8jj6
Structure of the NELF-BCE complex
Structural highlights
FunctionNELFB_HUMAN Essential component of the NELF complex, a complex that negatively regulates the elongation of transcription by RNA polymerase II. The NELF complex, which acts via an association with the DSIF complex and causes transcriptional pausing, is counteracted by the P-TEFb kinase complex. The NELF complex is involved in HIV-1 latency possibly involving recruitment of PCF11 to paused RNA polymerase II. Binds RNA which may help to stabilize the NELF complex on nucleic acid. In vitro, binds weakly to the HIV-1 TAR RNA which is located in the long terminal repeat (LTR) of HIV-1. May be able to induce chromatin unfolding.[1] [2] [3] [4] Publication Abstract from PubMedNegative elongation factor (NELF) is a four-subunit transcription elongation factor that mainly functions in maintaining the paused state of RNA polymerase II in eukaryotes. Upon binding to Pol II, NELF works synergistically with DRB sensitivity-inducing factor (DSIF) and inhibits transcription elongation of Pol II, which subsequently retains a stably paused state 20-60 base pairs downstream of the promoter. The promoter-proximal pausing of Pol II caused by NELF is a general mechanism of transcriptional regulation for most signal-responsive genes. To date, structural studies have significantly advanced our understanding of the molecular mechanisms of NELF. However, a high quality structural model clarifying the interaction details of this complex is still lacking. In this study, we solved the high resolution crystal structure of the NELF-B/C/E ternary complex. We observed detailed interactions between subunits and identified residues important for the association between NELF-B and NELF-E. Our work presents a precise model of the NELF complex, which will facilitate our understanding of its in vivo function. Structural basis of the human negative elongation factor NELF-B/C/E ternary complex.,Cao Y, Qin Y, Zhang W, Tian W, Ren Y, Ren J, Wang J, Wang M, Jiang J, Wang Z Biochem Biophys Res Commun. 2023 Oct 15;677:155-161. doi: , 10.1016/j.bbrc.2023.08.019. Epub 2023 Aug 10. PMID:37591184[5] From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine. References
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