Publications by authors named "Eun Il Jeong"
Article Synopsis
- The RAS-BRAF signaling pathway plays a crucial role in cell proliferation, with mutations often linked to various human cancers.
- Adenylate kinase 2 (AK2) has been identified as a BRAF-suppressor, inhibiting BRAF activity and downstream signaling in response to cellular energy states.
- Low levels of AK2 in hepatocellular carcinoma (HCC) patients correlate with increased BRAF activity and tumor growth, suggesting that AK2 serves as a negative regulator of BRAF linked to cellular metabolism.
Article Synopsis
- Toxic amyloid beta (Aβ) species contribute to synaptic dysfunction and neurotoxicity in Alzheimer's disease (AD), with gamma-secretase being a crucial link to amyloid accumulation.
- A study identifies pyruvate kinase M2 (PKM2) as a positive regulator of gamma-secretase, primarily expressed in the brains of people with AD and animal models.
- PKM2 expression is induced by hypoxia, enhancing gamma-secretase activity, which in turn increases Aβ production and worsens memory deficits in AD model mice.
In neurodegenerative diseases like Alzheimer's disease (AD), tau is hyperphosphorylated and forms aggregates and neurofibrillary tangles in affected neurons. Autophagy is critical to clear the aggregates of disease-associated proteins and is often altered in patients and animal models of AD. Because mechanistic target of rapamycin (mTOR) negatively regulates autophagy and is hyperactive in the brains of patients with AD, mTOR is an attractive therapeutic target for AD.
View Article and Find Full Text PDFCAV1/Caveolin1, an integral membrane protein, is involved in caveolae function and cellular signaling pathways. Here, we report that CAV1 is a positive regulator of autophagy under oxidative stress and cerebral ischemic injury. Treatment with hydrogen peroxide enhanced autophagy flux and caused the localization of BECN1 to the mitochondria, whereas these changes were impaired in the absence of CAV1.
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- Cerebral ischemia/reperfusion (I/R) leads to brain damage, and the study highlights the role of the E2-25K enzyme in this process, particularly its SUMOylation during oxidative stress.
- Disruption of E2-25K expression can protect neurons from death caused by oxygen/glucose deprivation and reoxygenation, while increased levels of E2-25K worsen those effects.
- The research suggests that E2-25K contributes to brain injury during I/R by inhibiting proteasome activity, which is linked to its SUMOylation at a specific site under stress conditions.
Fas-associated protein with death domain (FADD) plays a key role in extrinsic apoptosis. Here, we show that FADD is SUMOylated as an essential step during intrinsic necrosis. FADD was modified at multiple lysine residues (K120/125/149) by small ubiquitin-related modifier 2 (SUMO2) during necrosis caused by calcium ionophore A23187 and by ischemic damage.
View Article and Find Full Text PDFAlpha-synuclein has been implicated in the pathology of certain neurodegenerative diseases, including Parkinson disease (PD) and dementia with Lewy bodies (LBs). Overexpression of human alpha-synuclein in neuronal cells reduces cell viability, but the precise cellular and molecular mechanisms remain poorly understood. Gap junctional intercellular communication (GJIC) is thought to be essential for maintaining cellular homeostasis and growth control.
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