	2cer	43-46	major histocompatibility complex, class I, C	Homo sapiens	237-240
2790930-3	1989	The temporal appearance and magnitude of a PGI developing in either LLca-syngeneic or semi-syngeneic hosts, but not the allogeneic strains, suggested that the mechanism(s) involved in PGI development like the GVHR, was restricted by the MHC.	2cer	184-187	major histocompatibility complex, class I, C	Homo sapiens	237-240
2790930-5	1989	These observations were supported by the appearance of a LLca-induced PGI in various B10.A congenic strains carrying mutations at the I-A or I-E/I-J loci of the MHC.	2cer	70-73	major histocompatibility complex, class I, C	Homo sapiens	161-164
3181651-2	1988	Myosin extracted from tumours and electrophoresed on 6%-sodium dodecyl sulfate (SDS)glycerol gels was found to migrate as three distinct MHC components.	Sodium Dodecyl Sulfate	80-83	major histocompatibility complex, class I, C	Homo sapiens	137-140
3181651-2	1988	Myosin extracted from tumours and electrophoresed on 6%-sodium dodecyl sulfate (SDS)glycerol gels was found to migrate as three distinct MHC components.	Glycerol	84-92	major histocompatibility complex, class I, C	Homo sapiens	137-140
2450913-6	1988	T4 cells reacted with mAb to class I MHC Ag or beta 2 microglobulin and cross-linked with GaMIg proliferated vigorously in the presence of IL-2 or PMA.	gamig	90-95	major histocompatibility complex, class I, C	Homo sapiens	37-40
2450913-10	1988	Finally it was demonstrated that adding GaMIg to T4 cells reacted with mAb to class I MHC Ag but not CD11a resulted in an increase in intracellular calcium concentration.	gamig	40-45	major histocompatibility complex, class I, C	Homo sapiens	86-89
2450913-10	1988	Finally it was demonstrated that adding GaMIg to T4 cells reacted with mAb to class I MHC Ag but not CD11a resulted in an increase in intracellular calcium concentration.	Calcium	148-155	major histocompatibility complex, class I, C	Homo sapiens	86-89
2450913-11	1988	The data demonstrate that cross-linking class I MHC molecules results in the generation of at least one activation signal, a rise in intracellular calcium concentration, and, thereby, stimulates human T4 cells.	Calcium	147-154	major histocompatibility complex, class I, C	Homo sapiens	48-51
3355518-1	1988	Electrophoretic analysis in the presence of 33% glycerol of purified myosin from normal human muscle shows three distinct protein bands which are identified as type 1, 2B, and 2A myosin heavy chain (MHC) isoforms by affinity-purified polyclonal antibodies.	Glycerol	48-56	major histocompatibility complex, class I, C	Homo sapiens	199-202
2965021-7	1988	The combined results indicate that DC can directly present class I MHC alloantigen or class I MHC plus nominal antigen (e.g. minor H) to CD8+ cells and generate a Tc response by these cells without the requirement for CD4+ Th cells.	Technetium	163-165	major histocompatibility complex, class I, C	Homo sapiens	67-70
2965021-7	1988	The combined results indicate that DC can directly present class I MHC alloantigen or class I MHC plus nominal antigen (e.g. minor H) to CD8+ cells and generate a Tc response by these cells without the requirement for CD4+ Th cells.	Technetium	163-165	major histocompatibility complex, class I, C	Homo sapiens	94-97
3654756-4	1987	There are differences in where, when, and how myofibrillar alpha-actin and MHC are degraded and eliminated from TPA-myosacs.	Tetradecanoylphorbol Acetate	112-115	major histocompatibility complex, class I, C	Homo sapiens	75-78
2965021-2	1988	Generation of a secondary in vitro class II MHC-specific Tc response was totally CD4+ Th cell-dependent with both types of APC.	Technetium	57-59	major histocompatibility complex, class I, C	Homo sapiens	44-47
30978832-4	1987	Addition of salt (1.5 or 3.0%) or phosphate (0.5%) generally increased the extraction of MHC and actin from the myofibrillar protein fraction in both HB and CB preblends.	Salts	12-16	major histocompatibility complex, class I, C	Homo sapiens	89-92
