Articles tagged with Tumor Suppressors
Researchers at the University of Pennsylvania School of Medicine discovered how KSHV subverts a normal cell process to promote tumor growth. By tricking tumor suppressors VHL and p53 into being destroyed, KSHV allows cancer cells to grow unchecked.
A team of scientists led by Dr. Xiaojiang Chen have uncovered the molecular mechanism behind how a viral oncoprotein inactivates p53. The study reveals that the viral protein binds to p53, causing a conformational change that prevents it from binding to DNA and thus abolishes its tumor-suppressing function.
A University of Southern California-led research group used X-ray crystallography to study the struggle between LTag, a cancer-causing protein, and p53, a key tumor suppressor. The study found that LTag inhibits p53's role by tying up six molecules, but p53 fights back by preventing virus replication.
Dr. Hammarskjold's team reveals WT1(+KTS) promotes translation by facilitating mRNA transport and stability, highlighting links between transcription and post-transcriptional gene regulation. The study's findings suggest a crucial role for alternative splicing in regulating genes like WT1 during normal development and disease.
Researchers propose a new model of p53 regulation that suggests a novel anticancer strategy using Mdm2 and Mdm4. The study reveals that Mdm4 renders p53 inactive, while Mdm2 mainly controls the stability of p53's structure.
The APC tumor suppressor has a novel function in regulating Wnt signaling in the nucleus. In this new study, researchers demonstrate that APC opposes beta-catenin activity directly at Wnt target genes. The findings suggest that full-length APC protein is necessary to repress c-Myc gene expression and prevent colon cancer progression.
The WT1 gene is essential for male fertility and tumorigenesis. Research highlights its critical role in regulating cellular processes that lead to tumor formation and infertility.
The study found that phosphatase 2A activation modulates key cell survival molecules and induces growth suppression, cell differentiation, and apoptosis in BCR/ABL cell lines. Restoration of PP2A activity in CML-BC patient cells counteracted leukemia development.
Researchers at UCSD School of Medicine have discovered a natural tumor suppressor called PHLPP, which can be turned on in certain cancer cells to prevent tumor formation. By deleting a phosphate molecule from the Akt protein, PHLPP terminates cell-growth signaling and promotes programmed cell death.
Researchers discovered that DJ-1 negatively regulates PTEN function, suggesting a potential link between high DJ-1 levels and enhanced cancer cell survival. Elevated DJ-1 levels were associated with poor prognosis in lung cancer patients and may serve as a prognostic marker for cancer patients.
Researchers at Mayo Clinic have identified a new mechanism by which cancerous cell growth occurs, revealing that Skp2 degrades FOXO1, a tumor suppressor. This degradation abolishes FOXO1's ability to suppress tumors and can be reversed using chemicals that inhibit protein destruction.
Researchers have developed 'supermice' with an extra copy of the Ink4a/Arf tumor suppressor locus, revealing increased resistance to cancer. The study implies that differences in gene expression levels of tumor suppressors significantly contribute to the risk of developing cancers and may influence therapeutic development.