Molekulargenetisches Labor
Zentrum für Nephrologie und Stoffwechsel
Moldiag Erkrankungen Gene Support Kontakt

TNF-alpha induziertes Protein 3

Das TNFAIP3-Gen kodiert ein Zytokin, welches durch TNF-alpha induziert wird und and der Modulation von Immunantworten beteiligt ist. Mutationen führen zu einer autosomal dominanten Behçet-ähnlichen Krankheit des Kindesalters.

Gentests:

Klinisch Untersuchungsmethoden Familienuntersuchung
Bearbeitungszeit 5 Tage
Probentyp genomische DNS
Klinisch Untersuchungsmethoden Hochdurchsatz-Sequenzierung
Bearbeitungszeit 25 Tage
Probentyp genomische DNS
Forschung Untersuchungsmethoden Direkte Sequenzierung der proteinkodierenden Bereiche eines Gens
Bearbeitungszeit 25 Tage
Probentyp genomische DNS

Verknüpfte Erkrankungen:

Hereditäre Behçet-ähnliche Krankheit des Kindes
TNFAIP3

Referenzen:

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: 14. August 2020
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