30978832-4	1987	Addition of salt (1.5 or 3.0%) or phosphate (0.5%) generally increased the extraction of MHC and actin from the myofibrillar protein fraction in both HB and CB preblends.	Phosphates	34-43	major histocompatibility complex, class I, C	Homo sapiens	89-92
3654756-16	1987	TPA reversibly blocks incorporation of [35S]methionine into myofibrillar alpha-actin, MHC, myosin light chains 1 and 2, the tropomyosins, and troponin C. It does not block the synthesis of beta- or gamma-actins, the nonmyofibrillar MHC or light chains, tubulin, vimentin, desmin, or most household molecules.	Tetradecanoylphorbol Acetate	0-3	major histocompatibility complex, class I, C	Homo sapiens	86-89
3654756-16	1987	TPA reversibly blocks incorporation of [35S]methionine into myofibrillar alpha-actin, MHC, myosin light chains 1 and 2, the tropomyosins, and troponin C. It does not block the synthesis of beta- or gamma-actins, the nonmyofibrillar MHC or light chains, tubulin, vimentin, desmin, or most household molecules.	Tetradecanoylphorbol Acetate	0-3	major histocompatibility complex, class I, C	Homo sapiens	232-235
3597767-4	1987	The distribution of this new MHC isoform in the globe rotating muscles from different mammalian species was analysed using a panel of specific anti-myosin antibodies and comparing the histochemical myosin ATPase profile of muscle fibres with their isomyosin content.	isomyosin	248-257	major histocompatibility complex, class I, C	Homo sapiens	29-32
3616359-3	1987	Its definition requires: a) a family history of abnormalities of iron storage; b) an association with HLA; c) inadequate iron absorption in relation to iron stores in liver and other territories; d) the absence of any other known causes of iron overload.	Iron	121-125	major histocompatibility complex, class I, C	Homo sapiens	102-108
3616359-3	1987	Its definition requires: a) a family history of abnormalities of iron storage; b) an association with HLA; c) inadequate iron absorption in relation to iron stores in liver and other territories; d) the absence of any other known causes of iron overload.	Iron	121-125	major histocompatibility complex, class I, C	Homo sapiens	102-108
3616359-3	1987	Its definition requires: a) a family history of abnormalities of iron storage; b) an association with HLA; c) inadequate iron absorption in relation to iron stores in liver and other territories; d) the absence of any other known causes of iron overload.	Iron	121-125	major histocompatibility complex, class I, C	Homo sapiens	102-108
2434259-2	1986	A gene sequence coding for myosin heavy chain (MHC) of human cardiac muscle was isolated by screening a human genomic library with a 32P-labelled 1.1kb SacI restriction fragment from a previously characterized cDNA clone specifying the light meromyosin and 3" untranslated region of mRNA encoding rabbit cardiac alpha-MHC.	Phosphorus-32	133-136	major histocompatibility complex, class I, C	Homo sapiens	27-45
2434259-2	1986	A gene sequence coding for myosin heavy chain (MHC) of human cardiac muscle was isolated by screening a human genomic library with a 32P-labelled 1.1kb SacI restriction fragment from a previously characterized cDNA clone specifying the light meromyosin and 3" untranslated region of mRNA encoding rabbit cardiac alpha-MHC.	Phosphorus-32	133-136	major histocompatibility complex, class I, C	Homo sapiens	47-50
2434259-2	1986	A gene sequence coding for myosin heavy chain (MHC) of human cardiac muscle was isolated by screening a human genomic library with a 32P-labelled 1.1kb SacI restriction fragment from a previously characterized cDNA clone specifying the light meromyosin and 3" untranslated region of mRNA encoding rabbit cardiac alpha-MHC.	Phosphorus-32	133-136	major histocompatibility complex, class I, C	Homo sapiens	318-321
2434259-2	1986	A gene sequence coding for myosin heavy chain (MHC) of human cardiac muscle was isolated by screening a human genomic library with a 32P-labelled 1.1kb SacI restriction fragment from a previously characterized cDNA clone specifying the light meromyosin and 3" untranslated region of mRNA encoding rabbit cardiac alpha-MHC.	meromyosin	242-252	major histocompatibility complex, class I, C	Homo sapiens	27-45
