Ignet

Gene Information

Gene symbol: MICA

Gene name: MHC class I polypeptide-related sequence A

HGNC ID: 7090

Synonyms: PERB11.1

Related Genes

#	Gene Symbol	Number of hits
1	CALR	1 hits
2	CD274	1 hits
3	CD4	1 hits
4	CD8A	1 hits
5	CSF1	1 hits
6	CSF2	1 hits
7	CTLA4	1 hits
8	CXCL9	1 hits
9	HLA-A	1 hits
10	HLA-E	1 hits
11	IFNG	1 hits
12	IL2	1 hits
13	IRF7	1 hits
14	ITGAL	1 hits
15	KLRK1	1 hits
16	MICB	1 hits
17	MR1	1 hits
18	P4HB	1 hits
19	PDIA6	1 hits
20	STAT1	1 hits
21	STAT3	1 hits
22	TXNDC15	1 hits

Related Sentences

#	PMID	Sentence
1	9535555	Immunotherapy of acute lymphoblastic leukemia by vaccination with autologous leukemic cells transfected with a cDNA expression plasmid coding for an allogeneic HLA class I antigen combined with interleukin-2 treatment.
2	14695218	MICA/NKG2D-mediated immunogene therapy of experimental gliomas.
3	14695218	Tumor cells expressing ligands of the activating immunoreceptor NKG2D stimulate tumor immunity mediated by natural killer (NK), gammadelta T, and CD8(+) T cells.
4	14695218	We report that human glioma cells express the NKG2D ligands MICA, MICB, and members of the UL16-binding protein family constitutively.
5	14695218	However, glioma cells resist NK cell cytolysis because of high MHC class I antigen expression.
6	14695218	MICA/NKG2D-mediated immunogene therapy of experimental gliomas.
7	14695218	Tumor cells expressing ligands of the activating immunoreceptor NKG2D stimulate tumor immunity mediated by natural killer (NK), gammadelta T, and CD8(+) T cells.
8	14695218	We report that human glioma cells express the NKG2D ligands MICA, MICB, and members of the UL16-binding protein family constitutively.
9	14695218	However, glioma cells resist NK cell cytolysis because of high MHC class I antigen expression.
10	15585412	Here, we demonstrate that transfection of control plasmid DNA (that does not express a gene product) into tumor cell lines induces a dramatic (>10-fold) increase in the expression of the interferon (IFN)-regulated genes IRF7, STAT1, MIG (approved gene symbol CXCL9), MHCI (MICA), and CD11a (ITGAL) in tumor cell lines.
11	15585412	The antibody depletion study indicates that the underlying mechanism by which transfection of control DNA induces IFN-regulated genes is the induction of a secreting factor(s) such as IFN-beta.
12	15824323	This approach may be broadly improved by targeting the MHC class I chain-related protein A (MICA), which is frequently and abundantly expressed on most if not all types of epithelial cancers but not in normal tissues except intestinal mucosa.
13	15824323	Loading of DC with anti-MICA mAb-coated breast, melanoma, or ovarian tumor lines or uncultured ovarian cancer cells efficiently promoted TA cross-presentation and priming of multivalent anti-tumor CD8 and CD4 T cell responses.
14	16754847	Nonetheless, tumor cell shedding of NKG2D ligands, such as MHC class I chain-related protein A (MICA), results in immune suppression through down-regulation of NKG2D surface expression.
15	16754847	Here we show that some patients who respond to antibody-blockade of cytotoxic T lymphocyte-associated antigen 4 or vaccination with lethally irradiated, autologous tumor cells engineered to secrete granulocyte-macrophage colony-stimulating factor generate high titer antibodies against MICA.
16	16754847	These humoral reactions are associated with a reduction of circulating soluble MICA (sMICA) and an augmentation of natural killer (NK) cell and CD8(+) T lymphocyte cytotoxicity.
17	16754847	Together, these findings establish a key role for the NKG2D pathway in the clinical activity of cytotoxic T lymphocyte-associated antigen 4 antibody blockade and granulocyte-macrophage colony-stimulating factor secreting tumor cell vaccines.
18	16754847	Nonetheless, tumor cell shedding of NKG2D ligands, such as MHC class I chain-related protein A (MICA), results in immune suppression through down-regulation of NKG2D surface expression.
19	16754847	Here we show that some patients who respond to antibody-blockade of cytotoxic T lymphocyte-associated antigen 4 or vaccination with lethally irradiated, autologous tumor cells engineered to secrete granulocyte-macrophage colony-stimulating factor generate high titer antibodies against MICA.
20	16754847	These humoral reactions are associated with a reduction of circulating soluble MICA (sMICA) and an augmentation of natural killer (NK) cell and CD8(+) T lymphocyte cytotoxicity.
21	16754847	Together, these findings establish a key role for the NKG2D pathway in the clinical activity of cytotoxic T lymphocyte-associated antigen 4 antibody blockade and granulocyte-macrophage colony-stimulating factor secreting tumor cell vaccines.
22	16754847	Nonetheless, tumor cell shedding of NKG2D ligands, such as MHC class I chain-related protein A (MICA), results in immune suppression through down-regulation of NKG2D surface expression.
23	16754847	Here we show that some patients who respond to antibody-blockade of cytotoxic T lymphocyte-associated antigen 4 or vaccination with lethally irradiated, autologous tumor cells engineered to secrete granulocyte-macrophage colony-stimulating factor generate high titer antibodies against MICA.
24	16754847	These humoral reactions are associated with a reduction of circulating soluble MICA (sMICA) and an augmentation of natural killer (NK) cell and CD8(+) T lymphocyte cytotoxicity.
25	16754847	Together, these findings establish a key role for the NKG2D pathway in the clinical activity of cytotoxic T lymphocyte-associated antigen 4 antibody blockade and granulocyte-macrophage colony-stimulating factor secreting tumor cell vaccines.
26	17599917	The observed binding to the viral envelope spikes is the result of specific CD4-gp120 interaction, because binding was not observed with MICA-IgP, a construct that is identical to D1D2-IgP except that major histocompatibility complex Class I-related Chain A (MICA) replaces the CD4 moiety.
27	18202175	Here, we demonstrate that NKG2D, an activating receptor on natural killer (NK) cells, CD8(+) T lymphocytes, and MHC class I chain-related protein A (MICA), an NKG2D ligand induced in malignant plasma cells through DNA damage, contribute to the pathogenesis of MGUS and MM.
28	18202175	MICA expression is increased on plasma cells from MGUS patients compared with normal donors, whereas MM patients display intermediate MICA levels and a high expression of ERp5, a protein disulfide isomerase linked to MICA shedding (sMICA).
29	18202175	Here, we demonstrate that NKG2D, an activating receptor on natural killer (NK) cells, CD8(+) T lymphocytes, and MHC class I chain-related protein A (MICA), an NKG2D ligand induced in malignant plasma cells through DNA damage, contribute to the pathogenesis of MGUS and MM.
30	18202175	MICA expression is increased on plasma cells from MGUS patients compared with normal donors, whereas MM patients display intermediate MICA levels and a high expression of ERp5, a protein disulfide isomerase linked to MICA shedding (sMICA).
31	19008459	Toward this end, we screened a murine renal cell carcinoma cDNA expression library with sera from mice vaccinated with irradiated tumor cells engineered to secrete granulocyte macrophage colony-stimulating factor (GM-CSF).
32	19008459	High titer antibodies to human PDI were similarly induced in an acute myeloid leukemia patient who achieved a complete response after vaccination with irradiated, autologous GM-CSF-secreting tumor cells in the setting of nonmyeloablative allogeneic bone marrow transplantation.
33	19008459	Moreover, ERp5, a closely related disulfide isomerase involved in major histocompatibility complex (MHC) class I chain-related protein A (MICA) shedding, also evoked potent humoral reactions in diverse solid and hematologic malignancy patients who responded to GM-CSF-secreting tumor cell vaccines or antibody blockade of cytotoxic T lymphocyte-associated antigen 4 (CTLA-4).
34	23911739	Pneumococcal, HLA class I and II and major histocompatibility class I-related chain A (MICA) antibodies were determined by Luminex™ technology (xMAP™ Pneumococcal Immunity Panel and LABScreen™ Mixed beads, respectively) and HLA antibodies also by ELISA (Lambda Antigen Tray™).
35	23911739	Positive Luminex™ reactions were present in 63%, 67% and 63% (HLA class I), 47%, 47% and 55% (HLA class II) and 29%, 29% and 29% (MICA) pre-vaccination, at month 1 and 15, respectively.
36	23911739	Pneumococcal, HLA class I and II and major histocompatibility class I-related chain A (MICA) antibodies were determined by Luminex™ technology (xMAP™ Pneumococcal Immunity Panel and LABScreen™ Mixed beads, respectively) and HLA antibodies also by ELISA (Lambda Antigen Tray™).
37	23911739	Positive Luminex™ reactions were present in 63%, 67% and 63% (HLA class I), 47%, 47% and 55% (HLA class II) and 29%, 29% and 29% (MICA) pre-vaccination, at month 1 and 15, respectively.
38	24415578	Therefore, we analyzed a cohort of patients with a primary (n = 43) and subsequent recurrent uVIN lesion (n = 20), vaccine-treated uVIN patients (n = 12), patients with human papillomavirus (HPV)-induced vulvar carcinoma (n = 21) and healthy controls (n = 26) for the expression of classical HLA-class I/II and nonclassical HLA-E/-G and MHC class I chain-related molecule A (MICA).
39	24415578	Of the nonclassical molecules, MICA was downregulated in 80% of uVIN whereas HLA-E and -G were expressed in a minority of cases.
40	24415578	Therefore, we analyzed a cohort of patients with a primary (n = 43) and subsequent recurrent uVIN lesion (n = 20), vaccine-treated uVIN patients (n = 12), patients with human papillomavirus (HPV)-induced vulvar carcinoma (n = 21) and healthy controls (n = 26) for the expression of classical HLA-class I/II and nonclassical HLA-E/-G and MHC class I chain-related molecule A (MICA).
41	24415578	Of the nonclassical molecules, MICA was downregulated in 80% of uVIN whereas HLA-E and -G were expressed in a minority of cases.
42	25962106	Wogonin also promoted the secretion of calreticulin and high-mobility group protein 1 by tumor cells.
43	25962106	The dephosphorylation of STAT3 contributed to the decreased expression of B7H1 and MHC class I chain-related protein A, and the enhancement of calreticulin on the cell membrane.