Background: Clustered Regularly Interspaced Short Palindromic Repeats/CRISPR associated protein 9 (CRISPR/Cas9) has been wildly used to generate gene knockout models through inducing indels causing frame-shift. However, there are few studies concerning the post-transcript effects caused by CRISPR-mediated genome editing.
Results: In the present study, we showed that gene knockdown model also could be generated using CRISPR-mediated gene editing by disrupting the boundary of exon and intron in mice (C57BL/6 J). CRISPR induced indel at the boundary of exon and intron (5' splice site) caused alternative splicing and produced multiple different mRNAs, most of these mRNAs introduced premature termination codon causing down expression of the gene.
Conclusions: These results showed that alternative splicing mutants were able to generate through CRISPR-mediated genome editing by deleting the boundary of exon and intron causing disruption of 5' splice site. Although alternative splicing was an unexpected outcome, this finding could be developed as a technology to generate gene knockdown models or to investigate pre-mRNA splicing.
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http://dx.doi.org/10.1186/s12896-018-0472-8 | DOI Listing |
Sci Rep
December 2024
Guangdong Key Laboratory of Animal Conservation and Resource Utilization, Guangdong Public Laboratory of Wild Animal Conservation and Utilization, Institute of Zoology, Guangdong Academy of Sciences, Guangzhou, 510260, China.
Entomopathogenic nematodes (EPNs) associated with their symbiotic bacteria can effectively kill insect pests, in agriculture, forestry and floriculture. Industrial-scale production techniques for EPNs have been established, including solid and liquid monoculture systems. It is found that supplement of 0.
View Article and Find Full Text PDFFront Immunol
December 2024
Department of Otolaryngology, the Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Suzhou, Jiangsu, China.
Background: B-cell receptor-associated protein 31 (BCAP31) is a widely expressed transmembrane protein primarily located in the endoplasmic reticulum (ER), including the ER-mitochondria associated membranes. Emerging evidence suggests that BCAP31 may play a role in cancer development and progression, although its specific effects across different cancer types remain incompletely understood.
Methods: The raw data on BCAP31 expression in tumor and adjacent non-tumor (paracancerous) samples were obtained from the Broad Institute Cancer Cell Line Encyclopedia (CCLE) and UCSC databases.
Cytojournal
November 2024
Department of General Surgery, The First Affiliated Hospital of Anhui Medical University, Hefei, China.
Objective: Long non-coding RNAs (lncRNAs) participate in the formation, progression, and metastasis of cancer. This study aimed to explore the roles of the lncRNA ST8SIA6 antisense RNA 1 (ST8SIA6-AS1) in tumorigenesis and elucidate the underlying molecular mechanism of its upregulation in hepatocellular carcinoma (HCC).
Material And Methods: A total of 56 in-house pairs of HCC tissues were examined, and ST8SIA6-AS1 levels were determined through real-time polymerase chain reaction (PCR).
Cytojournal
November 2024
Department of Ultrasound, The Third Xiangya Hospital of Central South University, Changsha, China.
Objective: Thyroid cancer (TC) therapy, which is routinely used at present, can improve patients' survival rates. However, lymph node metastasis results in a higher degree of TC malignancy in patients who experience recurrence and/or death. The elucidation of new mechanisms of TC metastasis can help identify new therapeutic targets.
View Article and Find Full Text PDFCytojournal
November 2024
Department of Pathology, Xingtai Medical College, Xingtai, China.
Objective: Oral squamous cell carcinoma (OSCC) is a common malignant tumor worldwide. Surfeit 4 (SURF4) is a member of the surfeit gene family and plays a regulatory role in various cellular processes, such as protein transport and lipid metabolism. Therefore, this study aims to investigate the regulatory role and mechanisms of SURF4 in OSCC.
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