Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.4.25.1 (
proteasome
)
28,817
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Autophagy is one of the cellular adaptive processes that provide protection against many pathological conditions like infection, cancer, neurodegeneration, and aging. Recent evidences suggest that ubiquitination plays an important role in degradation of proteins or defective organelle either through
proteasome
or autophagy. In this study, we describe the role of
TRIM13
, ER resident ubiquitin E3 ligase in induction of autophagy and its role during ER stress. The ectopic expression of
TRIM13
in HEK-293 cells induces autophagy. Domain mapping showed that coiled-coil (CC) domain is required for induction of autophagy.
TRIM13
is stabilized during ER stress, interacts with p62/SQSTM1 and co-localizes with DFCP1.
TRIM13
regulates initiation of autophagy during ER stress and decreases the clonogenic ability of the cells. This study for the first time demonstrates the role of
TRIM13
in induction of autophagy which may play an important role in regulation of ER stress and may act as tumor suppressor.
...
PMID:TRIM13 regulates ER stress induced autophagy and clonogenic ability of the cells. 2217 86
Multiple myeloma (MM) is an incurable neoplasm caused by proliferation of malignant plasma cells in the bone marrow (BM). MM is characterized frequently by a complete or partial deletion of chromosome 13q14, seen in more than 50% of patients at diagnosis. Within this deleted region the tripartite motif containing 13 (
TRIM13
, also termed RFP2) gene product has been proposed to be a tumour suppressor gene (TSG). Here, we show that low expression levels of
TRIM13
in MM are associated with chromosome 13q deletion and poor clinical outcome. We present a functional analysis of
TRIM13
using a loss-of-function approach, and demonstrate that
TRIM13
downregulation decreases tumour cell survival as well as cell cycle progression and proliferation of MM cells. In addition, we provide evidence for the involvement of
TRIM13
downregulation in inhibiting the NF kappa B pathway and the activity of the 20S
proteasome
. Although this data does not support a role of
TRIM13
as a TSG, it substantiates important roles of
TRIM13
in MM tumour survival and proliferation, underscoring its potential role as a novel target for therapeutic intervention.
...
PMID:TRIM13 (RFP2) downregulation decreases tumour cell growth in multiple myeloma through inhibition of NF Kappa B pathway and proteasome activity. 2364 56
