Publication for PSMB8 and TAP1
| Species | Symbol | Function* | Entrez Gene ID* | Other ID | Gene coexpression |
CoexViewer |
|---|---|---|---|---|---|---|
| hsa | PSMB8 | proteasome 20S subunit beta 8 | 5696 | [link] | ||
| hsa | TAP1 | transporter 1, ATP binding cassette subfamily B member | 6890 |
| Pubmed ID | Priority | Text |
|---|---|---|
| 27098790 | 0.98 | PSMB8, PSMB9, TAP1, and TAP2 genes in the Chinese population. |
| 0.97 | PSMB8, TAP1, and TAP2 loci in PD patients. | |
| 0.97 | PSMB8, rs17587 in PSMB9, rs1135216 in TAP1, rs2228391, rs2228396, rs241447, rs241448, and rs4148876 in TAP2, respectively [Figure 1a]. | |
| 0.94 | PSMB8, PSMB9, TAP1, and TAP2 were genotyped through SNaPshot testing. | |
| 0.93 | PSMB8, PSMB9, TAP1, and TAP2 | |
| 0.93 | TAP1-PSMB8-TAP2 haplotype (AA-G-C-AGATC) was also found to be a slight association with PD, but no significance after the Bonferroni correction. | |
| 0.84 | PSMB8, PSMB9, TAP1, and TAP2 genes. | |
| 0.78 | PSMB8, PSMB9, TAP1, and TAP2 genes at chromosome 6 are located at an adjacent range from 32.859 Mb and 32.821 Mb and involved in the protein degradation and antigen presentation, suggesting a possible LD of the above SNPs with PD patients. | |
| 0.74 | PSMB8, TAP1, and TAP2 and PD (ii) the rs17587-G at PSMB9 may develop an increased risk of PD for Chinese female population. | |
| 28536458 | 0.98 | LMP7, TAP1 and TAP2 was measured by RT-qPCR before and after HDAC inhibition in MKL-2, WaGa, MKL-1 and BroLi cells (Fig. 3C). |
| 0.97 | TAP1 and TAP2 as well as the immunoproteasome subunits LMP2 and LMP7 are simultaneously down-regulated by histone hypoacetylation. | |
| 0.96 | TAP1, TAP2, LMP2 and LMP7 mRNA expression is shown in comparison to RPLP0. | |
| 0.94 | TAP1, TAP2, LMP2 or LMP7 promoter specific primers. | |
| 0.92 | LMP7, TAP1 and TAP2, (R squared = 0.32, p = 0.0006; supplementary Fig. S3A). | |
| 0.88 | TAP1, TAP2, LMP2 and LMP7 in the same data set (GSE22396). | |
| 0.69 | TAP1-, TAP2-, LMP2- and LMP7-specific mAbs (Fig. 2C), revealing that HLA-A and beta2m were expressed in all analyzed MCC cell lines, while TAP1 and LMP2, LMP7 expression was largely restricted to the MKL-2 cell line (Fig. 2C). | |
| 0.59 | LMP7 and the transporter complex which is composed of the subunits TAP1 and TAP2. | |
| 0.58 | LMP7, TAP1 and TAP2, mRNA levels (Fig. 2B). | |
| 21085187 | 0.98 | TAP1-PSMB8, TGFBR2, TNF, TSLP, TXNDC5, UVRAG, VDR, and XBP1; Supplementary Table S1 online), followed by a meta-analysis incorporating both the current and available previously published data, when possible. |
| 0.98 | TAP1-PSMB8 in two independent US non-Hispanic white cohorts: the first 230 cases and 188 controls (rs1135216, allelic P= 3.4E-03, Bonferroni-corrected P= 6.8E-03; genotypic P= 9.4E-03, Bonferroni-corrected P= 1.9E-02) and the second a family-based association study of 35 families (rs2071627, P= 5.7E-05, Bonferroni-corrected P= 1.1E-04). | |
| 0.94 | TAP1-PSMB8 region of the MHC seems to derive from LD with primary association signals in the MHC class I and class II regions. | |
| 0.90 | TAP1 and PSMB8 (previously, LMP7) are in close juxtaposition in the MHC class II region. | |
