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Catalytic Subunit - Crossref

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Last Updated: 13 January 2023

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Inhibition of the DNA-Dependent Protein Kinase Catalytic Subunit Radiosensitizes Malignant Glioma Cells by Inducing Autophagy

In general, IR cell death caused by cellular death is considered apoptotic. On the other hand, nonapoptotic cell death, autophagy, has recently piqued interest as a novel response of cancer cells to chemotherapy and IR. We investigated the role of DNA-PK in IR-induced apoptotic and autophagic cell death in human malignant glioma M059J and M059K cells in the current study. In M059J cells that lack the DNA-PK catalytic subunit of DNA-PK, Low-dose IR caused significant autophagic cell death. In M059J cells, low-dose IR inhibited the phosphorylation of p70S6K, a molecule downstream of the mammalian target of rapamycin associated with autophagy, but not in M059K cells. In addition, antisense oligonucleotides against DNA-PKcs radiosensitized other malignant glioma cell lines with DNA-PKcs, U373-MG and T98G, by inducing autophagy. Specific inhibition of DNA-PKcs may be a new way to radiosensitize malignant glioma cells by inducing autophagy.

Source link: https://doi.org/10.1158/0008-5472.can-04-4202


Identification of Potent Leads for Human cAMP Dependent Protein Kinase Catalytic Subunit Alpha: A Strategic Application of Virtual Screening for Cancer Therapeutics

Protein kinase A is one of the most important kinases implicated in cell signaling mechanism in humans. PKA catalytic subunits underwent several biological functions, including cell proliferation, cell cycle regulation, and cell survival of cells by operating on various substrates, including cAMP, G-proteins, and ATP molecules, which were all necessary for activation of protein kinase A. The amino acid residues constituting inhibitor interaction site were determined in Maestro v9. 0, the human PRKACA crystal structure in a complex with inhibitor complex was optimized, yielding a 2019 research. u2018796u2019 Following the introduction of human PRKACA and 21 lead molecules with good docking ratings were applied progressively to the prepared ligand dataset against a grid around centroid of the identified inhibitor interaction site of human PRKACA and 21 lead molecules with good docking scores were applied later to the prepared ligand dataset against a grid around centroid of the identified inhibitor interaction site of human PRKACA and 21 lead molecules with good docking scores were applied subsequently. Lead u20181 u2019u2019 with a poor docking result relative to other 20 lead molecules and 15 published inhibitors, it has been classified as the best competitive inhibitor of all. By establishing hydrogen bond, Leptosidin's promising inhibitory activity is further enhanced by further evidence from the development of binding orientations of human PRKACA-Leptosidin complex deciphering the Lead 1 blocks the active site residues Thr51, Glu121, Val123, Glu127, and Thr183. Leptosidin may be a futuristic perspective chemical compound to engineer drug molecule against human PRKACA in a variety of cancers, but further in vitro and in vivo research is required to establish the computational strategic prediction of PKA holoenzyme against cancer therapeutics.

Source link: https://doi.org/10.1038/npre.2010.4903.1


Ablation and Inhibition of the Immunoproteasome Catalytic Subunit LMP7 Attenuate Experimental Abdominal Aortic Aneurysm Formation in Mice

In this research, ApoE knockout or LMP7/ApoE double KO mice were infused with angiotensin II for up to 28 days, according to our results, LMP7 expression was significantly increased in AAA tissues from ApoE KO mice and human patients. Interestingly, LMP7/ApoE dKO mice showed a dramatic decline in infiltration of CD3+ T cells, especially CD4+ T cells in AAA tissues, relative to ApoE KO mice. Also, LMP7 ablation dramatically reduced the differentiation of CD4+ T cells into Th1 and Th17 cells, significantly reducing the expression of several transcriptional genes. Our findings suggest that LMP7 induces AAA formation in humans, and we have found, to our knowledge, new evidence that ablation or pharmacological inhibition of LMP7 induces AAA formation, and we may have identified LMP7 as a new therapeutic target for treating AAA in humans.

Source link: https://doi.org/10.4049/jimmunol.1800197


Regulation of the catalytic subunit (p34PSK-J3/cdk4) for the major D-type cyclin in mature B lymphocytes.

B cells that we rendered fit by IL 4 or low doses of anti-Ig, or, alternatively, elevated cdk4 protein levels were seen in vivo cdk4 cells that were not activated by phorbol ester or ionomycin alone. cyclin D2, not cyclin D1 or D3, was found in primary mature B lymphocytes in a subunit D-type cyclin D2 of the D2 protein, not cyclin D1 or D3. In response to mitogenic anti-Ig paralleled cdk4 expression, the production of cyclin D2 synthesis was consistent with that of resting B cells; however, IL-4 or low dose anti-Ig alone did not raise the rate of de novo cyclin D2 synthesis above that of resting B cells. In that only mitogenic factors that triggered DNA synthesis 1 lead to the formation of stable cyclin D2/cdk4 holoenzyme complexes during G1 phase expansion, only chromatic factors, not necessarily phosphates that phosphorylated retinoblastoma, was demonstrated, only human physiology 2 lead to the production of stable cyclin D2/cdk4 holoenzyme complexes during G1 phase progression, phosphorylation phosphate dk4 induced synthesis 1 synthesis 1 led to the development of cyclin D2 chron D2 zyme complexedk4 cytome complexes cytome gratesy cytogendk4 cdk4 cytome complexedodenzyme cellular cytogenomics, and phosphorylated cytogendk4 oligooenzyme cytos, but 2 cytome est oenzyme cytogendk4 cyto.

Source link: https://doi.org/10.4049/jimmunol.156.2.539

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions