CTPS1 (CTP Synthase 1)

INHBA promotes gemcitabine resistance in PC by stabilizing CTPS1 and enhancing pyrimidine metabolism, making it a potential target for chemosensitization in PC.

Circ_0000437 is upregulated in breast cancer tissues and cells, and its high expression promotes proliferation, invasion, migration and EMT of breast cancer cells through the let-7b-5p/CTPS1 axis.

While targeting CTPS1 may offer opportunities to enhance radiosensitivity of cancer patients, challenges related to specificity and off-target effects require further studies. This article highlights an emerging role of H1 modification in the DNA damage repair and discusses the therapeutic potential of manipulating H1 deamidation in cancer treatment.

Our findings not only elucidate a novel regulatory mechanism of hCTPS1 activity but also deepen the understanding of how metabolic enzymes utilize filamentation as a conserved strategy for functional regulation. This study opens new avenues for targeting hCTPS1 in therapeutic interventions.

qRT-PCR validation of key genes (LcDXS3, LcHMGS1, LcMDS, and LcTPS19) confirmed the reliability of the transcriptome data, with LcDXS3 exhibiting pronounced declines in expression after 6 h (2.76-fold decrease) and 12 h (2.63-fold decrease) of darkness treatment. These findings provide novel insights into the photoregulatory mechanisms governing terpenoid metabolism in L. cubeba.

Moreover, high expression of CTPS1 was associated with resistance to cancer radiotherapy, in both mouse xenograft models and clinical cohorts. These findings provide new insights into how linker histones regulate dynamic chromatin alterations in the DNA damage response.

Among these proteins, CTP synthase 1 (CTPS1) and Thymidylate synthetase (TYMS), both of which play roles in nucleotide metabolism, are found to be significantly associated with the survival outcomes of patients with lung cancer. Insufficient ablation can cause alterations in nucleotide metabolism, potentially leading to recurrence and metastasis.

A detailed illustration of gmctool is presented for multiple myeloma (MM), an incurable hematological malignancy. We provide in vitro experimental evidence for the essentiality of CTPS1 (CTPS synthase) and UAP1 (UDP-N-Acetylglucosamine Pyrophosphorylase 1) in specific MM patient subgroups.

This combination induced replicative stress and caspase-mediated cell death and was highly effective in resistant/refractory patient samples with TP53 deletion and/or mutation and in TP53 -/- NCI-H929 xenografted NOD-scid IL2Rgamma mice. Our in vitro, ex vivo, and in vivo data provide the rationale for combined CTPS1 and ATR inhibition for the treatment of p53-deficient patients.

Overall, miR-519e-5p slows the proliferation, invasion, migration, and EMT of BC by binding to CTPS1. This study offers a new direction for BC treatment.

CTPS1-OE decreased sensitivity to bortezomib, whereas CTPS1-sh increased sensitivity to bortezomib in MM cell lines...Additionally, CTPS1 was closely related to several co-expressed genes such as MYC and the bone marrow immune microenvironment. In conclusion, CTPS1 is a significant prognostic biomarker for patients with MM, suggesting a potential therapeutic target.

Our previous studies have implicated phosphoribosyl formylglycinamidine synthase (PFAS) and phosphoribosyl pyrophosphate amidotransferase (PPAT) in deamidating retinoic acid-inducible gene I (RIG-I) and evading dsRNA-induced innate immune defense in herpesvirus infection. Overall, these studies have uncovered an unconventional enzymatic activity of cellular GATs in metabolism and immune defense, offering a molecular link intimately coupling these fundamental biological processes.