| 0.76 | TAP1-PSMB8 region SNPs reflect LD with these primary MHC class I and class II association signals. | |
| 0.73 | TAP1-PSMB8 with GV is secondary to linkage disequilibrium (LD) with primary associated loci located elsewhere in the MHC class I and class II gene regions. | |
| 0.57 | TAP1-PSMB8 (rs3819721, P = 5.2E-06) seems to derive from linkage disequilibrium with major primary signals in the MHC class I and class II regions. | |
| 27634283 | 0.98 | TAP1, TAP2, PSMB8, and PSMB9 in both founder mice were further confirmed by using real-time PCR and western blotting, respectively (Fig. 1C,D). |
| 0.97 | TAP1, TAP2, PSMB8, and PSMB9). | |
| 0.93 | TAP1, TAP2, PSMB8, and PSMB9 in splenocytes from WT or hTAP-LMP mice as analyzed by qRT-PCR and normalized to 18S rRNA levels. | |
| 0.56 | TAP1 (65 kDa), TAP2 (75 kDa), PSMB8 (23/28 kDa), and PSMB9 (22 kDa) in WT or hTAP-LMP mice was determined by western blotting; beta-actin (42 kDa) was used as an internal control. | |
| 0.53 | TAP1, TAP2, PSMB8, and PSMB9 genes (hTAP-LMP mice) was generated, and we found that reconstitution of the hTAP-LMP gene cluster notably improved human HLA-I antigen presentation and restricted CTL responses. | |
| 19756593 | 0.98 | LMP7, LMP10, HLA class I heavy chain, tapasin, TAP1, TAP2 and ERp57) and MHC class I-related antigen (MICA). |
| 0.98 | LMP7 and LMP10, the TAP subunits TAP1 and TAP2, and tapasin. | |
| 0.95 | LMP7, LMP10, TAP1 and ERp57 than normal superficial urothelium (see Table 1 for P values; Fig. 1). | |
| 17316446 | 0.98 | LMP7 and LMP10; peptide transporters TAP1 and TAP2; and chaperones Calnexin, Calreticulin, ERp57, and Tapasin. |
| 0.97 | TAP1, Tapasin and LMP2 (5 cases), Calreticulin (4 cases), LMP7 (2 cases), and Calnexin and ERp57 (1 case). | |
| 20419139 | 0.98 | TAP-1, TAP-2, TPN, CNX, CLR, ERp57, LMP2, LMP7) and the transcription factors RFX5 and CIITA in undifferentiated Shef-1 and NT2 cells, compared to the control, Pitout cell line. |
| 0.76 | TAP-1, TAP-2, TPN, ERp57, CNX, CLR and LMP7 genes was induced in differentiated cells, although the level of up-regulation varied. | |
| 23024775 | 0.97 | TAP1, LMP7, tapasin, CRT, and ERp57 had an inverse correlation with lymph node metastasis (Figure 2C). |
| 0.96 | TAP1, TAP2, LMP2, LMP7, ERAP1, tapasin and ERp57 from normal expression to partial loss or total loss of expression in cervical tissue specimens in Immunohistochemical analysis. | |
| 0.95 | TAP1, TAP2, LMP7, tapasin, and ERp57 gene promoters. | |
| 0.92 | TAP1, LMP7, and ERp57 protein expression and tumor differentiation grade. | |
| 0.92 | TAP1, TAP2, and LMP7 protein expression in esophageal squamous cell carcinoma, colon cancer, renal cancer, and melanoma. | |
| 0.90 | TAP1, TAP2, LMP2, LMP7, ERAP1, tapasin, and ERp57, due to the downregulation of these genes in cervical cancer or precursor lesions, for methylation status of CpG islands at the promoter region in SiHa cervical carcinoma cells by bisulfite-sequencing approach. | |
| 0.88 | TAP1, TAP2, LMP2, LMP7, ERAP1, tapasin and ERp57 was statistically significant for CIN cases compared to normal controls. | |
| 0.84 | TAP1, LMP7, and ERp57 with changes in protein expression. | |
| 0.83 | TAP-1, TAP-2, LMP2, LMP7, Tapasin, ERAP1, CNX, CRT and ERp57) in cervical cancer. | |
