Regulation and Functional Roles of Chemokines in Liver Diseases

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]
Cao, S., Liu, M., Sehrawat, T. S., & Shah, V. H. (2021). Regulation and functional roles of chemokines in liver diseases. Nature Reviews Gastroenterology & Hepatology, 1–18. https://doi.org/10.1038/s41575-021-00444-2 Cite
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IMFINZI and Tremelimumab with Chemotherapy Demonstrated Overall Survival Benefit in POSEIDON Trial for 1st-Line Stage IV Non-small Cell Lung Cancer

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 Launched to Revolutionize Treatment of Liver Diseases by Targeting the Microbiome-Gut-Liver Axis

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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A Kinome Screen Reveals That Nemo-Like Kinase Is a Key Suppressor of Hepatic Gluconeogenesis

Using a gluconeogenesis-targeted kinome screening approach combined with transcriptome analyses, we uncovered Nemo-like kinase (NLK) as a potent suppressor of HGP.
[Cell Metabolism]
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
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Adenine Base Editing and Prime Editing of Chemically Derived Hepatic Progenitors Rescue Genetic Liver Disease

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]
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
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A Mutation in SLC37A4 Causes a Dominantly Inherited Congenital Disorder of Glycosylation Characterized by Liver Dysfunction

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]
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
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Supramolecular Self-Assembled Nanofibers Efficiently Activate the Precursor of Hepatocyte Growth Factor for Angiogenesis in Myocardial Infarction Therapy

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]
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
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Tspan5 Promotes Epithelial-Mesenchymal Transition and Tumour Metastasis of Hepatocellular Carcinoma by Activating Notch Signalling

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.
[Molecular Oncology]
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
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Morphine May Act via DDX49 to Inhibit Hepatocellular Carcinoma Cell Growth

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.
[Aging]
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Histone Deacetylase Inhibitor Resminostat in Combination with Sorafenib Counteracts Platelet-Mediated Pro-tumoral Effects in Hepatocellular Carcinoma

The impact of platelets on the sorafenib and resminostat drug effects in hepatocellular carcinoma cells was explored.
[Scientific Reports]
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
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Macrophage Potentiates the Recovery of Liver Zonation and Metabolic Function after Acute Liver Injury

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.
[Scientific Reports]
Miura, A., Hosono, T., & Seki, T. (2021). Macrophage potentiates the recovery of liver zonation and metabolic function after acute liver injury. Scientific Reports, 11(1), 9730. https://doi.org/10.1038/s41598-021-88989-9 Cite
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