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pancreatic cancer cells

MAP4K4 Promotes Pancreatic Tumorigenesis via Phosphorylation and Activation of Mixed Lineage Kinase 3

[Oncogene] Researchers identified MLK3 as a direct downstream target of MAP4K4. The MAP4K4 and MLK3 associated with each other, and MAP4K4 phosphorylates MLK3 on Thr738 and increased MLK3 kinase activity and downstream signaling.

Combinational Blockade of MET and PD-L1 Improves Pancreatic Cancer Immunotherapeutic Efficacy

[Journal of Experimental & Clinical Cancer Research] Kaplan–Meier plotter was used to analyze the prognostic significance of each of the all-known receptor tyrosine kinases to date in immune “hot” and “cold” pancreatic cancers.

circPTPN22 Attenuates Immune Microenvironment of Pancreatic Cancer via STAT3 Acetylation

[Cancer Gene Therapy] Cell counting kit-8 assay and colony formation assay were used to measure the proliferation of pancreatic cancer cells. RNA immunoprecipitation and Western blot were employed for investigation the binding between circPTPN22 and STAT3.

GSK2126458 Has the Potential to Inhibit the Proliferation of Pancreatic Cancer Uncovered by Bioinformatics Analysis and Pharmacological Experiments

[Journal of Translational Medicine] Researchers identified key genes and pathways in the development of pancreatic cancer and provide targets for the treatment of pancreatic cancer.

Inhibition of Acid Ceramidase Elicits Mitochondrial Dysfunction and Oxidative Stress in Pancreatic Cancer Cells

[Cancer Science] The effects of gene therapy using small interfering RNA and short hairpin RNA (shRNA) for acid ceramidase inhibition with its mechanisms for pancreatic cancer were investigated.

Signaling Profiles in HEK 293T Cells Co-Expressing GLP-1 and GIP Receptors

[Acta Pharmacologica Sinica] Scientists showed that when the two receptors were co-expressed in HEK 293T cells with comparable receptor ratio to pancreatic cancer cells, glucose-dependent insulinotropic polypeptide (GIP) predominately induced cAMP accumulation while Glucagon-like peptide-1 (GLP-1) was biased towards β-arrestin 2 recruitment.

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