| 0.82 | TAP1, TAP2, LMP2, LMP7, calnexin, calreticulin, ERp57, and tapasin staining shown in Figure S1), Panels A1-C1 depict normal uterine cervix tissue with normal protein expression. | |
| 0.79 | transporter associated with antigen processing (TAP1/2), low molecular mass protein (LMP2, LMP7), endoplasmic reticulum aminopeptidase 1(ERAP1), chaperone molecules include calreticulin (CLR), calnexin (CNX) and ERp57, and this was proved again by analysis of transcription of the same genes in addition to three genes HLA-A, B and C coding for HLA-I. By bisulfite sequencing approach, we identified target CpG islands methylated at the gene promoter region of TAP1, TAP2, LMP7, tapasin and ERp57 in cervical carcinoma cells. | |
| 0.77 | TAP1, TAP2, LMP7, ERAP1, tapasin, and ERp57 protein expression positively associated with HLA-I expression in CIN lesions, whereas ss2-m, TAP1, TAP2, LMP2, LMP7, ERAP1, ERp57, and tapasin expression positively associated with HLA-I in the cancerous lesions. | |
| 0.70 | TAP1, LMP7, and ERp57 genes in CSCC tissue as compared to CIN and normal tissues. | |
| 0.67 | TAP-1, TAP-2, LMP2, LMP7, Tapasin, ERAP1, CNX, CRT and ERp57) were analyzed by Semi-quantitative RT-PCR in normal uterine cervix tissue, CIN and CSCC. | |
| 0.51 | TAP1, LMP7, and ERp57 indicated a significant increase in methylation level of most of the CpG sites at target CpG islands of TAP1, LMP7, and ERp57 genes in CSCC compared to controls, whereas no statistical significance was found between CIN and the control (P>0.05). | |
| 25749172 | 0.97 | LMP7 and possibly LMP2, as well as lower nuclear expression of LMP10 and a higher expression of TAP1 in TSCC as compared to BOTSCC (Table 2, Table 3). |
| 0.97 | TAP1 and TAP2, and also between LMP2 and LMP7, irrespective of HPV status (Table 4). | |
| 0.96 | TAP1 and TAP2, as well as between LMP2 and LMP7, irrespective of tumor HPV status. | |
| 0.95 | TAP1 and TAP2 was correlated, as was LMP2 to LMP7. | |
| 0.95 | LMP7, TAP1, TAP2, and HLA class I correlated to clinical outcome in HNSCC. | |
| 0.94 | TAP1, TAP2, LMP2, and LMP7, between 127 and 147 of the 151 included TSCC and BOTSCC samples were stained and evaluated for nuclear and cytoplasmic expression. | |
| 0.93 | LMP7, LMP10, TAP1, and TAP2, affecting the formation of peptide presenting HLA-b2m complexes, seemed of importance. | |
| 0.93 | LMP7, and LMP10 are subunits of the immunoproteasome, responsible for the processing of proteins to peptides, while TAP1 and TAP2 transport peptides from the cytoplasm to the endoplasmic reticulum. | |
| 0.92 | LMP7 expression was correlated to TAP2, irrespective of HPV status, and to TAP1 in HPV-negative tumors (Table 5). | |
| 0.92 | TAP1, TAP2, LMP2, and LMP7 expression in the HNSCC study by Meissner et al. were also somewhat higher than those presented here, but in line with our data, TAP1 was less frequently reduced than TAP2. | |
| 0.90 | TAP1, TAP2, LMP2, and LMP7 were analyzed only for patients treated with curative intent, and separately for patients with HPV-positive and HPV-negative tumors (Figure 2), since the former usually have a better clinical outcome. | |
