Kyung-Min No
Ewha Womans University · Agricultural and Biological Sciences
About the Lab
Professor Kyung-Min No's research lab focuses on the molecular and epigenetic mechanisms underlying neuronal cell death and survival, particularly in the context of ischemic brain injury. The lab investigates transcriptional regulation by factors such as REST/NRSF and their roles in controlling genes critical for synaptic function and neuronal vulnerability. A central theme is the epigenetic regulation of neural gene expression through chromatin modifications, including histone variants like H3.3, and the functional significance of intragenic CpG islands in development and disease. The lab also explores cellular signaling pathways, such as PI3K/Akt and anoikis-related mechanisms, that modulate neuronal survival under stress conditions.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15A subset of genes implicated in genetic and acquired neurological disorders encode proteins essential to neural patterning and neurogenesis. The gene silencing transcription factor neuronal repressor element-1 silencing transcription factor (REST)/neuron-restrictive silencer factor (NRSF) plays a critical role in elaboration of the neuronal phenotype. In neural progenitor and non-neural cells, REST acts by repression of a subset of neural genes important to synaptic plasticity and synaptic remod
Transient global ischemia is a neuronal insult that induces delayed, selective death of hippocampal CA1 pyramidal neurons. A mechanism underlying ischemia-induced cell death is activation of the gene silencing transcription factor REST (repressor element-1 silencing transcription factor)/NRSF (neuron-restrictive silencing factor) and REST-dependent suppression of the AMPA receptor subunit GluR2 in CA1 neurons destined to die. Here we show that REST regulates an additional gene target, OPRM1 (mu
Mature oocyte cytoplasm can reprogram somatic cell nuclei to the pluripotent state through a series of sequential events including protein exchange between the donor nucleus and ooplasm, chromatin remodeling, and pluripotency gene reactivation. Maternal factors that are responsible for this reprogramming process remain largely unidentified. Here, we demonstrate that knockdown of histone variant H3.3 in mouse oocytes results in compromised reprogramming and down-regulation of key pluripotency gen
Transient forebrain or global ischemia induces delayed neuronal death in vulnerable CA1 pyramidal cells with many features of apoptosis. A brief period of ischemia, i.e., ischemic preconditioning, affords robust protection of CA1 neurons against a subsequent more prolonged ischemic challenge. Here we show that preconditioning acts via PI3K/Akt signaling to block the ischemia-induced cascade involving mitochondrial translocation of Bad, assembly of Bad with Bcl-x(L), cleavage of Bcl-x(L) to form
CpG, 5'-C-phosphate-G-3', islands (CGIs) have long been known for their association with enhancers, silencers, and promoters, and for their epigenetic signatures. They are maintained in embryonic stem cells (ESCs) in a poised but inactive state via the formation of bivalent chromatin containing both active and repressive marks. CGIs also occur within coding sequences, where their functional role has remained obscure. Intragenic CGIs (iCGIs) are largely absent from housekeeping genes, but they ar
Delayed death of serum-starved PC12 cells on a poly-L-lysine (PLL) matrix was observed, even in the presence of NGF. NGF blocked the apoptotic death of attached but not detached cells, which suggests that delayed death may be related to cell detachment from the PLL matrix. Iron selectively blocked this anoikis-like death by increasing cell attachment. Interestingly, the addition of > 10 microM FeCl2 to the culture medium generated gelatinous iron precipitates, and the removal of the precipitates
Objective: To retrospectively compare the imaging characteristics of retropharyngeal density and associated findings for Kawasaki disease with those for non-Kawasaki disease, and identify the distinguishing features which aid the CT diagnosis of Kawasaki disease with retropharyngeal low density. Materials and Methods: Among the enhanced neck CT performed in children less than 8-years old with clinical presentation of fever and cervical lymphadenopathy over a 6-year period, only cases with retrop
TRIM2 is a mammalian E3 ligase with particularly high expression in Purkinje neurons, where it contributes to neuronal development and homeostasis. The understanding of ubiquitin E3 ligase function hinges on thoroughly identifying their cellular targets, but the transient nature of signaling complexes leading to ubiquitination poses a significant challenge for detailed mechanistic studies. Here, we tailored a recently developed ubiquitin-specific proximity labeling tool to identify substrates of
BACKGROUND: Long dismissed as mere genomic parasites, transposable elements (TEs) are now recognized as major drivers of genome evolution. TEs serve as a source of cell-type specific cis-regulatory elements, influencing gene expression and observable phenotypes. However, the precise TE regulatory roles in different contexts remain largely unexplored and the impact of TEs on transcriptional regulatory networks and contribution to disease risk is likely deeply underestimated. RESULTS: Using a mult
목적: 자궁근종과 자궁선근증 환자에서 자궁동맥색전술 시행 후 통증의 정도를 24시간 동안 평가하여 정맥 내 진통제와 함께 추가로 사용하는 경피 펜타닐 패치의 통증 조절에 대한 효과를 알아보았다. 대상과 방법: 자궁근종과 자궁선근증으로 자궁동맥색전술을 시행 받은 42명의 환자를 대상으로, 마약성 진통제 페티딘과 비스테로이드성 소염제를 정맥 내 투여받은 군(A군)과 추가로 경피 펜타닐 패치를 부착한 군(B군)으로 각각 21명씩 분류하였다. 색전술 시행 후 24시간 동안의 통증 지각 정도를 구두통증척도에 따라 0-10점으로 평가하여 시간에 따른 통증 정도를 분석하였다. 또한, 두 군의 통증 정도, 페티딘 투여량, 부작용 발생을 비교하였다. 결과: 전체 환자에서 색전술 6시간 후에 통증의 정도가 가장 심했으며, 이때의 평균 구두통증척도는 A군 8.2 ± 0.7점, B군 6.3 ± 0.7점으로 유의한 차이가 있었다(p < 0.05). A군에서는 평균 114.3 ± 59.5 mg의 페티딘이 투
Additional file 2.
Abstract Background Long dismissed as mere genomic parasites, transposable elements (TEs) are now recognized as major drivers of genome evolution. TEs serve as a source of cell-type specific cis-regulatory elements, influencing gene expression and observable phenotypes. However, the precise TE regulatory roles in different contexts remain largely unexplored and the impact of TEs on transcriptional regulatory networks and contribution to disease risk is likely deeply underestimated. Results Using
Additional file 1.
Abstract Background Long dismissed as mere genomic parasites, transposable elements (TEs) are now recognized as major drivers of genome evolution. TEs serve as a source of cell-type specific cis-regulatory elements, influencing gene expression and observable phenotypes. However, the precise TE regulatory roles in different contexts remain largely unexplored and the impact of TEs on transcriptional regulatory networks and contribution to disease risk is likely deeply underestimated. Results Using
Additional file 1.
Research Areas
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