Publications by authors named "Joseph B Black"
Despite curative-intent local therapy, approximately 27% to 53% of prostate cancer (PCa) patients experience prostate-specific antigen (PSA) recurrence, known as biochemical recurrence (BCR). BCR significantly raises the risk of PCa-related morbidity and mortality, yet there is no consensus on optimal management. Prostate-specific membrane antigen-positron emission tomography (PSMA PET) has emerged as highly sensitive imaging, distinguishing local recurrences from distant metastases, crucially influencing treatment decisions.
View Article and Find Full Text PDFThe monomer-binding protein profilin 1 (PFN1) plays a crucial role in actin polymerization. However, mutations in PFN1 are also linked to hereditary amyotrophic lateral sclerosis, resulting in a broad range of cellular pathologies which cannot be explained by its primary function as a cytosolic actin assembly factor. This implies that there are important, undiscovered roles for PFN1 in cellular physiology.
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- Profilin 1 (PFN1) plays a crucial role in both actin assembly and microtubule growth, but its primary mechanism of influencing microtubules—either directly by regulating tubulin or indirectly through actin polymerization—remains unclear.
- By adjusting PFN1 levels, actin filament formation, and actomyosin function, researchers found that reducing these elements led to adaptive changes in the microtubule cytoskeleton, especially in neuronal cells.
- Importantly, these microtubule alterations were reversible with the restoration of actomyosin, suggesting PFN1 mainly regulates microtubules through actin, and that disturbances in actin may result in significant functional changes in other
Article Synopsis
- * Long-term depletion of F-actin or actomyosin contractility leads to increased levels of acetylated microtubules and intermediate filaments, especially in neuronal processes.
- * Restoring F-actin and myosin activity can reverse changes in microtubules, but changes due to actin depletion can disrupt microtubule transport, potentially leading to neurodegenerative symptoms.
Article Synopsis
- Profilin 1 (PFN1) is crucial for forming actin filaments and its absence leads to an increase in mitophagy, the process that removes damaged mitochondria.
- Despite the heightened activity in removing defective mitochondria, PFN1 knockout cells still accumulate dysfunctional mitochondria, indicating a failure in quality control.
- PFN1 not only influences mitochondria's shape and function from within but also its ALS mutants worsen mitochondrial problems, hinting at a new understanding of PFN1's role in both mitochondrial regulation and ALS pathology.
Progression of prostate cancer (PC) to terminal castration-resistant PC (CRPC) involves a diverse set of intermediates, and androgen receptor (AR) is the key mediator of PC initiation and progression to CRPC. Hence, identification of factors involved in the regulation of AR expression and function is a necessary first-step to improve disease outcome. In this study, we identified ubiquitous βArrestin 1 (βArr1) as a regulator of AR function in CRPC.
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- RNA splicing of U12-type introns is crucial for cell differentiation in humans, but its role in plants, specifically maize, is still unclear.
- The maize protein ROUGH ENDOSPERM3 (RGH3) is similar to the human splicing factor ZRSR2, and mutations in RGH3 lead to cell differentiation issues in maize endosperm.
- Retained U12-type introns in maize mutants indicate splicing defects, affecting key biological pathways and suggesting that U12 splicing is vital for proper cell development across different species.
Treatment options for metastatic renal cell carcinoma (RCC) are limited. In this study, we investigated impact of prostaglandin E2 (PGE2) receptor 4 (EP4) on RCC metastasis. We found that knockdown of EP4 in two RCC cell lines, ACHN and SN12C, does not affect xenograft tumor take or growth rate in mice, but reduces metastasis by decreasing tumor intravasation.
View Article and Find Full Text PDFFeedback regulation of G protein-coupled receptor signaling by GRKs and arrestins.
Semin Cell Dev Biol
February 2016
GPCRs are ubiquitous in mammalian cells and present intricate mechanisms for cellular signaling and communication. Mechanistically, GPCR signaling was identified to occur vectorially through heterotrimeric G proteins that are negatively regulated by GRK and arrestin effectors. Emerging evidence highlights additional roles for GRK and Arrestin partners, and establishes the existence of interconnected feedback pathways that collectively define GPCR signaling.
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