| 0.89 | TAP1, TAP2, LMP2, and LMP7, we have used commercially available antibodies and we have trusted the manufacturers' descriptions of their specificity. | |
| 0.84 | TAP1, TAP2, LMP2, and LMP7 expression in HPV-positive and HPV-negative tumors, while, as presented in Tertipis et al., there was a minor difference with regard to cytoplasmic LMP10 expression . | |
| 0.83 | TAP1, TAP2, LMP2, and LMP7 in these tumors in relation to HPV status, HLA class I expression, each other, and clinical outcome was therefore investigated. | |
| 0.74 | LMP7 was absent or weak in a substantial fraction (33-59%) of the tumors, while LMP10 was reduced in even more (87%) of the tumors, whereas TAP1 only had a reduced expression in 9%. | |
| 28700671 | 0.97 | PSMB8 rs2071464 was associated with generalized and active vitiligo from Gujarat whereas TAP1 rs1135216 showed no association. |
| 0.96 | PSMB8 and TAP1 were measured in the PBMCs of 91 patients and 96 controls by using qPCR. | |
| 0.96 | TAP1-PSMB8 region in GWAS and the meta-analysis study in GV patients; however, no association was observed for TAP1 rs1135216 and PSMB8 rs2071627 SNPs. | |
| 0.95 | PSMB8 and TAP1 are needed to delineate the role of defective antigen processing and presentation pathways in vitiligo pathogenesis. | |
| 0.94 | PSMB8 rs2071464 SNP with GV as well as with the disease activity (AV); however, TAP1 rs1135216 SNP was not associated with vitiligo in Gujarat. | |
| 0.93 | proteasome subunit beta 8 (PSMB8) and transporter associated with antigen processing 1 (TAP1), involved in antigen processing and presentation have been reported to be associated with several autoimmune diseases including vitiligo. | |
| 0.93 | TAP1-PSMB8 seems to derive from linkage disequilibrium with major primary signals in the MHC class I and class II regions. | |
| 0.83 | PSMB8-TAP1 region of the MHC has been reported to derive from LD with primary association signals in the MHC class I and class II regions. | |
| 0.82 | PSMB8 rs2071464 and TAP1 rs1135216 single nucleotide polymorphisms and to estimate the expression of PSMB8 and TAP1 in patients with vitiligo and unaffected controls from Gujarat. | |
| 0.78 | PSMB8 or TAP1 proteins could potentially affect the antigenic repertoire expressed on the cell surface and may alter peripheral tolerance. | |
| 0.77 | PSMB8 and TAP1 polymorphisms in patients with vitiligo (Table 7); however, studies revealing the impact of these polymorphisms at transcript and protein levels are few. | |
| 0.75 | PSMB8 rs2071464 polymorphism was genotyped using polymerase chain reaction- restriction fragment length polymorphism (PCR-RFLP) and TAP1 rs1135216 polymorphism was genotyped by amplification refractory mutation system-polymerase chain reaction (ARMS-PCR) in 378 patients with vitiligo and 509 controls. | |
| 0.75 | TAP1 exon 10 A/G polymorphism with vitiligo in Saudi population but not for PSMB8 intron 6 G/T polymorphism. | |
| 0.70 | proteasome subunit beta 8 (PSMB8) and transporter associated with antigen processing 1 (TAP1) polymorphisms and their transcript levels in vitiligo from Gujarat | |
| 0.55 | proteasome subunit beta 8 (PSMB8) and transporter associated with antigen processing 1 (TAP1) have been reported to be associated with several autoimmune diseases including vitiligo. | |
