Results 71 to 80 of about 1,681,356 (252)
Matrix Stiffness Induces Endothelial Network Senescence
Using a 3D human in vitro model that decouples mechanical stress from inflammatory or biochemical signals, matrix stiffening induces a senescence phenotype in endothelial networks. This mechano‐induced senescence activates Notch signaling, and pharmacologic Notch inhibition attenuates this stiffness‐induced senescence.
Jiyeon Song +6 more
wiley +1 more source
Objective : p16 is cyclin-dependent kinase (CDK) inhibitor which decelerates cell cycle by inactivating CDKs that phosphorylate retinoblastoma protein (pRb). In cervical carcinogenesis, abnormality of p16 gene such as methylation of p16 gene promoter was investigated as an important factor. The aims of our study are to investigate the expression of p16
Seob Jeon +5 more
openaire +1 more source
Alteration of p16 and p15 genes in human uterine tumours [PDF]
The roles of the p16 and p15 inhibitor of cyclin-dependent kinase tumour suppressor genes were examined in human uterine cervical and endometrial cancers. p16 mRNA, examined by reverse transcription polymerase chain reaction (RT-PCR), was significantly reduced in five of 19 (26%) cervical and four of 25 (16%) endometrial tumours.
Nakashima, R +11 more
openaire +2 more sources
Alterations of p16(INK4A) and p15(INK4B) genes in gastric carcinomas
BACKGROUND. It has been suggested that cyclin-dependent kinase inhibitors (CDKIs), including p16 and p15, are tumor suppressor genes. Alterations of CDKIs have been found in most types of cancer.
Seo, Jin Y. +9 more
core +1 more source
ABSTRACT Osteoarthritis (OA) is a progressive and disabling joint disease driven by oxidative stress, chondrocyte senescence and extracellular matrix (ECM) degradation, yet lacks effective disease‐modifying treatments. In this study, we identified miR‐197‐3p as a previously unrecognized, cartilage‐protective miRNA significantly downregulated in both ...
Xuejie Cai +11 more
wiley +1 more source
Aberrations of the p14(ARF) and p16(INK4a) genes in renal cell carcinomas.
The INK4a / ARF locus on chromosome 9p21, which encodes two distinct genes, p14(ARF) and p16(INK4a), is frequently altered in human neoplasms. To investigate the potential roles of p14(ARF) and p16(INK4a) genes in human renal cell carcinomas (RCCs), we ...
Nakamura, M. +8 more
core +1 more source
NSUN2‐mediated m5C modification cooperates with ALYREF to stabilize and export IP3R3 mRNA, increasing IP3R3 expression and Ca2 + overload in chondrocytes. This signaling promotes mitochondrial dysfunction, NLRP3 inflammasome activation, and senescence, thereby accelerating osteoarthritis progression.
Guping Mao +8 more
wiley +1 more source
p16(INK4A) positively regulates p21(WAF1) expression by suppressing AUF1-dependent mRNA decay. [PDF]
BACKGROUND: p16(INK4a) and p21(WAF1) are two independent cyclin-dependent kinase inhibitors encoded by the CDKN2A and CDKN1A genes, respectively. p16(INK4a) and p21(WAF1) are similarly involved in various anti-cancer processes, including the regulation ...
Huda H Al-Khalaf, Abdelilah Aboussekhra
doaj +1 more source
Expression of p16 induces transcriptional downregulation of the RB gene [PDF]
The RB and p16(INK4A) tumor suppressor genes function in the same pathway of cell cycle control. Previous evidence indicates that the p16(INK4A) gene is transcriptionally repressed by the RB gene product, pRB. In this study using human ovarian cancer cell lines, we found that RB protein and mRNA were expressed at higher levels in cell lines lacking p16
X, Fang +10 more
openaire +2 more sources
In the pathological context of osteoarthritis (OA), the phosphorylation of AKT1 at Ser473 enhances its binding to Lys140 of Insig1, which facilitates the formation of AKT1–Insig1 complex. Subsequently, the activation of AKT1 promotes the phosphorylation of Insig1 at Ser189, potentially enhancing the dissociation of Insig1 from sterol regulatory element‑
Xiaoqi Zhang +19 more
wiley +1 more source

