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: UNIPROT:P04637 (
p53
)
77,613
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The
p53 protein
arrests the cell cycle at the G1 phase when stabilized by the interaction between ribosomal proteins and HDM2 under growth-inhibitory conditions. Meanwhile,
p53
, when translocated to the mitochondria in response to cell death signals, induces apoptosis via transcription-independent mechanisms. In this report, we demonstrate that the
mitochondrial ribosomal protein L41
(
MRPL41
) enhances
p53
stability and contributes to
p53
-induced apoptosis in response to growth-inhibitory conditions such as actinomycin D treatment and serum starvation. An analysis of
MRPL41
expression in paired normal and tumor tissues revealed lower expression in tumor tissue. Ectopic
MRPL41
expression resulted in inhibition of the growth of cancer cells in tissue culture and tumor growth in nude mice. We discovered that
MRPL41
protein is localized in the mitochondria, stabilizes the
p53 protein
, and enhances its translocation to the mitochondria, thereby inducing apoptosis. Interestingly, in the absence of
p53
,
MRPL41
stabilizes the p27(Kip1) protein and arrests the cell cycle at the G1 phase. These results suggest that
MRPL41
plays an important role in
p53
-induced mitochondrion-dependent apoptosis and
MRPL41
exerts a tumor-suppressive effect in association with
p53
and p27 (Kip1).
...
PMID:Mitochondrial ribosomal protein L41 suppresses cell growth in association with p53 and p27Kip1. 1602 96
Ribosomal proteins not only act as components of the translation apparatus but also regulate cell proliferation and apoptosis. A previous study reported that
MRPL41
plays an important role in
p53
-dependent apoptosis. It also showed that
MRPL41
arrests the cell cycle by stabilizing p27(Kip1) in the absence of
p53
. This study found that
MRPL41
mediates the p21(WAF1/CIP1)-mediated G1 arrest in response to serum starvation. The cells were released from serum starvation-induced G1 arrest via the siRNA-mediated blocking of
MRPL41
expression. Overall, these results suggest that
MRPL41
arrests the cell cycle by increasing the p21(WAF1/CIP1) and p27(Kip1) levels under the growth inhibitory conditions.
...
PMID:Mitochondrial ribosomal protein L41 mediates serum starvation-induced cell-cycle arrest through an increase of p21(WAF1/CIP1). 1625 47
Ribosomal biogenesis is correlated with cell cycle, cell proliferation, cell growth and tumorigenesis. Some oncogenes and tumor suppressors are involved in regulating the formation of mature ribosome and affecting the ribosomal biogenesis. In previous studies, the
mitochondrial ribosomal protein L41
was reported to be involved in cell proliferation regulating through p21(WAF1/CIP1) and
p53
pathway. In this report, we have identified a mitochondrial ribosomal protein S36 (mMRPS36), which is localized in the mitochondria, and demonstrated that overexpression of mMRPS36 in cells retards the cell proliferation and delays cell cycle progression. In addition, the mMRPS36 overexpression induces p21(WAF1/CIP1) expression, and regulates the expression and phosphorylation of
p53
. Our result also indicate that overexpression of mMRPS36 affects the mitochondrial function. These results suggest that mMRPS36 plays an important role in mitochondrial ribosomal biogenesis, which may cause nucleolar stress, thereby leading to cell cycle delay.
...
PMID:Mitochondrial ribosomal protein S36 delays cell cycle progression in association with p53 modification and p21(WAF1/CIP1) expression. 1713 59