| 23526983 | 0.97 | TAP-1 peptide was demonstrated, and, increase and/or rescue in the expression of TAP-2, LMP-2 and LMP-7 peptides were demonstrated when down-regulation of IGF-1 by IGF-1 antisense RNA or when blockade of the IGF-1 receptor (IGF-1R) by its monoclonal antibody occurred. |
| 0.96 | TAP-1, TAP-2, tightly linked to LMP-2 and LMP-7 are multiple components of the endogenous, antigen presentation pathway machinery. | |
| 0.96 | TAP-1; B, TAP-2; C, LMP-7; and D, LMP-2. | |
| 0.94 | TAP-1, TAP-2, LMP-2 and LMP-7, respectively. | |
| 0.87 | TAP-1 and LMP-7 peptides, and, rescue in expression of TAP-2 and LMP-2 peptides following the exogenous addition of 10ug/ml IGF-1R mAb into cell culture medium for 48 hours were demonstrated by Western Blot. | |
| 0.85 | TAP-1, TAP-2, LMP-2 and LMP-7 mRNA | |
| 0.76 | TAP-1 and LMP-7 Peptides, and, Rescued Expression of TAP-2, LMP-2 Peptides and the B-7.1 Molecule | |
| 0.74 | TAP-1, TAP-2, LMP-2 and LMP-7 components of the endogenous antigen presentation pathway. | |
| 0.74 | TAP-1 was increased in HG-2, HG-5 and HG-9 (p<0.05); expression in TAP-2 was increased in HG-2 (p<0.001) and HG-3 (p<0.05); expression in LMP-7 was enhanced in HG-2 (p<0.001), HG-5 and HG-9 (p<0.05); and, expression in LMP-2 was up-regulated in HG-2 (p<0.001), HG-5 and HG-9 (p<0,05). | |
| 30648121 | 0.97 | LMP7, TAP1, and TAP2 Transcripts in the Three sHCC Cell Lines |
| 0.97 | TAP1 and LMP7 downregulation. | |
| 0.95 | TAP1 and LMP7 are directly or indirectly involved in the formation of an effective peptide-loading platform for HLA class I-beta 2m-peptide complex stabilization. | |
| 0.86 | LMP7, TAP1, and TAP2 were markedly lower in the sHCC29 and sHCC63 cells than those in the sHCC74 cells. | |
| 0.84 | LMP7, TAP1, and TAP2 mRNA in the three newly established sHCC cell lines cultured in the presence or absence of IFN-gamma (300 U/mL, 48 h). | |
| 0.69 | TAP1 was expressed at a low frequency in the two beta 2m-negative cell lines, and while LMP2 was abundantly expressed in all of three cell lines, LMP7 expression was detectable only at a very low percentage of sHCC63 cells (Figure 3(c)). | |
| 28718425 | 0.97 | LMP7 and TAP1. |
| 0.97 | LMP7 and TAP1. | |
| 0.96 | LMP7, TAP1), was associated with poor survival in melanoma and bladder cancer patients, indicating that abnormal epigenetic changes in NLRC5 within cancer cells significantly impact clinical outcomes. | |
| 0.92 | LMP7 and TAP1. | |
| 0.90 | LMP7 and TAP1.. | |
| 22134332 | 0.97 | TAP-1, TAP-2, LMP-7, and LMP-10 expressions differed among the cancer cell lines. |
| 0.96 | TAP-1, TAP-2, LMP-7 and LMP-10. | |
| 0.96 | TAP-1, TAP-2, LMP-7, and LMP-10, which differed among cultured cell lines. | |
| 0.61 | TAP-1, TAP-2, LMP-7, LMP-10). | |
| 27213585 | 0.97 | TAP1 (2.1-fold, P<0.001), LMP7 (3.0-fold, P<0.001), and HLA class I (2.5-fold, P<0.001) in comparison to JAK1 wildtype endometrial cancers (Figure 2). |
| 0.95 | LMP7 expression in contrast to TAP1 (P=0.001 vs. P=0.381). | |
| 0.91 | TAP1, LMP7, HLA class I and presence of CD8-positive T-cells in the MSI endometrial cancers (Table 2). | |
