Publications by authors named "Hye-Yeong Ha"

Article Synopsis
  • Induced pluripotent stem cells (iPSCs) are promising for regenerative medicine and can be derived from umbilical cord blood (UCB) cells, which are abundant and have low immune rejection rates.
  • CD34-UCB cells specifically from the group O/D-negative blood type were reprogrammed to create universal iPSCs for generating red blood cells (RBCs).
  • The newly formed iPSCs display characteristics of pluripotent stem cells, paving the way for advanced therapies, particularly in blood transfusion.
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Induced pluripotent stem cell (iPS) technology may be advantageous for the study of genetic aberrations in terms of recapitulating the full manifestation of pathological features in vitro, identifying underlying pathways, and developing personalized therapeutics rather than procuring somatic cells from patients. Here, we derived an iPSC line from a patient with reciprocal chromosome translocation, t(1;5)(p31.1;35.

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The Korea National Stem Cell Bank has been banking pluripotent stem cell (PSC) lines since 2012. Quality-controlled and ethically sourced cell lines were developed for distribution. Currently (as of 2020), among the 69 deposited lines, 4 research-grade human embryonic stem cell (hESC) lines and 19 induced pluripotent stem cell (iPSC) lines have been distributed.

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Human induced pluripotent stem cells with indefinite propagation in vitro provide a potential donor source of cells including erythroid cells for human therapy. Since group O D-negative (RhD) blood cells are considered as universal donors for transfusion, it is compelling to derive iPSC line from group O/RhD sample as a new cellular source to generate universal RBCs. The resulting iPSC line derived from group O/RhD somatic source showed typical features of pluripotent stem cells and could provide an unprecedented cellular tool to develop universal therapeutics for blood transfusion.

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Human pluripotent stem cells (hPSCs) have promising therapeutic applications due to their infinite capacity for self-renewal and pluripotency. Genomic stability is imperative for the clinical use of hPSCs; however, copy number variation (CNV), especially recurrent CNV at 20q11.21, may contribute genomic instability of hPSCs.

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We generated a human induced pluripotent stem cell (hiPSC) line, KSCBi003-A, from adipose tissue-derived mesenchymal stem cells (Ad-MSCs) using a Sendai virus-based gene delivery system. We confirmed that the KSCBi003-A has a normal karyotype and short tandem repeat (STR)-based identities that match the parent cells. We also confirmed that the cell line expresses pluripotent stem cell markers such as Nanog, OCT4, SSEA-4, TRA-1-60, and TRA-1-81.

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We generated human induced pluripotent stem cells (KSCBi002-B and KSCBi002-B-1) from the dermal fibroblasts of a donor using a modified RNA-based gene delivery method. According to GTG-banding analysis, the generated KSCBi002-B line has a cytogenetic abnormality (46,XY, t(1;4)(q21;q25)) that is distinct from that of the donor, whereas KSCBi002-B-1 has a normal karyotype (46,XY). These cell lines can be useful as a model for characterizing the hiPSCs generated by a non-viral and non-integrative system, or as a chromosomal balanced translocation model.

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Article Synopsis
  • Induced pluripotent stem cells (iPSCs) can be created by introducing specific factors into mature cells, allowing for potential treatments and research applications.
  • Banking iPSCs that represent a diverse range of the population is crucial for effective clinical use, particularly through homozygous human leukocyte antigen (HLA) iPSCs.
  • A study in Korea identified and reprogrammed the most common homozygous HLA types from the population, resulting in 13 high-quality iPSC lines that possess strong pluripotency and normal genetics, paving the way for their use in clinical research and therapy.
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Urinary cells can be an ideal source for generating hiPSCs and progenitors, as they are easily accessible, non-invasive, and universally available. We generated human induced pluripotent stem cells (hiPSCs) from the urinary cells of a healthy donor using a Sendai virus-based gene delivery method. The generated hiPSC line, KSCBi001-A, has a normal karyotype (46,XY).

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We generated human induced pluripotent stem cells (hiPSCs) from dermal fibroblasts using a Sendai virus (SeV)-based gene delivery method. The generated hiPSC line, KSCBi002-A, has a normal karyotype (46,XY). The pluripotency and differentiation capacity were characterized by comparison with those of a human embryonic stem cell line.

