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Chemical Structure| 115144-35-9 Chemical Structure| 115144-35-9
Chemical Structure| 115144-35-9

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D-Luciferin is the natural substrate of luciferase (Luc), catalyzing the characteristic yellow-green light emission of fireflies. The luciferase (Luc) gene is commonly used as a reporter gene in research and active molecule screening, ideal for detecting low levels of gene expression due to minimal background interference from chemiluminescence.

Synonyms: Firefly luciferin potassium; Beetle Luciferin potassium; D-Luciferin (potassium salt)

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Lin, Chuman ; Li, Zhiyang ; Zhu, Xiaotong ; Zhou, Wanbing ; Lu, Xiansheng ; Zheng, Jiali , et al.

Abstract: The abnormal arginine metabolism is characteristic of tumor cell metabolism in colorectal cancer (CRC). However, the mechanisms underlying arginine metabolic reprogramming and how altered metabolism in turn enhances CRC tumorigenicity are poorly understood. Protein post-translational modifications (PTMs) are crucial for regulating protein function, activity, and interactions. Here, the study reports that arginine levels are elevated in CRC, accompanied by the high expression of arginase-1 (ARG1) but low levels of ARG1 β-hydroxybutyrylation (Kbhb) and its oncogenic role in CRC in a catalytic-activity-independent manner. Mechanistically, low-level ARG1-Kbhb-induced arginine metabolic reprogramming by decreasing the interaction of ARG1 with SLC3A2 in CRC cells inhibits the efflux of arginine, thereby increasing intracellular arginine levels to promote tumorigenicity. P300 is identified as the “writer” of Kbhb. Inducing ARG1-Kbhb at the Lys313 residue by β-hydroxybutyrate (BHB) promotes the interaction of ARG1 with SLC3A2, resulting in the efflux of arginine in CRC cells. Together, these findings reveal valuable insights into arginine metabolism reprogramming involving the ARG1-Kbhb/P300/SLC3A2 signaling axis, thereby bridging the connection between metabolic reprogramming and PTMs, which may shed light on the therapeutic potential of combining BHB with ARG1 inhibitor through the conventional enzymatic role and nonenzymatic metabolic function of ARG1 for CRC.

Keywords: β-hydroxybutyrylation ; ARG1 ; arginine metabolism reprogramming ; colorectal cancer

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Zheng, Weiwei ; Shen, Peiliang ; Yu, Chang ; Tang, Yu ; Qian, Cheng ; Yang, Chunmei , et al.

Abstract: Tumor cell extravasation across endothelial barrier has been recognized as a pivotal event in orchestrating metastasis formation. This event is initiated by the interactions of extravasating tumor cells with endothelial cells (ECs). Therefore, targeting the crosstalk between tumor cells and ECs might be a promising therapeutic strategy to prevent metastasis. In this study, we demonstrated that Rh1, one of the main ingredients of ginseng, hindered the invasion of breast cancer (BC) cells as well as diminished the permeability of ECs both in vitro and in vivo, which was responsible for the attenuated tumor cell extravasation across endothelium. Noteworthily, we showed that ECs were capable of inducing the epithelial-mesenchymal transition (EMT) and invadopodia of BC cells that are essential for tumor cell migration and invasion through limiting the nuclear translocation of hematopoietically expressed homeobox (HHEX). The decreased nuclear HHEX paved the way for initiating the CCL20/CCR6 signaling axis, which in turn contributed to damaged endothelial junctions, uncovering a new crosstalk mode between tumor cells and ECs. Intriguingly, Rh1 inhibited the kinase activity of casein kinase II subunit alpha (CK2α) and further promoted the nuclear translocation of HHEX in the BC cells, which resulted in the disrupted crosstalk between chemokine (C-C motif) ligand 20 (CCL20) in the BC cells and chemokine (C-C motif) receptor 6 (CCR6) in the ECs. The prohibited CCL20-CCR6 axis by Rh1 enhanced vascular integrity and diminished tumor cell motility. Taken together, our data suggest that Rh1 serves as an effective natural CK2α inhibitor that can be further optimized to be a therapeutic agent for reducing tumor cell extravasation.

Keywords: Ginsenoside Rh1 ; Tumor cell extravasation ; CCL20 ; Endothelial permeability ; HHEX ; CK2α

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Product Details of D-Luciferin potassium

CAS No. :115144-35-9
Formula : C11H7KN2O3S2
M.W : 318.41
SMILES Code : O=C([C@@H]1N=C(C2=NC3=CC=C(O)C=C3S2)SC1)[O-].[K+]
Synonyms :
Firefly luciferin potassium; Beetle Luciferin potassium; D-Luciferin (potassium salt)
MDL No. :MFCD00044928

Safety of D-Luciferin potassium

GHS Pictogram:
Signal Word:Warning
Hazard Statements:H302-H315-H319-H335
Precautionary Statements:P261-P305+P351+P338
 

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