| 0.82 | LMP7 and HLA class I with no effect on TAP1 expression and the number of CD8-positive T-cells in JAK1 mutant endometrial cancer tissue samples. | |
| 18704411 | 0.97 | LMP7 and TAP1 had a low expression or were not detectable in all the cell lines tested. |
| 0.97 | TAP1, TAP2, LMP2 and LMP7 mRNA in the six RCC cell lines under basal conditions and following a 48 h incubation at 37 C with IFN-gamma (300 U/ml). | |
| 0.62 | TAP1, TAP2, LMP2 and LMP7 mRNAs under basal conditions; the level of each component mRNA was augmented in all the cell lines following incubation with IFN-gamma (Fig. 3a-f). | |
| 24480782 | 0.97 | LMP7, TAP1, TAP2, and the protein chaperones calnexin, tapasin, and calreticulin (Supplemental Table 1). |
| 0.71 | LMP7, and LMP10; the peptide transporters TAP1 and TAP2; and the chaperones calnexin (2/3 cell lines) and tapasin (3/3 cell lines). | |
| 25305756 | 0.97 | TAP1/PSMB8 locus |
| 0.96 | TAP1/PSMB8, and HLA-DP loci), chr.1q32 (CFHR3,1-delta locus), chr.8p23 (DEFA locus), chr.17p13 (TNFSF13 locus), and chr.22q12 (HORMAD2 locus). | |
| 25796583 | 0.97 | TAP1) and low molecular weight peptide 7 (LMP7) is significantly associated with decreased survival in human papilloma virus (HPV) associated cervical carcinoma (Mehta et al.). |
| 0.92 | TAP1, LMP7 and ERAP1 expression is associated with decreased survival in HPV-mediated cervical carcinoma in Dutch patients (Mehta et al.). | |
| 25874709 | 0.97 | TAP1, TAP2, LMP2, LMP7, tapasin) in a high risk population of HCV infection in China. |
| 0.61 | TAP1, TAP2, LMP2, LMP7, HLA-DMA, HLA-DMB, HLA-DOA, and HLA-DOB. | |
| 26440127 | 0.97 | LMP7, LMP10 (MECL1), TAP1 and TAP2. |
| 0.97 | LMP7, LMP10, TAP1, TAP2, calnexin, calreticulin, ERp57 and tapasin.29, 33 Chikamatsu et al.34 report that CD44+ putative head and neck CSC/CIC showed expression levels of LMP2, LMP7, LMP10 (MECL1), TAP1 and tapasin that were equal to those in CD44- cells, whereas CD44+ cells showed a lower expression level of TAP2 than that in CD44- cells (Fig. 1). | |
| 29743639 | 0.97 | TAP1), IFI35 (Interferon induced protein 35) and Proteasome subunit beta 8 (PSMB8) mRNA expression. |
| 28129744 | 0.96 | PSMB8, PSMB9 and TAP1 (bold) on chromosome 6 reported previously as potential VL-associated genetic loci. |
| 0.95 | PSMB8, PTPN6, MX1, MX2, IFIT1, TOMM34, IFIT3, SERPING1, NCF4, TAP1 and ISG15) in the VL-blood profile (representing TFs, receptors, kinases, proteases, phosphatases, enzymes and other general proteins) that are significantly "over-connected" with objects both within the VL-blood profile as well as the larger metabase (Table 2). | |
| 0.89 | PSMB8, (Additional file 4: Figure S1)]; b) Type II IFN (IFN-gamma) signaling pathway [IRF9, PRKCD, EIF2AK2 (PKR), STAT1 (Fig. 4)]; c) IFN signaling related to inflammation [MICB, IRF9, ISG20, STAT1, TAP1, MX2, IFI44, PTPN6 (Fig. 3b)]; d) Cytokine related pathways (28 in total) (Fig. 3c) (IL-13 signaling (STAT1, PTPN6, STAT6, PRKCD] and IL-2 activation (NFKB2, HMGA1, PTPN6 and SYK, among others). | |
| 0.89 | PSMB8 (chr6p21.3), PSMB9 (chr6p21.3) and TAP1 (chr6p21.3) overlap with putative VL susceptibility loci. | |
| 0.85 | PSMB8, PSMB9 and TAP1) described as potential VL-associated genetic susceptibility loci. | |
