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Catabolic Pathway - Crossref

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Last Updated: 10 September 2022

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Progress in structural and functional study of the bacterial phenylacetic acid catabolic pathway, its role in pathogenicity and antibiotic resistance

In this report, we have summarized the PAA distribution in microbes, the latest structural and functional research progress of the enzyme families of the bacterial PAA pathway, as well as their involvement in bacterial pathogenicity and antibiotic resistance. The enzymes of the bacterial PAA pathway have demonstrated promise as an antimicrobial drug target for biotechnological applications in metabolic engineering.

Source link: https://doi.org/10.3389/fmicb.2022.964019


Coordinated Transcriptional and Catabolic Programs Support Iron-Dependent Adaptation to RAS–MAPK Pathway Inhibition in Pancreatic Cancer

The reasons that contributed to pancreatic duct carcinoma cell proliferation to pharmacologic inhibition of RAS-u2013MAPK signaling are largely unknown. We find transcriptional antagonism among c-MYC and the master transcription factors for lysosome gene expression, the MiT/TFE proteins, by using transcriptome and chromatin immunoprecipitation profiling of PDA cells treated with the MEK inhibitor trametinib. Factors influencing c-MYC and MiT/TFE factors' competition for binding to lysosome gene promoters to fine-tune gene expression are demonstrated under baseline conditions. MiT/TFE-dependent lysosome biogenesis has been reported in response to the downregulation of PDA cells or patient organoids with MEKi. Ferritinophagy promotes mitochondrial iron production and increased mitochondrial respiration. During adaptation to KRASu2013MAPK inhibition, lowering iron availability sensitizes PDA cells to MEKi, highlighting a critical and targetable reliance on lysosome-dependent iron supply during adaptation to KRAS-u2013MAPK inhibition. Increased autophagyu2013lysosome production is required for increased ferritinophagy-mediated iron supply, which aids mitochondrial respiration in the case of therapy stress.

Source link: https://doi.org/10.1158/2159-8290.cd-22-0044


Activation of the ubiquitin pathway in rat skeletal muscle by catabolic doses of glucocorticoids

Rats were injected daily with corticosterone for 7 days to see if catabolic glucocorticoids promote the ubiquitin pathway in conjunction with their reported proteolytic effect in skeletal muscle. Around the 3-MH peaks, ubiquitin pathway mRNAs in skeletal muscle were screened for skeletal muscle. On day 3, a second more significant peak of induction of pUb mRNA was present. On day 3 and 4, a rise in pUb mRNA was observed in the soleus, induction of E2-14k mRNA, which culminated in 216 and 28% of controls, while an increase in pUb mRNA was observed on days 3 and 4. At days 3 and 4, a rise in proteasome C8 subunit mRNA accumulation was also observed in the soleus. The comparison between CTC's catabolic effects and the activation of the ubiquitin pathway in muscles of CTC-treated rats clearly points to the presence of this system in glucocorticoid-induced muscular atrophy.

Source link: https://doi.org/10.1152/ajpcell.1997.272.3.c1007


Abstract 3808: MYCN coordinately regulates the entire polyamine gene pathway to drive polyamine biosynthesis in neuroblastoma, with expression of every synthetic and catabolic polyamine pathway gene being highly prognostic of clinical outcome.

The New Approaches to Neuroblastoma Treatment consortium USA's coordinating a refractory neuroblastoma trial will begin soon, and celecoxib and SAT1 inhibition by high-dose difluoromethylornithine will be used soon, according to ODC1 inhibition by high-dose difluoromethylornithine and SAT1 induction by celecoxib. We have now investigated the prognostic role of all polyamine pathway genes in a large population of neuroblastoma tumors. MYCN's chromatin immunoprecipitation revealed that polyamine genes' activation and repression of polyamine genes were analyzed by chromatin immunoprecipitation. Polyamine gene promoters were cloned into luciferase reporter vector vectors and tested as a result of MYCN expression. Results: All polyamine pathway genes were highly predictive of neuroblastoma development, according to the author. A correlation of high MYCN expression in the presence or absence of MYCN expression was found in neuroblastoma cell lines, but an inverse correlation of low MYCN with low catabolic polyamine gene expression was found in neuroblastoma cell lines. MYCN affiliates with biosynthetic gene promoters, according to ChIP assays, by binding to E-box addresses in order to enable transcription. MYCN, on the other hand, binds the catabolic genes in close proximity to the transcription start sites by interacting with the Sp1 protein in order to repress transcription of these genes. Assays, direct activation by MYCN of biosynthetic genes and catabolic genes down-regulation by MYCN of catabolic genes was confirmed by luciferase activity assays. The complete polyamine gene pathway to induce polyamine biosynthesis in neuroblastoma is coordinated by MYCN, with the expression of every synthetic and catabolic polyamine pathway gene being highly predictive of clinical outcomes.

