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|β-Amanitin is a cyclic peptide toxin in the poisonous Amanita phalloides mushroom. β-Amanitin inhibits eukaryotic RNA polymerase II and III. β-Amanitin inhibits protein synthesis. β-Amanitin can be us...|
With advanced technology and years of experience, BOC Sciences focuses on producing and manufacturing various cytotoxins, which effectively target RNA Polymerase II and III.
The eukaryotic genome is transcribed by the multi-subunit enzymes RNA polymerase I (Pol I), RNA polymerase II (Pol II), and RNA polymerase III (Pol III), which catalyze DNA-dependent RNA synthesis. Pol III transcribes genes encoding short, untranslated RNAs, including transfer RNAs, 5S ribosomal RNA (rRNA), spliceosomal U6 small nuclear RNA (snRNA), and signal recognition particle 7SL RNA. Pol III transcription is coregulated with Pol I activity, accounting for up to 80% of nuclear gene transcription in growing cells. Pol III activity is a critical determinant of cell growth. However, subsequent studies and contemporary genome-wide approaches have identified additional targets for RNA Pols, particularly for RNA Pol II and RNA Pol III. The specificity of transcription reflects the structurally distinct subunit compositions of the three classes of RNA Pol, which contain both common and unique subunits. Indeed, recent detailed structural studies demonstrate that, although the active center region and core enzymes are similar, each RNA Pol exhibits significant structural differences on its surface, consistent with the gene class-specific functions of each RNA Pol.
RNA polymerase III (Pol III) genes are involved in fundamental processes such as ribosome and protein biogenesis, RNA processing, and protein transport. The rate of protein synthesis strongly correlates with the cellular content of rRNA and transfer RNA (tRNA), and therefore cells need to sustain high rates of RNA Pol I and Pol III transcription to produce a million ribosomes per cell generation. RNA polymerase II is a multi-protein complex, one of three RNA enzymes found in the eukaryotic cell nucleus. Protein-coding genes are transcribed by RNA polymerase II (Pol II) into messenger RNAs (mRNA) in eukaryotes. These short-lived RNA species have a variety of characteristics and are extensively regulated from production to degradation. Deregulation of Pol II and Pol III transcription has been implicated in a variety of human diseases. In particular, elevated Pol III activity is a recurring feature of mouse and human tumors.
The altered gene expression patterns associated with malignant transformation have generally been attributed as a downstream consequence of mutations in genes that encode cellular signaling molecules, such as growth factor receptors, kinases, small GTPases and other intracellular adaptor molecules. However, it became evident that genomic rearrangements or mutations in sequence-specific DNA-binding RNA Pol transcriptional activators and repressors were either crucial drivers or contained secondary mutations required for the malignant transformation of a broad range of cell types. Perhaps the most prototypical examples of such sequence-specific transcription factors are MYC and p53, the oncogenic and tumor-suppressive activity of which, respectively, is nearly ubiquitously deregulated during malignant transformation. Many cancer therapeutics reportedly acts through the inhibition of mRNA and tRNA synthesis. β-Amanitin is a potent inhibitor of RNA polymerase II and III in antibody-drug conjugate (ADC) applications.