| 28622390 | 0.96 | PSMB8 (Fig 1D), PSMB9 (Fig 1E), TAP1 (Fig 1F), and TAPBP (Fig 1G). |
| 0.92 | PSMB8, CALR, PSMB9/TAP1 (shared promoter), CD58, and TAPBP. | |
| 0.89 | PSMB8, PSMB9, and TAP1). | |
| 20140259 | 0.96 | TAP1 and TAP2, the chaperon protein tapasin, and the subunits of the multicatalytic proteasome (PA28, LMP2, LMP7, and LMP10). |
| 0.58 | TAP1, TAP2, tapasin, PA28, LMP2, LMP7, and LMP10 proteins (Figure 4). | |
| 24728075 | 0.96 | TAP1, PSMB8, PSMB9, HLA-DQB1, HLA-DQB2, HLA-DMA, and HLA-DOA. |
| 0.92 | TAP1, PSMB8, PSMB9, HLA-DQB1, HLA-DQB2, HLA-DMA, and HLA-DOA reside. | |
| 29073155 | 0.96 | TAP1, LMP2 and LMP7 are all located within a narrow region of the class II cluster of the major histocompatibility complex on chromosome 6. |
| 0.84 | TAP1 and mutant LMP7, decreased the risk of ESCC in the Kazakh population. | |
| 26405558 | 0.96 | TAP1 and PSMB8. |
| 20221424 | 0.95 | PSMB8, PSMB9, TAP1 and TAP2 as well as proteins involved in MHC class I and class II presentation. |
| 0.94 | PSMB8, PSMB9) and transporter 1, ATP-binding cassette sub-family B (MDR/TAP) (TAP1) and transporter 2, ATP-binding cassette sub-family B (MDR/TAP) (TAP2). | |
| 27264839 | 0.95 | TAP1 (3%), HLA-A and HLA-B (3% respectively) and PSMB7 (LMP7, 3%). |
| 0.87 | LMP7, LMP10, TAP1, TAP2, Tapasin, Calreticulin, Calnexin, ERp57, beta2-microglobulin) and HLA class I loci (HLA-A, HLA-B and HLA-C). | |
| 28058287 | 0.94 | TAP1 and LMP7. |
| 0.93 | TAP1 and LMP7 in Huh7.5 cells treated with IL-27. | |
| 0.84 | TAP1 increased from 6 hrs post stimulation (p=0.0001) and LMP7 significantly increased increased from 24 hours (p=0.0132) post-stimulation with IL-27 ( Figure 3B). | |
| 0.80 | TAP1, transporter associated with antigen processing 1; LMP-7, low molecular mass polypeptide 7. | |
| 0.55 | TAP1 and LMP7. | |
| 27332624 | 0.94 | TAP1, neighboring both PSMB8 and PSMB9. |
| 0.93 | PSMB8 and TAP1, consistent with an increased frequency of antigen-presenting cells in LSG tissue from the SS cases. | |
| 20628381 | 0.91 | TAP-1, LMP-7, and tapasin were downregulated or lost in HER2 high-expressing TE4 in comparison to HER2 low-expressing TE1 (Figure 5). |
| 0.87 | LMP-7, TAP-1, or tapasin between siHER2 and control transfectants in both cell lines (Figure 5). | |
| 0.85 | TAP-1, LMP-7, and tapasin were downregulated or lost in HER2 high-expressing TE4 in comparison to HER2 low-expressing TE1, we could not detect significant alterations in the expressions of LMP2, LMP7, Tap1, and tapasin between ESCC treated with HER2-siRNA and the control. | |
| 0.71 | LMP7, Tap1, and tapasin) were assessed by western blot analysis against TE1 (HER2 low) and TE4 (HER2 high) transfected with siRNA targeting HER2 (siHER2) or the control (siCont). | |
| 17622526 | 0.90 | LMP7 and LMP10 subunits); and transported from the cytoplasm to the endoplasmic reticulum by TAP (transporter associated with antigen presentation) which is composed of TAP1 and TAP2 subunits. |
| 0.85 | LMP7, LMP10, TAP1, TAP2, ERAP1, tapasin, calreticulin, calnexin and ERp57. | |
| 0.66 | TAP1, LMP7 (for OS only) and ERAP1 expression, combined with the aforementioned prognostic factors. | |