2434259-2	1986	A gene sequence coding for myosin heavy chain (MHC) of human cardiac muscle was isolated by screening a human genomic library with a 32P-labelled 1.1kb SacI restriction fragment from a previously characterized cDNA clone specifying the light meromyosin and 3" untranslated region of mRNA encoding rabbit cardiac alpha-MHC.	meromyosin	242-252	major histocompatibility complex, class I, C	Homo sapiens	47-50
2434259-7	1986	It also showed that lambda HCMHC8 spanned 14 kb of DNA and contained exon segments estimated to code for two-thirds of a MHC including the carboxylic acid terminus.	Carboxylic Acids	139-154	major histocompatibility complex, class I, C	Homo sapiens	29-32
3009364-3	1986	Homology searches in protein data banks revealed the presence of the peptide SDGR in the alpha 2 domain of MHC class I antigens, and a variant of RGDS, Arg-Phe-Asp-Ser (RFDS), was found highly conserved in MHC class I (alpha 1 domain) and class II antigens (beta 1 domain).	Arginine	152-155	major histocompatibility complex, class I, C	Homo sapiens	206-209
2421254-2	1986	In this report, we present the complete DNA sequence of two different adult human skeletal muscle MHC cDNA clones, one of which encodes the entire light meromyosin (LMM) segment of MHC and represents the longest described MHC cDNA sequence.	meromyosin	153-163	major histocompatibility complex, class I, C	Homo sapiens	98-101
2421254-2	1986	In this report, we present the complete DNA sequence of two different adult human skeletal muscle MHC cDNA clones, one of which encodes the entire light meromyosin (LMM) segment of MHC and represents the longest described MHC cDNA sequence.	meromyosin	153-163	major histocompatibility complex, class I, C	Homo sapiens	181-184
2421254-2	1986	In this report, we present the complete DNA sequence of two different adult human skeletal muscle MHC cDNA clones, one of which encodes the entire light meromyosin (LMM) segment of MHC and represents the longest described MHC cDNA sequence.	meromyosin	153-163	major histocompatibility complex, class I, C	Homo sapiens	181-184
2936964-5	1986	Here, we show that a fluorescein-labelled synthetic peptide, together with Texas red-labelled class II MHC antigen, I-Ad, stimulates the production of interleukin-2 by a peptide-specific I-Ad-restricted T-cell hybridoma when reconstituted in a lipid membrane on a glass substrate.	Texas red	75-84	major histocompatibility complex, class I, C	Homo sapiens	103-106
3997878-2	1985	MHC was alkylated with N-ethylmaleimide, purified by Sepharose-4B chromatography, and cleaved with cyanogen bromide.	Ethylmaleimide	23-39	major histocompatibility complex, class I, C	Homo sapiens	0-3
2425369-0	1986	Inhibition of MHC product induction may contribute to the immunosuppressive action of ciclosporin.	Cyclosporine	86-97	major histocompatibility complex, class I, C	Homo sapiens	14-17
3997878-2	1985	MHC was alkylated with N-ethylmaleimide, purified by Sepharose-4B chromatography, and cleaved with cyanogen bromide.	Sepharose	53-65	major histocompatibility complex, class I, C	Homo sapiens	0-3
3997878-2	1985	MHC was alkylated with N-ethylmaleimide, purified by Sepharose-4B chromatography, and cleaved with cyanogen bromide.	Cyanogen Bromide	99-115	major histocompatibility complex, class I, C	Homo sapiens	0-3
3997878-6	1985	Comparison of the homologous MHC sequences shows two positions at which MHC from dystrophic chicks differs from that of the White Leghorn chicks *(Glu----Gln and Met----Ile).	Glutamic Acid	147-150	major histocompatibility complex, class I, C	Homo sapiens	29-32
3997878-6	1985	Comparison of the homologous MHC sequences shows two positions at which MHC from dystrophic chicks differs from that of the White Leghorn chicks *(Glu----Gln and Met----Ile).	Glutamic Acid	147-150	major histocompatibility complex, class I, C	Homo sapiens	72-75
3997878-6	1985	Comparison of the homologous MHC sequences shows two positions at which MHC from dystrophic chicks differs from that of the White Leghorn chicks *(Glu----Gln and Met----Ile).	Glutamine	154-157	major histocompatibility complex, class I, C	Homo sapiens	29-32
