Publication for B2m and H2-K1

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
mmu	B2m	beta-2 microglobulin	12010			[link]
mmu	H2-K1	histocompatibility 2, K1, K region	14972

Pubmed ID	Priority	Text
22939644	0.98	beta2m knockdown and is decreased in neurons overexpressing H2-Kb.
	0.96	beta2m siRNA, and decreased in neurons overexpressing H2-Kb.
	0.91	H2-Kb and H2-Db (KbDb-/-), and mice deficient in CD3zeta, exhibit defects in LGN refinement that mimic those found in beta2m-/- mice (Figure 2b).
22445338	0.98	beta2m is necessary for stable cell surface expression of the majority of MHCI proteins, it is likely that the increase in levels of Kb and Db is accompanied by increased cell surface expression following MCAO.
	0.95	Kb, Db, beta2m and PirB following MCAO is associated with known PirB signaling components in brain.
25811463	0.98	B2m, Tap1, Psmb9, classical MHCI genes (H2-K, H2-D), and the non-classical MHCI gene H2-M3.
	0.88	H2-K, H2-D, B2m, Psmb9, and Tap1), validating the quality of the ChIP-seq analysis (Table 1, Figs. 3A, S2A).
30071035	0.98	H-2Kb and H-2Db, we propose that preservation of the heavy chain-beta2m heterodimer is sufficient for class I molecules to exit early secretory pathway.
	0.96	H-2Kb via C84-C139 disulfide bond improves the conformational stability of the peptide-receptive class I-beta2m heterodimer.
26861112	0.98	H2-K and H2-D, but also beta-2 microglobulin (B2m) and selected non-classical MHCI genes by occupying a specific SXY sequence in their promoter.
21358642	0.97	beta2m knockdown (KD) increased glutamatergic synapse density, while overexpression (OE) of a GFP-tagged MHCI subtype, H2-Kb, decreased it.
	0.96	beta2m KD dramatically increases, and H2-Kb OE strongly decreases, glutamatergic synaptic transmission.
	0.93	beta2m KD increases, and H2-Kb OE decreases, GABAergic synaptic transmission.
	0.89	H2-Kb-CFP: 0.97+-0.05, p=0.60, n=11 dendrites, 5 cells; e beta 2m, 1.07+-0.06, p=0.41, n= 5 dendrites, 5 cells).
19945389	0.97	beta2m-/-TAP1-/- mice, which lack cell surface expression of all MHCIs, implying that H2-Kb and H2-Db can account for observed changes in synapse plasticity.
	0.97	H2-Kb and H2-Db mRNA and protein are present in neurons within LGN and visual cortex, we propose that these specific classical MHCI family members are not only required for activity-dependent refinement and plasticity in the visual system, but can account for the majority of the abnormalities observed in the visual system of beta2m-/-TAP1-/- mice.
22711889	0.97	H2-Kb) and beta2m were also reduced in the spleen and thymus of Nlrc5-deficient mice (Fig. 1D).
	0.86	H2-Kb) and beta2m at the protein level in Nlrc5-deficient splenocytes and thymocytes (Fig. 3B).
27229916	0.97	beta2M-/-, TAP-/-, and MHCI deficient mice all lack efficient or appropriate synaptic pruning during development while over-expression of the H2-Kb heavy chain of MHCI in cultured neurons results in a decrease in synapse density of both excitatory GluN2A/B and inhibitory gamma-aminobutyric acid synapses.
30337538	0.97	H-2K, D, L) are highly polymorphic glycoproteins associated with beta2-microglobulin (beta2m), expressed on the cell surface of nucleated cells.
23776170	0.96	H-2 Kb, Db mouse beta2-m triple KO mice that express a significant amount of transgenic molecules at the cell surface resulting in substantial restoration of their CD8+ T cell peripheral compartment, which appears endowed with a well-diversified TCR repertoire.
	0.96	beta2-m-associated H-2 Kb molecules could also lyse virus-infected cells expressing beta2-m-free H-2 Kb molecules inferring presentation by some beta2-m-free H-2 Kb molecules of the "correct" viral peptides.
	0.95	H-2 Kb, Db, mouse beta2-m triple-KO context, cell-surface expression was observed in all strains that in all cases was substantially higher (roughly 10-fold) than the expression of the HLA-A*02:01 monochains in HHD II mice.
11714758	0.96	beta2m- spleen cells to BALB.B and (BALB/c x BALB.B)F1 mice (both expressing H-2Kb), we found that the cell surface level of Ly49C was strongly downregulated on donor NK1.1+ cells (Fig. 4 A, right graph).
	0.56	beta2m-/Ly49A+ cells acquire H-2Dd but not H-2Kb after transfer of NK cells to (BALB/c x BALB.B)F1 mice.