| 24212778 | 0.90 | LMP7, TAP-1, TAP2, and tapasin, can be epigenetically regulated in certain tumors. |
| 0.84 | LMP7), transporters associated with antigen processing (TAP1, TAP2) and the TAP-associated glycoprotein (tapasin) gene in tumor cells. | |
| 0.65 | TAP1, TAP2, LMP2, LMP7, Tapasin and MHC class I) involved in antigen processing and presentation via the MHC class I in melanoma cells. | |
| 18331636 | 0.90 | TAP1, TAP2, PSMB8 and PSMB9), were down-regulated, thus contributing to viral immune escape from this pathway and other genes involved in apoptosis, nucleic acid metabolism, cytoskeleton signaling as well as interferon-mediated antiviral response were also modulated during PrV infection. |
| 0.82 | TAP1 and TAP2 genes encoding immunoproteasome catalytic subunits, PSMB8 and PSMB9, involved in the MHC class I antigenic presentation pathway was also detected in our experiment. | |
| 22588558 | 0.90 | LMP7 (P<0.001), TAP1 (P<0.001), tapasin (P=0.019) and HLA-A (P<0.001) was observed in NPC. |
| 25548428 | 0.89 | TAP1-rs5735883 and PSMB8-rs37360 have been studied in Saudi vitiligo cases, but no significant associations have been found. |
| 31019512 | 0.85 | TAP1, TAP2, PSMB8, PSMB9. |
| 31767055 | 0.84 | PSMB8, PSMB9, PSMB10, TAP1, TAP2, ERAP1, ERAP2, CANX, CALR, PDIA3, TAPBP, B2M, HLA-A, HLA-B and HLA-C (Figure 1:source data 1). |
| 28051153 | 0.83 | PSMB8, PSMB9 and PSMB10), proteasome activators PSME1 and PSME2 and transporter genes TAP1 and TAP2 across cancer cells, and eight datasets representing breast cancer tumour tissue's. |
| 22727420 | 0.82 | TAP-1 gene lies ~ 1 Kb upstream from the initial translational codon of LMP7. |
| 31024628 | 0.76 | TAP1, and TAP2) and genes involved in the immune response (NOD2, IFITM1, PSMB8, TXK, and AIM2). |
| 16389301 | 0.73 | LMP7, and LMP10; (2) transporters associated with antigen processing (TAP): TAP1 and TAP2; (3) the chaperone proteins: calnexin, calreticulin, and tapasin; and (4) MHC class I heavy chain and beta2-microglobulin. |
| 26313662 | 0.73 | TAP1, LMP2, LMP7, ERAP2 and ERp57, the P-value for the interaction term was significant (P<0.0012). |
| 31888082 | 0.73 | TAP1-PSMB8 and HLA-DP), on chromosome 1q32 (CFHR3-CFHR1), on chromosome 8p23 (DEFA), on chromosome 17p13 (TNFSF13) and on chromosome 22q12 (HORMAD2), new signals were identified, 4 of which in three new loci: Integrin alpha M- Integrin alpha X (ITGAM-ITGAX) on the 16p11 chromosome, implicated in the adhesion and migration of leukocytes and in phagocytosis complement-mediated by monocytes and macrophages and associated with the development of erythematous systemic lupus; CARD9, on chromosome 9q34, implicated in the activation of nuclear factor NF-kappaB in macrophages, which gives an increased risk of ulcerative colitis and Crohn's disease; and VAV3, on chromosome 1p13, implicated in the development of B and T lymphocytes and in the antigen presentation process. |
| 25528575 | 0.59 | TAP1, TAP2, LMP2, LMP7, and tapasin), which are involved in antigen processing and presentation. |
| 28081217 | 0.59 | TAP1/TAP2 and PSMB8/PSMB9. |
| 26158850 | 0.55 | Psmb8, Psmb9, Tap1, Tap2, Tapbp and Erap1. |
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