3997878-6	1985	Comparison of the homologous MHC sequences shows two positions at which MHC from dystrophic chicks differs from that of the White Leghorn chicks *(Glu----Gln and Met----Ile).	Glutamine	154-157	major histocompatibility complex, class I, C	Homo sapiens	72-75
2580010-4	1985	In contrast, the same T cell clones were only minimally affected in their ability to respond to similarly chloroquine-treated APC expressing allogeneic MHC products.	Chloroquine	106-117	major histocompatibility complex, class I, C	Homo sapiens	152-155
6489465-4	1984	We demonstrate that the calmodulin antagonist trifluoperazine (TFP) enhances the apparent rate of endocytosis of liposomes bound to MHC class I molecules.	Trifluoperazine	46-61	major histocompatibility complex, class I, C	Homo sapiens	132-135
2579032-9	1985	In contrast, 5-azaC resulted in some cases in increased density of MHC antigens.	Azacitidine	13-19	major histocompatibility complex, class I, C	Homo sapiens	67-70
6198102-3	1984	The MHC product occurred in a KCl extract of cells and behaved genetically and serologically as I-J.	Potassium Chloride	30-33	major histocompatibility complex, class I, C	Homo sapiens	4-7
6334644-7	1984	Soluble or Sepharose-bound anti-Ti monoclonal antibodies, like physiologic ligand (antigen/MHC), enhanced proliferative responses to purified IL-2 by inducing a 6-fold increase in surface IL-2 receptor expression.	Sepharose	11-20	major histocompatibility complex, class I, C	Homo sapiens	91-94
6086718-1	1984	Complementary DNA (cDNA) clones corresponding to the major histocompatibility (MHC) class III antigen, complement protein C2, have been isolated from human liver cDNA libraries with the use of a complex mixture of synthetic oligonucleotides (17 mer) that contains 576 different oligonucleotide sequences.	Oligonucleotides	224-240	major histocompatibility complex, class I, C	Homo sapiens	79-82
6086718-1	1984	Complementary DNA (cDNA) clones corresponding to the major histocompatibility (MHC) class III antigen, complement protein C2, have been isolated from human liver cDNA libraries with the use of a complex mixture of synthetic oligonucleotides (17 mer) that contains 576 different oligonucleotide sequences.	Oligonucleotides	224-239	major histocompatibility complex, class I, C	Homo sapiens	79-82
6198102-4	1984	Cells armed with anti-picryl or anti-"oxazolone" TsF could be triggered by the corresponding "bis-picryl-L-lysine" and "bis-oxazolone-L-lysine" together with MHC.	picryl	22-28	major histocompatibility complex, class I, C	Homo sapiens	158-161
6198102-4	1984	Cells armed with anti-picryl or anti-"oxazolone" TsF could be triggered by the corresponding "bis-picryl-L-lysine" and "bis-oxazolone-L-lysine" together with MHC.	Oxazolone	38-47	major histocompatibility complex, class I, C	Homo sapiens	158-161
6226585-2	1983	This correlation, and the large body of (largely) circumstantial but still quite convincing data, suggests that these Ly and Leu molecules play a very important role in T cell responses by actually interacting with monomorphic MHC class specific determinants.	Lysine	118-120	major histocompatibility complex, class I, C	Homo sapiens	227-230
6226585-2	1983	This correlation, and the large body of (largely) circumstantial but still quite convincing data, suggests that these Ly and Leu molecules play a very important role in T cell responses by actually interacting with monomorphic MHC class specific determinants.	Leucine	125-128	major histocompatibility complex, class I, C	Homo sapiens	227-230
6947265-6	1981	When MHC [3H]mRNPs were encapsulated into liposomes and subsequently delivered to myoblasts and myotubes, the mRNPs were taken up by the cells at both stages of differentiation.	Tritium	10-12	major histocompatibility complex, class I, C	Homo sapiens	5-8
6947265-7	1981	However, the MHC [3H]mRNPs taken up by the myoblasts remained as free cytoplasmic particles (80-120S), whereas in myotubes the incorporated mRNP RA was associated with polysomes.	Tritium	18-20	major histocompatibility complex, class I, C	Homo sapiens	13-16