18299400	0.96	H2Kb, and Qa2 MHC I molecules were abrogated in beta2m-deficient EL4 cells, but were restored in beta2m transfectants (Fig. 1 A).
	0.95	beta2m transfectants is probably explained by the lower expression of H2Db and H2Kb on beta2m transfectants compared with WT cells (Fig. 1 A).
19220912	0.96	H2Kb, H2Db and beta2m were unaffected in glucose-deprived or palmitate-treated cells (Figure 4A).
23531237	0.96	H-2K/D, Tap1, or CD8alpha was not as profound as that observed in beta2m BXSB.Yaa mice, suggesting that more than one mechanism likely accounts for the protective effect of beta2m in lupus.
9182675	0.95	H-2Kb-specific CTL have been generated against beta2m- cells, and H-2Kb molecules can be detected at the surface of Con A-stimulated beta2m-/- splenocytes, implying residual expression of beta2m-free, H-2Kb heavy chains.
	0.95	beta2m-free H-2Kb heavy chains and the relatively low expression level (for which we do not have definitive explanation) of HHD monochains by HHD (heterozygous) transgenic H-2Db beta2m double knockout mice, the results reported indicate efficient usage of the HLA-A2.1 monochain both at the educational and effector levels by the mouse CD8+ T lymphocytes.
	0.89	beta2m-/- mice, H-2Kb-restricted CTL can be positively selected in the presence of exogenously added beta2m and peptides.
14517277	0.95	H-2k hosts that were additionally deficient for beta2m, a deficiency that has been shown to further reduce NK cell activity.
	0.93	H-2k hosts, but this difference disappeared in H-2k hosts that lacked beta2m (Fig. 5 A, open squares), suggesting that the lower survival in H-2k might reflect the activity of a small number of residual NK cells in the gammac- hosts (Fig. 2; reference).
	0.81	H-2k mice that lacked beta2m, showing that the lack of CD4+ T cells in H-2k mice is not due to negative selection by the H-2k class I molecules.
9419210	0.95	H-2Kb-restricted peptides, stabilize MHC class I expression on the surface of beta2m-/- macrophages and that the H-2Db peptide complexes were recognized by CD8+ CTLs.
	0.92	beta2m, free H-2Db molecules are transported to the cell surface but H-2Kb molecules are not.
16769997	0.94	beta2m-/-H-2Db-/-H-2Kb-/- mice (Fig. 3 A), and even more reduced to 10-fold lower values and some times totally abrogated in beta2m-/-I-Abeta-/- hosts (Fig. 4).
	0.91	beta2m-/-H-2Db-/-H-2Kb-/- tetra KO hosts, which should express very low levels of MHC class I. We found that removal of additional MHC class I molecules induced a major delay in OT-1 cell accumulation.
24523508	0.94	beta2m-heterozygous mice express nearly wild-type levels of H-2Kb (Supplementary Figure 1.) Since Tregs differ from Tconv cells in their expression of Foxp3, we next considered the possibility that the elevated MHC class I expression in Tregs was mediated by Foxp3.
26802986	0.94	beta2m-/-TAP-/- values (p=0.09), suggesting that loss of H-2K and H-2D could fully explain the initial synapse elimination defects in beta2m-/-TAP-/- mice.
8976180	0.89	H-2Kb heavy chain which are obscured upon proper folding and subsequent assembly with beta2-microglobulin (KU1: residues 49-54; KU2: residues 23-30; KU4: residues 193-198).
26910923	0.89	H-2Kb mAbs with killer MPs implied that H-2Kb-Ig dimers coupled onto the PLGA MPs displayed the correct conformation, because the anti-H-2Kb mAbs (clone AF6-88.5) recognizes a framework epitope expressed on the beta2 m-associated H-2Kb heavy chain.
10075972	0.85	beta2m-/- cells, whereas conformed H-2Kb was detected at lower levels, in line with previously published results (27, 28; Fig. 1).
27855706	0.84	beta2m (Fig. 1b) in the context of transgenes HLA-A11 and HLA-B27 restored normal expression of endogenous mouse class I (H2-Kb and H2-Db) molecules.
21335486	0.74	H2Kb involving beta2m is involved in interaction with Ly49C.
19625641	0.60	H-2Kb tetramers (Asn107Ala, Lys62Glu, Ser31Leu or Ala, Arg8Asp or Ala) can be rationalized because these are contact residues to either MHC or beta2m, several others (Thr81Ala, Leu29Ala, and Lys12Glu) cannot be easily explained, although Thr81 resides at the edge of the H-2Kb interface with CD8alpha1.
31112530	0.54	H-2Kb and B2m mRNA levels tended to be higher in alphaKO cells, but the differences were not statistically significant.