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NUMB dysfunction defines a novel mechanism underlying hyperuricemia and gout.
Cell Discov
October 2024
Department of Microbiology, Tumor and Cell Biology, Karolinska Institute, Stockholm, Sweden.
Article Synopsis
- - Genetic defects in uric acid excretion, particularly involving a variant of the NUMB gene, contribute to hyperuricemia and gout, a condition characterized by elevated uric acid levels.
- - Researchers discovered this variant through genome-wide sequencing in a family with hereditary gout, revealing that it affects the protein's function, causing it to redistribute improperly within cells.
- - The study highlights the role of the NUMB protein in regulating the uric acid transporter ABCG2, showing that loss of NUMB function leads to decreased uric acid excretion and increased serum urate levels, as demonstrated in a genetically modified mouse model.
Exosomal long non-coding RNA TRPM2-AS promotes angiogenesis in gallbladder cancer through interacting with PABPC1 to activate NOTCH1 signaling pathway.
Mol Cancer
March 2024
Division of Biliary Surgery, Department of General Surgery, West China Hospital, Sichuan University, Chengdu, 610041, P. R. China.
Background: Abnormal angiogenesis is crucial for gallbladder cancer (GBC) tumor growth and invasion, highlighting the importance of elucidating the mechanisms underlying this process. LncRNA (long non-coding RNA) is widely involved in the malignancy of GBC. However, conclusive evidence confirming the correlation between lncRNAs and angiogenesis in GBC is lacking.
View Article and Find Full Text PDFNOTCH localizes to mitochondria through the TBC1D15-FIS1 interaction and is stabilized via blockade of E3 ligase and CDK8 recruitment to reprogram tumor-initiating cells.
Exp Mol Med
February 2024
Departments of Molecular Microbiology and Immunology, University of Southern California, Los Angeles, CA, USA.
The P53-destabilizing TBC1D15-NOTCH protein interaction promotes self-renewal of tumor-initiating stem-like cells (TICs); however, the mechanisms governing the regulation of this pathway have not been fully elucidated. Here, we show that TBC1D15 stabilizes NOTCH and c-JUN through blockade of E3 ligase and CDK8 recruitment to phosphodegron sequences. Chromatin immunoprecipitation (ChIP-seq) analysis was performed to determine whether TBC1D15-dependent NOTCH1 binding occurs in TICs or non-TICs.
View Article and Find Full Text PDFNaturally occurring genetic diseases caused by de novo variants in domestic animals.
Anim Genet
June 2024
CIIMAR - Interdisciplinary Centre of Marine and Environmental Research, University of Porto, Porto, Portugal.
With the advent of next-generation sequencing, an increasing number of cases of de novo variants in domestic animals have been reported in scientific literature primarily associated with clinically severe phenotypes. The emergence of new variants at each generation is a crucial aspect in understanding the pathology of early-onset diseases in animals and can provide valuable insights into similar diseases in humans. With the aim of collecting deleterious de novo variants in domestic animals, we searched the scientific literature and compiled reports on 42 de novo variants in 31 genes in domestic animals.
View Article and Find Full Text PDFUbiquilin-4 induces immune escape in gastric cancer by activating the notch signaling pathway.
Cell Oncol (Dordr)
February 2024
Department of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Purpose: We aimed to investigate the role of ubiquilin-4 in predicting the immunotherapy response in gastric cancer.
Methods: Retrospective RNA-sequencing and immunohistochemical analysis were performed for patients with gastric cancer who received programmed death-1 blockade therapy after recurrence. Multiplex immunohistochemistry identified immune cell types in gastric cancer tissues.
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