• Molecules and Cells
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• 제25권3호
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• pp.428-437
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• 2008

To identify transcriptional markers for beef traits related to meat tenderness and moisture, we measured the transcriptome of the Longissimus dorsi skeletal muscle in 10 Korean native cattle (KNC). We analyzed the correlation between the beef transcriptome and measurements of four different beef traits, shear force (SF), water holding capacity (WHC), cooking loss (CL), and loin eye area (LEA). We obtained non-overlapping and unique panels of genes showing strong correlations (${\mid}r{\mid}$ > 0.8) with SF, WHC, CL, and LEA, respectively. Functional studies of these genes indicated that SF was mainly related to energy metabolism, and LEA to rRNA processing. Interestingly, our data suggested that WHC is influenced by protein metabolism. Overall, the skeletal muscle transcriptome pointed to the importance of energy and protein metabolism in determining meat quality after the aging process. The panels of transcripts for beef traits may be useful for predicting meat tenderness and moisture.

• BMB Reports
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• 제50권11호
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• pp.546-553
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• 2017

Aging is a natural and gradual process in human life. It is influenced by heredity, environment, lifestyle, and disease. DNA methylation varies with age, and the ability to predict the age of donor using DNA from evidence materials at a crime scene is of considerable value in forensic investigations. Recently, many studies have reported age prediction models based on DNA methylation from various tissues and body fluids. Those models seem to be very promising because of their high prediction accuracies. In this review, the changes of age-associated DNA methylation and the age prediction models for various tissues and body fluids were examined, and then the applicability of the DNA methylation-based age prediction method to the forensic investigations was discussed. This will improve the understandings about DNA methylation markers and their potential to be used as biomarkers in the forensic field, as well as the clinical field.

• BMB Reports
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• 제35권1호
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• pp.67-86
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• 2002

Three routes have been identified triggering neuronal death under physiological and pathological conditions. Excess activation of ionotropic glutamate receptors cause influx and accumulation of $Ca^{2+}$ and $Na^+$ that result in rapid swelling and subsequent neuronal death within a few hours. The second route is caused by oxidative stress due to accumulation of reactive oxygen and nitrogen species. Apoptosis or programmed cell death that often occurs during developmental process has been coined as additional route to pathological neuronal death in the mature nervous system. Evidence is being accumulated that excitotoxicity, oxidative stress, and apoptosis propagate through distinctive and mutually exclusive signal transduction pathway and contribute to neuronal loss following hypoxic-ischemic brain injury. Thus, the therapeutic intervention of hypoxic-ischemic neuronal injury should be aimed to prevent excitotoxicity, oxidative stress, and apoptosis in a concerted way.

• Molecules and Cells
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• 제38권8호
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• pp.677-684
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• 2015

Osteoarthritis (OA) is one of the most prevalent forms of joint disorder, associated with a tremendous socioeconomic burden worldwide. Various non-genetic and lifestyle-related factors such as aging and obesity have been recognized as major risk factors for OA, underscoring the potential role for epigenetic regulation in the pathogenesis of the disease. OA-associated epigenetic aberrations have been noted at the level of DNA methylation and histone modification in chondrocytes. These epigenetic regulations are implicated in driving an imbalance between the expression of catabolic and anabolic factors, leading eventually to osteoarthritic cartilage destruction. Cellular senescence and metabolic abnormalities driven by OA-associated risk factors appear to accompany epigenetic drifts in chondrocytes. Notably, molecular events associated with metabolic disorders influence epigenetic regulation in chondrocytes, supporting the notion that OA is a metabolic disease. Here, we review accumulating evidence supporting a role for epigenetics in the regulation of cartilage homeostasis and OA pathogenesis.

• BMB Reports
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• 제52권1호
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• pp.35-41
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• 2019

Cellular senescence, a permanent state of cell cycle arrest, is believed to have originally evolved to limit the proliferation of old or damaged cells. However, it has been recently shown that cellular senescence is a physiological and pathological program contributing to embryogenesis, immune response, and wound repair, as well as aging and age-related diseases. Unlike replicative senescence associated with telomere attrition, premature senescence rapidly occurs in response to various intrinsic and extrinsic insults. Thus, cellular senescence has also been considered suppressive mechanism of tumorigenesis. Current studies have revealed that therapy-induced senescence (TIS), a type of senescence caused by traditional cancer therapy, could play a critical role in cancer treatment. In this review, we outline the key features and the molecular pathways of cellular senescence. Better understanding of cellular senescence will provide insights into the development of powerful strategies to control cellular senescence for therapeutic benefit. Lastly, we discuss existing strategies for the induction of cancer cell senescence to improve efficacy of anticancer therapy.

