Scientists provide an overview of chemokine biology, with a particular focus on the genetic and epigenetic regulation of chemokine transcription as well as on the cell type-specific production of chemokines by liver cells and liver-associated immune cells.
[Nature Reviews Gastroenterology & Hepatology]
POSEIDON was a Phase III trial of AstraZeneca’s IMFINZI® (durvalumab) plus platinum-based chemotherapy or IMFINZI, tremelimumab and chemotherapy versus chemotherapy alone in the 1st-line treatment of patients with Stage IV (metastatic) non-small cell lung cancer (NSCLC).
[Business Wire, Inc.]
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NovoBiome, Inc. launched to revolutionize treatment of liver diseases by targeting the microbiome-gut-liver axis.
[NovoBiome, Inc. (Globenews Wire, Inc.)]
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Using a gluconeogenesis-targeted kinome screening approach combined with transcriptome analyses, we uncovered Nemo-like kinase (NLK) as a potent suppressor of HGP.
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Ji, Y.-X., Wang, Y., Li, P.-L., Cai, L., Wang, X.-M., Bai, L., Liu, Z., Tian, H., Tian, S., Zhang, P., Zhang, X.-J., Cheng, X., Yuan, Y., She, Z.-G., Hu, Y., & Li, H. (2021). A kinome screen reveals that Nemo-like kinase is a key suppressor of hepatic gluconeogenesis. Cell Metabolism, 0(0). https://doi.org/10.1016/j.cmet.2021.04.006 Cite
we reprogrammed hepatocytes from a mouse model of hereditary tyrosinemia type 1 (HT1) into expandable CdHs and successfully corrected the disease-causing mutation using both adenine base editors (ABEs) and prime editors (PEs).
[Cell Stem Cell]
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Kim, Y., Hong, S.-A., Yu, J., Eom, J., Jang, K., Yoon, S., Hong, D. H., Seo, D., Lee, S.-N., Woo, J.-S., Jeong, J., Bae, S., & Choi, D. (2021). Adenine base editing and prime editing of chemically derived hepatic progenitors rescue genetic liver disease. Cell Stem Cell, 0(0). https://doi.org/10.1016/j.stem.2021.04.010 Cite
Scientists generated a CRISPR base-edited hepatoma cell line harboring the c.1267C>T variant. These cells replicated the secreted abnormalities seen in serum N-glycosylation, and a portion of the mutant protein appears to relocate to a distinct, non-Golgi compartment, possibly endoplasmic reticulum exit sites.
[American Journal of Human Genetics]
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Ng, B. G., Sosicka, P., Fenaille, F., Harroche, A., Vuillaumier-Barrot, S., Porterfield, M., Xia, Z.-J., Wagner, S., Bamshad, M. J., Vergnes-Boiteux, M.-C., Cholet, S., Dalton, S., Dell, A., Dupré, T., Fiore, M., Haslam, S. M., Huguenin, Y., Kumagai, T., Kulik, M., … Freeze, H. H. (2021). A mutation in SLC37A4 causes a dominantly inherited congenital disorder of glycosylation characterized by liver dysfunction. The American Journal of Human Genetics, 0(0). https://doi.org/10.1016/j.ajhg.2021.04.013 Cite
Investigators designed supramolecular nanofibers self-assembled by compound 1, which could strongly activate the hepatocyte growth factor precursor and initiate hepatocyte growth factor–Met signaling.
[ACS Applied Materials & interfaces]
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Guo, W., Feng, W., Huang, J., Zhang, J., Fan, X., Ma, S., Li, M., Zhan, J., Cai, Y., & Chen, M. (2021). Supramolecular Self-Assembled Nanofibers Efficiently Activate the Precursor of Hepatocyte Growth Factor for Angiogenesis in Myocardial Infarction Therapy. ACS Applied Materials & Interfaces. https://doi.org/10.1021/acsami.0c23153 Cite
Mechanistic studies revealed that Tspan5 promoted cell migration and tumour metastasis by increasing the enzymatic maturation of ADAM10 and activating Notch signalling via the increase of the cleavage of the Notch1 receptor catalysed by the γ‐secretase complex.
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Xie, Q., Guo, H., He, P., Deng, H., Gao, Y., Dong, N., Niu, W., Liu, T., Li, M., Wang, S., Wu, Y., & Li, J.-L. (n.d.). Tspan5 promotes epithelial-mesenchymal transition and tumour metastasis of hepatocellular carcinoma by activating Notch signalling. Molecular Oncology, n/a(n/a). https://doi.org/https://doi.org/10.1002/1878-0261.12980 Cite
Scientists showed that morphine could inhibit hepatocellular carcinoma (HCC) cell proliferation. They further showed that DEAD-box helicase 49 (DDX49 ) was up-regulated in HCC tumors, and that knocking down the DDX49 gene decreases tumor formation in vivo and in vitro, as well as reduces tumor metastasis in vivo.
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The impact of platelets on the sorafenib and resminostat drug effects in hepatocellular carcinoma cells was explored.
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Streubel, G., Schrepfer, S., Kallus, H., Parnitzke, U., Wulff, T., Hermann, F., Borgmann, M., & Hamm, S. (2021). Histone deacetylase inhibitor resminostat in combination with sorafenib counteracts platelet-mediated pro-tumoral effects in hepatocellular carcinoma. Scientific Reports, 11(1), 9587. https://doi.org/10.1038/s41598-021-88983-1 Cite
We employed a mouse model of carbon tetrachloride (CCl4) induced-acute liver injury with clodronate-induced macrophage depletion to clarify the impact of liver injury on liver metabolism and recovery dynamics of metabolic function and liver zonation during regeneration.