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Phosphorylation-induced SUMOylation promotes Ulk4 condensation at ciliary tip to transduce Hedgehog signal.
bioRxiv
November 2024
Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Hedgehog (Hh) signaling controls embryonic development and adult tissue homeostasis through the Gli family of transcription factors. In vertebrates, Hh signal transduction depends on the primary cilium where Gli is thought to be activated at the ciliary tip, but the underlying mechanism has remained poorly understood. Here we provide evidence that two Unc-51-like kinase (Ulk) family members Stk36 and Ulk4 regulate Gli2 ciliary tip localization and activation through phosphorylation and SUMOylation-mediated condensation in response to Shh.
View Article and Find Full Text PDFConditioned Medium From Reactive Astrocytes Inhibits Proliferation, Resistance, and Migration of p53-Mutant Glioblastoma Spheroid Through GLI-1 Downregulation.
J Cell Biochem
September 2024
Programa de Pós-Graduação em Anatomia Patológica, Hospital Universitário Clementino Fraga Filho, Universidade Federal do Rio de Janeiro (UFRJ), Rio de Janeiro, Brazil.
Glioblastoma (GBM) aggressiveness is partly driven by the reactivation of signaling pathways such as Sonic hedgehog (SHH) and the interaction with its microenvironment. SHH pathway activation is one of the phenomena behind the glial transformation in response to tumor growth. The reactivation of the SHH signaling cascade during GBM-astrocyte interaction is highly relevant to understanding the mechanisms used by the tumor to modulate the adjacent stroma.
View Article and Find Full Text PDFIdentification of truncated variants in GLI family zinc finger 3 (GLI3) associated with polydactyly.
J Orthop Surg Res
July 2024
Department of Hand and Microsurgery, Xiangya Hospital, Central South University, Changsha, 410000, China.
Background: Polydactyly is a prevalent congenital anomaly with an incidence of 2.14 per 1000 live births in China. GLI family zinc finger 3 (GLI3) is a classical causative gene of polydactyly, and serves as a pivotal transcription factor in the hedgehog signaling pathway, regulating the development of the anterior-posterior axis in limbs.
View Article and Find Full Text PDFDownregulation of Glis3 in INS1 cells exposed to chronically elevated glucose contributes to glucotoxicity-associated β cell dysfunction.
Islets
December 2024
Department of Biological Sciences, Murray State University, Murray, KY, USA.
Chronically elevated levels of glucose are deleterious to pancreatic β cells and contribute to β cell dysfunction, which is characterized by decreased insulin production and a loss of β cell identity. The Krüppel-like transcription factor, Glis3 has previously been shown to positively regulate insulin transcription and mutations within the Glis3 locus have been associated with the development of several pathologies including type 2 diabetes mellitus. In this report, we show that Glis3 is significantly downregulated at the transcriptional level in INS1 832/13 cells within hours of being subjected to high glucose concentrations and that diminished expression of Glis3 is at least partly attributable to increased oxidative stress.
View Article and Find Full Text PDFGLI1 Coamplification in Well-Differentiated/Dedifferentiated Liposarcomas: Clinicopathologic and Molecular Analysis of 92 Cases.
Mod Pathol
June 2024
Department of Pathology and Laboratory Medicine, Memorial Sloan Kettering Cancer Center, New York, New York. Electronic address:
GLI1(12q13.3) amplification is identified in a subset of mesenchymal neoplasms with a distinct nested round cell/epithelioid phenotype. MDM2 and CDK4 genes are situated along the oncogenic 12q13-15 segment, amplification of which defines well-differentiated liposarcoma (WDLPS)/dedifferentiated liposarcoma (DDLPS).
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