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Ribosomal RNA transcription refers to the synthesis of ribosomal RNA (rRNA) from ribosomal DNA (rDNA) by RNA polymerase I (for most rRNAs) and RNA polymerase III (for 5S rRNA) in eukaryotic cells[2][4][1]. This process occurs predominantly in the nucleolus and is essential for ribosome biogenesis, since rRNA forms the catalytic and structural core of the ribosome which carries out translation of mRNA into protein[1][2][5]. rRNA transcription is tightly regulated and highly active in growing and proliferating cells, accounting for up to 60% of total cellular transcription in mammals[2][3]. Disruption or dysregulation of rRNA transcription is linked to diseases such as cancer and developmental syndromes, where hyperactive or defective ribosome synthesis alters cellular protein production and homeostasis[4][2]. Drugs targeting this process usually inhibit RNA polymerase I, leading to decreased ribosome production, nucleolar stress, and potentially activating p53-mediated cell death pathways[2][4]. Ribosomal RNA transcription is not a molecule or receptor; it is a biological process or cellular function. The correct molecular targets for this process would be components such as RNA polymerase I, TIF-IA (Transcription Initiation Factor IA), or UBF (Upstream Binding Factor), which regulate rRNA transcription. Thus, this entry is technically not a suitable "target molecule/receptor" for pharmacological intervention, but drugs do target the process via enzymes and cofactors of the transcription apparatus[4][2].
Inhibition of RNA polymerase I-mediated rRNA transcription; Disruption of ribosome biogenesis, leading to nucleolar stress and activation of p53-dependent pathways
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