• BMB Reports
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• 제56권8호
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• pp.426-438
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• 2023

Muscle wasting in end-stage renal disease (ESRD) is an escalating issue due to the increasing global prevalence of ESRD and its significant clinical impact, including a close association with elevated mortality risk. The phenomenon of muscle wasting in ESRD, which exceeds the rate of muscle loss observed in the normal aging process, arises from multifactorial processes. This review paper aims to provide a comprehensive understanding of muscle wasting in ESRD, covering its epidemiology, underlying molecular mechanisms, and current and emerging therapeutic interventions. It delves into the assessment techniques for muscle mass and function, before exploring the intricate metabolic and molecular pathways that lead to muscle atrophy in ESRD patients. We further discuss various strategies to mitigate muscle wasting, including nutritional, pharmacological, exercise, and physical modalities intervention. This review seeks to provide a solid foundation for future research in this area, fostering a deeper understanding of muscle wasting in ESRD, and paving the way for the development of novel strategies to improve patient outcomes.

• BMB Reports
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• 제48권12호
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• pp.677-684
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• 2015

Cardiovascular function is regulated by the rhythmicity of circadian, infradian and ultradian clocks. Specific time scales of different cell types drive their functions: circadian gene regulation at hours scale, activation-inactivation cycles of ion channels at millisecond scales, the heart's beating rate at hundreds of millisecond scales, and low frequency autonomic signaling at cycles of tens of seconds. Heart rate and rhythm are modulated by a hierarchical clock system: autonomic signaling from the brain releases neurotransmitters from the vagus and sympathetic nerves to the heart's pacemaker cells and activate receptors on the cell. These receptors activating ultradian clock functions embedded within pacemaker cells include sarcoplasmic reticulum rhythmic spontaneous Ca²⁺ cycling, rhythmic ion channel current activation and inactivation, and rhythmic oscillatory mitochondria ATP production. Here we summarize the evidence that intrinsic pacemaker cell mechanisms are the end effector of the hierarchical brain-heart circadian clock system.

• Molecules and Cells
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• 제41권1호
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• pp.65-72
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• 2018

Autophagy is an evolutionally conserved cytoplasmic degradation system in which varieties of materials are sequestered by a double membrane structure, autophagosome, and delivered to the lysosomes for the degradation. Due to the wide varieties of targets, autophagic activity is essential for cellular homeostasis. Recent genetic evidence indicates that autophagy has a crucial role in the regulation of animal lifespan. Basal level of autophagic activity is elevated in many longevity paradigms and the activity is required for lifespan extension. In most cases, genes involved in autophagy and lysosomal function are induced by several transcription factors including HLH-30/TFEB, PHA-4/FOXA and MML-1/Mondo in long-lived animals. Pharmacological treatments have been shown to extend lifespan through activation of autophagy, indicating autophagy could be a potential and promising target to modulate animal lifespan. Here we summarize recent progress regarding the role of autophagy in lifespan regulation.

• Mass Spectrometry Letters
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• 제7권4호
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• pp.85-90
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• 2016

Post-translational modifications (PTMs) of proteins regulate self-renewal and differentiation in embryonic stem cells (ESCs). Nitration of tyrosine residues of proteins in ESCs modulates their downstream pathways, which can affect self-renewal and differentiation. However, protein tyrosine nitration (PTN) in ESCs has been rarely studied. We reviewed 23 nitrated sites in stem cell proteins. Functional enrichment analysis showed that these nitrated proteins are involved in signal transduction, cell adhesion and migration, and cell proliferation in ESCs. Comparison between the nitrated and known phosphorylated sites revealed that 7 nitrated sites had overlapping phosphorylated sites, indicating functional links of PTNs to their associated signaling pathways in ESCs. Therefore, nitrated proteome provides a basis for understanding potential roles of PTN in self-renewal and differentiation of ESCs.

• 대한의사협회지
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• 제61권11호
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• pp.644-648
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• 2018

The incidence of skin cancer has continuously increased in Korea, probably due to sun exposure and increases in the aging population. Ultraviolet light, a well-known risk factor for skin cancer, can cause DNA damage, mutation, and immune suppression, followed by abnormal proliferation. To prevent photocarcinogenesis, the appropriate use of sunscreen should be emphasized. Using broad-spectrum sunscreens with sun protection factor values of 15 or higher and frequent reapplication are recommended. Controversy exists about whether vitamin D synthesis is inhibited by the use of sunscreen. However, considering that skin cancer most commonly develops on the head and neck area, applying it to the face and neck is reasonable in terms of balancing the risk-benefit ratio.