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SHH

A Self-Amplifying Loop of YAP and SHH Drives Formation and Expansion of Heterotopic Ossification

[Science Translational Medicine] In mouse models of progressive osseous heteroplasia, a disease caused by null mutations in GNAS, researchers found that Gnas−/− mesenchymal cells secreted Sonic hedgehog (SHH), which induced osteoblast differentiation of the surrounding wild-type cells.

ETV4 Promotes Breast Cancer Cell Stemness by Activating Glycolysis and CXCR4-Mediated Sonic Hedgehog Signaling

[Cell Death Discovery] Regulation of cancer cell metabolism rewiring and stemness is not completely understood. Scientists reported that ETV4 is a key transcription factor in regulating glycolytic gene expression.

A Potential Role for Somatostatin Signaling in Regulating Retinal Neurogenesis

[Scientific Reports] By analyzing retinal explants treated with selective ligands that target these receptors, we found that Sstr2-dependent somatostatin signaling induces a modest, dose-dependent inhibition of photoreceptor generation, while correspondingly increasing the relative fraction of primary progenitor cells.

NKX6-1 Mediates Cancer Stem-Like Properties and Regulates Sonic Hedgehog Signaling in Leiomyosarcoma

[Journal of Biomedical Science] NKX6-1 enhanced in vitro tumor cell aggressiveness via upregulation of cell proliferation and anchorage-independent growth and promoted in vivo tumor growth.

Disease-Relevant Single Cell Photonic Signatures Identify S100β Stem Cells and their Myogenic Progeny in Vascular Lesions

[Stem Cell Reviews and Reports] Researchers evaluated single cell photonics as a discriminator of cell phenotype in vitro before the presence of vascular stem cells within vascular lesions.

Acetylation of KLF5 Maintains EMT and Tumorigenicity to Cause Chemoresistant Bone Metastasis in Prostate Cancer

[Nature Communications] Investigators report that bone-borne TGF-β induced the acetylation of transcription factor KLF5 in prostate cancer bone metastases, and acetylated KLF5 caused osteoclastogenesis and bone metastatic lesions by activating CXCR4, which led to IL-11 secretion, and stimulated SHH/IL-6 paracrine signaling.

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