한양대학교 · Biochemistry, Genetics and Molecular Biology
Suresh Ramakrishna 교수의 연구실은 유전자 편집 기술과 암 치료의 융합을 핵심으로 삼고 있습니다. CRISPR/Cas9 기반의 정밀한 유전자 편집 기술 개발과 함께, 이를 활용한 암의 조기 진단 및 맞춤형 치료 전략을 연구하고 있습니다. 특히, 단백질 분해 조절 메커니즘과 탈유비퀴틴 효소(DUBs)의 역할을 통해 암 진행을 규명하고자 하며, 나노소재 기반의 다기능 치료·진단 플랫폼 개발에도 주력하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
RNA-guided endonucleases (RGENs) derived from the CRISPR/Cas system represent an efficient tool for genome editing. RGENs consist of two components: Cas9 protein and guide RNA. Plasmid-mediated delivery of these components into cells can result in uncontrolled integration of the plasmid sequence into the host genome, and unwanted immune responses and potential safety problems that can be caused by the bacterial sequences. Furthermore, this delivery method requires transfection tools. Here we sho
The theranostic term is a revolutionary topic in cancer treatment, combining therapeutic and diagnostic. Theranostic provides an opportunity for diagnosis and response assessment during treatment. Therefore, a single approach can determine an effective line of treatment. The real-time monitoring of therapeutic strategy aimed to be reached by co-delivery of imaging and pharmaceutical agents. The nanoscale carriers are promising platforms in theranostic applications. Although, it is worth bearing
A number of transcriptional factors are required for pluripotency of stem cells. NANOG, a homeobox transcription factor, plays a critical role in regulating embryonic stem cell (ESC) pluripotency. The expression level of NANOG is tightly regulated, and perturbation in its expression level can lead to significant difference in the morphology, expression of cell surface markers, and growth factor dependence of human and mouse ESCs. Here, we demonstrate that the proteolysis of human NANOG is regula
Cancer remains a life-threatening disease and accounts for the major mortality rates worldwide. The practice of using biomarkers for early detection, staging, and customized therapy may increase cancer patients' survival. Deubiquitinating enzymes (DUBs) are a family of proteases that remove ubiquitin tags from proteins of interest undergoing proteasomal degradation. DUBs play several functional roles other than deubiquitination. One of the important roles of DUBs is regulation of tumor progressi
The use of paired Cas9 nickases instead of Cas9 nuclease drastically reduces off-target effects. Because both nickases must function for a nickase pair to make a double-strand break, the efficiency of paired nickases can intuitively be expected to be lower than that of either corresponding nuclease alone. Here, we carefully compared the gene-disrupting efficiency of Cas9 paired nickases with that of nucleases. Interestingly, the T7E1 assay and deep sequencing showed that on-target efficiency of
Antibiotic resistance ranks among the top threats to humanity. Due to the frequent use of antibiotics, society is facing a high prevalence of multidrug resistant pathogens, which have managed to evolve mechanisms that help them evade the last line of therapeutics. An alternative to antibiotics could involve the use of bacteriophages (phages), which are the natural predators of bacterial cells. In earlier times, phages were implemented as therapeutic agents for a century but were mainly replaced
Deubiquitylating enzymes (DUBs) reverse the ubiquitylation of target proteins, thereby regulating diverse cellular functions. In contrast to the plethora of research being conducted on the ability of DUBs to counter the degradation of cellular proteins or auto-ubiquitylated E3 ligases, very little is known about the mechanisms of DUB regulation. In this review paper, we summarize a novel possible mechanism of DUB deubiquitylation by other DUBs. The available data suggest the need for further exp
<b>Background:</b> Cisplatin is one of the frontline anticancer agents. However, development of cisplatin-resistance limits the therapeutic efficacy of cisplatin-based treatment. The expression of microtubule-associated serine/threonine kinase 1 (MAST1) is a primary factor driving cisplatin-resistance in cancers by rewiring the MEK pathway. However, the mechanisms responsible for MAST1 regulation in conferring drug resistance is unknown. <b>Methods:</b> We implemented a CRISPR/Cas9-based, genome
SDS3 is a key component of the histone deacetylase (HDAC)-dependent Sin3A co-repressor complex, serving to maintain its HDAC activity. Here, we report both exogenous and endogenous functional interaction between deubiquitinating enzyme USP17 and human SDS3 by MALDI-TOF-MS, co-immunoprecipitation assay, and GST pull-down assay. In this study, we demonstrated that SDS3 readily undergoes endogenous polyubiquitination, which is associated specifically with Lys-63-branched polyubiquitin chains and no