- Cancer-related Molecular Pathways
- Chemical Synthesis and Analysis
- Click Chemistry and Applications
- Neuroblastoma Research and Treatments
- Crystallization and Solubility Studies
- X-ray Diffraction in Crystallography
- Neuroendocrine Tumor Research Advances
- PI3K/AKT/mTOR signaling in cancer
- Hedgehog Signaling Pathway Studies
- Supramolecular Self-Assembly in Materials
- Renal and related cancers
- Hippo pathway signaling and YAP/TAZ
- Growth Hormone and Insulin-like Growth Factors
- Lung Cancer Research Studies
- Cell death mechanisms and regulation
- Epigenetics and DNA Methylation
- Crystallography and molecular interactions
Tumor progression is suppressed by inherent cellular mechanisms such as apoptosis. The p53 tumor suppressor gene the most commonly mutated in human cancer and plays a pivotal role suppression. RPRM target of known to be involved suppression, but its molecular function has remained elusive. Here, we report that Reprimo (the protein product ) secreted extrinsically induces apoptosis recipient cells. We identified FAT1, FAT4, CELSR1, CELSR2, CELSR3, members protocadherin family, receptors for...
The PHLDA family (pleckstrin homology‐like domain family) of genes consists 3 members: 1 , 2 and . Both are phosphatidylinositol ( PIP ) binding proteins function as repressors Akt. They have tumor suppressive functions, mainly through Akt inhibition. Several reports suggest that also has a function; however, the precise molecular functions remain to be elucidated. Through comprehensive screen for p53 target genes, we identified novel target, show ability repress in manner similar 2....
Insulin signaling often plays a role in the regulation of cancer, including tumor initiation, progression, and response to treatment. In addition, insulin-regulated PI3K-Akt-mTOR pathway an important islet cell proliferation, this is hyperactivated human non-functional pancreatic neuroendocrine tumors (PanNETs). We, therefore, investigated effect very low carbohydrate diet (ketogenic diet) on mouse model that develops PanNETs ask how reduced might affect development progression PanNET. We...
Protein–protein interactions (PPIs) are often mediated by helical, strand and/or coil secondary structures at the interface regions. We previously showed that non-naturally occurring, stable helical trimers of bicyclic β-amino acids (Abh) with all-trans amide bonds can block p53–MDM2/MDMX α-helix–helix interaction, which plays a role in regulating p53 function. Here, we conducted docking and molecular dynamics calculations to guide structural optimization our reported compounds, focusing on...
We have discovered that β-amino acid homooligomers with cis- or trans-amide conformation can fold themselves into highly ordered helices. Moreover, unlike α-amino peptides, which are significantly stabilized by intramolecular hydrogen bonding, these helical structures autogenous conformations stable without the aid of bonding and irrespective solvent (protic/aprotic/halogenated) temperature. A structural overlap comparison cis/trans bicyclic β-proline typical α-helix structure peptides...
Our NMR, IR/Raman, CD spectroscopic, and X-ray crystallographic studies, as well accelerated molecular dynamics simulations, showed that alternating hybrid α/β-peptides containing a bicyclic β-proline surrogate form unique extended curved folds, regardless of the peptide length solvent environment. It is suggested β/PPII structures are preferred in insulating α-alanine moieties between rigid structures. These peptides inhibit p53-MDM2 p53-MDMX protein–protein interactions.
ABSTRACT Insulin signaling often plays a role in the regulation of cancer including tumor initiation, progression, and response to treatment. In addition, insulin-regulated PI3K-Akt-mTOR pathway an important islet cell proliferation this is hyperactivated human non-functional pancreatic neuroendocrine tumors (PanNETs). We therefore investigated effect very low carbohydrate diet (ketogenic diet) on mouse model that develops PanNETs ask how reduced might affect development progression PanNET....