Source link: https://doi.org/10.1158/1538-7445.am2013-3808


Abstract 2736: Thymidine catabolic and salvage pathways are responsible for the heterogeneity of anticancer agent dT-QX in liver cancer cells

Abstract Thymidine analog 3u2032-deoxythymidine phenylquinoxaline conjugate is selectively killed cancer cell lines in tumor cell lines while remaining highly toxic to normal liver cells. However, dT-QX's cytotoxicity was not the same among cell lines of the same type cancer. The expression of enzymes of these two pathways were determined and compared among various cell lines of liver cancer. The alterations in liver cancer cell lines were shown by our initial findings, indicating a dramatic change in the enzyme profiles of thymidine catabolic and salvage pathways. With various structural analogs tested on these liver cancer cell lines, variation on the cytotoxic activity was even found. Our results showed that thymidine catabolic and salvage pathways were antagonistic toward each other, and thus were responsible for the heterogeneity of dT-QX in liver cancer cells. The heterogeneity of anticancer agent dT-QX in liver cancer cells is attributed to Thymidine catabolic and salvage pathways.

Source link: https://doi.org/10.1158/1538-7445.am2014-2736


Procalcitonin N-Terminal Peptide Causes Catabolic Effects via the Hypothalamus and Prostaglandin-Dependent Pathways

N-PCT transfer from intracerebroventricular delivery of N-PCT to free-feeding male rats led to a significant decrease in longer-term food intake and body weight gain. N-PCT raises the responsiveness of proopiomelanocortin anorexigenic neurons in the hypothalamus's arcuate nucleus, and we further demonstrate that N-PCT enhances the central effects produced by N-PCT, and that provocon synthesis of prostaglandins is vital for the central effects induced by N-PCT.

Source link: https://doi.org/10.1159/000155137


Synthesis and Physicochemical Characterization of D -Tagatose-1-Phosphate: The Substrate of the Tagatose-1-Phosphate Kinase in the Phosphotransferase System-Mediated D -Tagatose Catabolic Pathway of Bacillus licheniformis

In tagatose-grown cells of Klebsiella pneumoniae, we present the first enzymatic synthesis of D -tagatose-1-phosphate by the multicomponent phosphatase system. The Bacillus licheniformis PTS-mediated D -tagatose catabolic pathway was used by Tag-1P to characterize the putative tagatose-1-phosphate kinase of the Bacillus licheniformis PTS-mediated D -tagatose catabolic pathway. The conversion of the phosphate moiety from PEP to a B. licheniformis tagatose-specific Enzyme II in E. coli is inefficient, particularly because we observe it in vivo. It is demonstrated by the PTS general cytoplasmic components of B. subtilis, HPr, and Enzyme I that the phosphate transfer can be restored.

Source link: https://doi.org/10.1159/000370115


SEMA6D, Negatively Regulated by miR-7, Contributes to C28/I2 chondrocyte’s Catabolic and Anabolic Activities via p38 Signaling Pathway

In vitro and in vivo, we found that Semaphorin 6D was a direct target gene of miR-7 and had a negative regulatory association with SEMA6D. According to H&E and Safranin O-Fast green staining and a U03bcCT review, SEMA6D could increase OA in rat OA models. SEMA6D has been shown to facilitate the synthesis of C28/I2 chondrocytes and reduces their catabolism, according to a further analysis by SEMA6D.

Source link: https://doi.org/10.1155/2022/9674221

* 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