Laboratory for Molecular Diagnostics
Center for Nephrology and Metabolic Disorders
Moldiag Diseases Genes Support Contact

Tumor necrosis factor alpha-induced protein 3

The TNFAIP3 gene encodes a cytokine which is involved in the TNF pathway. Mutations cause autosomal dominant pediatric Behçet-like disease.

Genetests:

Clinic Method Carrier testing
Turnaround 5 days
Specimen type genomic DNA
Clinic Method Massive parallel sequencing
Turnaround 25 days
Specimen type genomic DNA
Research Method Genomic sequencing of the entire coding region
Turnaround 25 days
Specimen type genomic DNA

Related Diseases:

Hereditary pediatric Behçet-like disease
TNFAIP3

References:

1.

Dixit VM et al. (1990) Tumor necrosis factor-alpha induction of novel gene products in human endothelial cells including a macrophage-specific chemotaxin.

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2.

Wertz IE et al. (2015) Phosphorylation and linear ubiquitin direct A20 inhibition of inflammation.

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3.

Zhou Q et al. (2016) Loss-of-function mutations in TNFAIP3 leading to A20 haploinsufficiency cause an early-onset autoinflammatory disease.

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4.

Liu X et al. (2014) Interleukin-17 (IL-17)-induced microRNA 873 (miR-873) contributes to the pathogenesis of experimental autoimmune encephalomyelitis by targeting A20 ubiquitin-editing enzyme.

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5.

Vande Walle L et al. (2014) Negative regulation of the NLRP3 inflammasome by A20 protects against arthritis.

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6.

Ma L et al. (2014) Role of A20 in interferon-α-mediated functional restoration of myeloid dendritic cells in patients with chronic hepatitis C.

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7.

Lu TT et al. (2013) Dimerization and ubiquitin mediated recruitment of A20, a complex deubiquitinating enzyme.

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8.

Matmati M et al. (2011) A20 (TNFAIP3) deficiency in myeloid cells triggers erosive polyarthritis resembling rheumatoid arthritis.

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9.

Shembade N et al. (2010) Inhibition of NF-kappaB signaling by A20 through disruption of ubiquitin enzyme complexes.

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10.

Ferch U et al. (2009) Inhibition of MALT1 protease activity is selectively toxic for activated B cell-like diffuse large B cell lymphoma cells.

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11.

Compagno M et al. (2009) Mutations of multiple genes cause deregulation of NF-kappaB in diffuse large B-cell lymphoma.

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12.

Kato M et al. (2009) Frequent inactivation of A20 in B-cell lymphomas.

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13.

Schmitz R et al. (2009) TNFAIP3 (A20) is a tumor suppressor gene in Hodgkin lymphoma and primary mediastinal B cell lymphoma.

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14.

Braggio E et al. (2009) Identification of copy number abnormalities and inactivating mutations in two negative regulators of nuclear factor-kappaB signaling pathways in Waldenstrom's macroglobulinemia.

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15.

Song XT et al. (2008) A20 is an antigen presentation attenuator, and its inhibition overcomes regulatory T cell-mediated suppression.

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16.

Coornaert B et al. (2008) T cell antigen receptor stimulation induces MALT1 paracaspase-mediated cleavage of the NF-kappaB inhibitor A20.

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17.

Wolfrum S et al. (2007) The protective effect of A20 on atherosclerosis in apolipoprotein E-deficient mice is associated with reduced expression of NF-kappaB target genes.

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18.

Vendrell JA et al. (2007) A20/TNFAIP3, a new estrogen-regulated gene that confers tamoxifen resistance in breast cancer cells.

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19.

Boone DL et al. (2004) The ubiquitin-modifying enzyme A20 is required for termination of Toll-like receptor responses.

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20.

Wertz IE et al. (2004) De-ubiquitination and ubiquitin ligase domains of A20 downregulate NF-kappaB signalling.

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21.

Cook SA et al. (2003) A20 is dynamically regulated in the heart and inhibits the hypertrophic response.

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22.

O'Reilly SM et al. (2003) Regulation of Toll-like receptor 4 signalling by A20 zinc finger protein.

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23.

Lee EG et al. (2000) Failure to regulate TNF-induced NF-kappaB and cell death responses in A20-deficient mice.

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24.

Opipari AW et al. (1990) The A20 cDNA induced by tumor necrosis factor alpha encodes a novel type of zinc finger protein.

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25.
Update: Aug. 14, 2020
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