[ China Pharmaceutical Network Technology News ] Long non-coding RNA, once considered to be the "dark matter" of human genes, is now an important scientific frontier in the post-gene era, and many members of its family have been widely involved in the regulation of various important life activities. . On May 5th, the international academic journal Cell published the latest research results of Chen Lingling's research group. This result reveals the important function and mechanism of action of the long non-coding RNA SLERT in the nucleolar nucleolar nucleoside.
The Chen Lingling research group of the Institute of Biochemistry and Cell Biology of the Chinese Academy of Sciences recently discovered a new long non-coding RNA (ribonucleic acid) and named it SLERT. This achievement is expected to provide potential targets and directions for drug design and targeted therapy for diseases such as cancer.
In the study, Chen Lingling's research team used gene coding technology to accurately knock out SLERT located in the nucleolus of the cell and found that the deletion of SLERT resulted in a decrease in the transcriptional activity of RNA polymerase I.
The researchers found that knocking out SLERT can inhibit the growth rate of tumors in model mice, and injecting SLERT-suppressing tumor cells into mice, the growth rate of tumors in vivo is lower than that of mice injected with ordinary tumor cells, which is also a related tumor. Targeted therapy offers new targets.
Ribosomal RNA (rRNA) binds to proteins to form ribosomes and is an assembly machine for protein biosynthesis. Human cells contain about 400 copies of ribosomal DNA sequences, but only half can be converted to rRNA. Insufficient transcription of rRNA will lead to bone marrow failure anemia, and excessive transcription may lead to a variety of cancers.
The mystery of this differential transcriptional regulation has long been unsolved. Now Chen Lingling's research on SLERT has proposed a new mechanism to answer this mystery. That is, transcriptional regulation of RNA polymerase I by the SLERT-DDX21 loop controls the difference in rRNA transcription. This new mechanism provides a new direction for drug design for diseases such as cancer.
The study also elucidated the molecular mechanism between protein, DNA and RNA in cell kernels, and analyzed the regulation of the size of DDX21 loop on the regulation of RNA polymerase I transcription and the control of SLERT on DDX21 loop, revealing a new perspective. The new mechanism of RNA polymerase I transcription also provides a new direction for further study of cell nucleolar structure and function.
(Scientists' new results are expected to provide potential targets and directions for cancer treatment)
The Chen Lingling research group of the Institute of Biochemistry and Cell Biology of the Chinese Academy of Sciences recently discovered a new long non-coding RNA (ribonucleic acid) and named it SLERT. This achievement is expected to provide potential targets and directions for drug design and targeted therapy for diseases such as cancer.
In the study, Chen Lingling's research team used gene coding technology to accurately knock out SLERT located in the nucleolus of the cell and found that the deletion of SLERT resulted in a decrease in the transcriptional activity of RNA polymerase I.
The researchers found that knocking out SLERT can inhibit the growth rate of tumors in model mice, and injecting SLERT-suppressing tumor cells into mice, the growth rate of tumors in vivo is lower than that of mice injected with ordinary tumor cells, which is also a related tumor. Targeted therapy offers new targets.
Ribosomal RNA (rRNA) binds to proteins to form ribosomes and is an assembly machine for protein biosynthesis. Human cells contain about 400 copies of ribosomal DNA sequences, but only half can be converted to rRNA. Insufficient transcription of rRNA will lead to bone marrow failure anemia, and excessive transcription may lead to a variety of cancers.
The mystery of this differential transcriptional regulation has long been unsolved. Now Chen Lingling's research on SLERT has proposed a new mechanism to answer this mystery. That is, transcriptional regulation of RNA polymerase I by the SLERT-DDX21 loop controls the difference in rRNA transcription. This new mechanism provides a new direction for drug design for diseases such as cancer.
The study also elucidated the molecular mechanism between protein, DNA and RNA in cell kernels, and analyzed the regulation of the size of DDX21 loop on the regulation of RNA polymerase I transcription and the control of SLERT on DDX21 loop, revealing a new perspective. The new mechanism of RNA polymerase I transcription also provides a new direction for further study of cell nucleolar structure and function.
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