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A role of NF-B and the proteasome in autoimmunity

100%

Hayashi T. , Faustman D.

nr 5

353-365

Type 1 diabetes (also known as insulin-dependent diabetes mellitus or juvenile-onset diabetes) is usually caused by T cell-mediated autoimmunity, with a prediabetic state characterized by the production of autoantibodies specific for proteins expressed by pancreatic beta cells. The non-obese diabetic (NOD) mouse is a spontaneous model of type 1 diabetes with a strong genetic component that maps to the major histocompatibility complex (MHC) region of the genome. A specific proteasome defect has been identified in NOD mouse lymphocytes that results from down-regulation of expression of the proteasome subunit LMP2, which is encoded by a gene in the MHC genomic region. This defect both prevents the proteolytic processing required for the production and activation of the transcription factor nuclear facktor-kappaB (NF-kappaB), which plays important roles in immune and inflammatory responses, as well as increases the susceptibility of the affected cells to apoptosis induced by tumor necrosis factor alpha (TNF-alpha). The proteasome dysfunction is both tissue and developmental stage specific and likely contributes to disease pathogenesis and tissue targeting.

Ribophagy ? the novel degradation system of the ribosome

75%

Bakowska-Zywicka K. , Tyczewska A.

nr 1

99-103

Recently biochemists have discovered a new pathway by which the cell selectively degrades ribosomes. The pathway is called ribophagy. Two proteins were identified as crucial for the selective degradation of ribosomes by autophagy: ubiquitin-specific protease 3 (Ubp3) and Ubp3-associated cofactor, Bre5. This fact strengthens the connections between the autophagy and proteasome pathways of protein degradations.