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Background: Embryonic stem cells (ESCs) can be expanded infinitely and have the potential to differentiate into hematopoietic stem cells (HSCs); thus, they are considered a useful source of cells for HSC production. Although several technical methods for engineering HSCs from pluripotent stem cells have been developed, clinical application of HSCs engineered from pluripotent stem cells is restricted because of the possibility of xenogeneic contamination resulting from the use of murine materials.

Methods: Human ESCs (CHA-hES15) were cultured on growth factor-reduced Matrigel-coated dishes in the mTeSR1 serum-free medium.

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Although there are a number of weaknesses for clinical use, pluripotent stem cells are valuable sources for patient-specific cell therapies against various diseases. Backed-up by a huge number of basic researches, neuronal differentiation mechanism is well established and pluripotent stem cell therapies against neurological disorders are getting closer to clinical application. However, there are increasing needs for standardization of the sourcing pluripotent stem cells by establishing stem cell registries and banking.

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We previously reported that mice lacking JSAP1 (jsap1-/-) were lethal and the brain of jsap1-/- at E18.5 exhibited multiple types of developmental defects, which included impaired axon projection of the corpus callosum and anterior commissures. In the current study, we examined whether the early telencephalic commissures were formed abnormally from the beginning of initial development or whether they arose normally, but have been progressively lost their maintenance in the absence of JSAP1.

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Important cellular processes such as cell fate are likely to be controlled by an elaborate orchestration of multiple signaling pathways, many of which are still not well understood or known. Because protein kinases, the members of a large family of proteins involved in modulating many known signaling pathways, are likely to play important roles in balancing multiple signals to modulate cell fate, we focused our initial search for chemical reagents that regulate stem cell fate among known inhibitors of protein kinases. We have screened 41 characterized inhibitors of six major protein kinase subfamilies to alter the orchestration of multiple signaling pathways involved in differentiation of stem cells.

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Article Synopsis
  • Recent research indicates that mice lacking JSAP1 (JNK/stress-activated protein kinase-associated protein 1) experience respiratory failure shortly after birth due to developmental issues in their lungs.
  • Histological examination revealed no significant abnormalities until E16.5, but by then, important lung structures like alveoli were not developing properly in the jsap1(-/-) mice, despite normal levels of surfactant-secreting cells.
  • The study found altered expression of several proteins and transcription factors critical for lung development, suggesting that JSAP1 is essential for the proper formation of the cytoskeletal structure and chaperone proteins in developing lungs, which, when impaired, can lead to morphogenetic defects.
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This study reports the roles of extracellular superoxide dismutase (EC-SOD) in the cutaneous inflammation and hyperplasia with 12-O-tetradecanoylphorbol-3-acetate (TPA) application in EC-SOD transgenic mice (Tg EC-SOD). Topical double TPA treatment induced the various inflammatory changes including the epidermal thickness, elevated the PCNA-labeling index, the edema formation, and increased production of hydrogen peroxide (H2O2) in wild type mice (WT). These changes were markedly suppressed in TPA-treated Tg EC-SOD.

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The roles of JSAP1 and JIP1 in cell adhesion and spreading were examined using mouse embryonic fibroblasts (MEFs) deficient in JIP1 (JIP1-KO), JSAP1 (JSAP1-KO), and in both JIP1 and JSAP1 (double-KO), and by using their wild type. After being plated on fibronectin-coated culture plates, wild type MEFs rapidly adhered and differentiated to typical longitudinal fibroblasts in 4 h. JSAP1-KO MEFs showed a similar sequence of adhesion and cell spreading, but their adhesion was weak, and cell spreading sequence proceeded in a delayed manner compared with the wild type.

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Article Synopsis
  • Researchers found that a part of a protein called betaCTF99 can harm brain cells in mice as they get older.
  • In older mice, this protein led to changes that made it harder for brain cells to stay healthy and affected their ability to think clearly and feel less anxious.
  • Overall, the study suggests that having too much of this betaCTF99 protein could lead to brain problems similar to Alzheimer's disease as the mice age.
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The JNK interacting protein, JSAP1, has been identified as a scaffold protein for mitogen-activated protein kinase (MAPK) signaling pathways and as a linker protein for the cargo transport along the axons. To investigate the physiological function of JSAP1 in vivo, we generated mice lacking JSAP1. The JSAP1 null mutation produced various developmental deficits in the brain, including an axon guidance defect of the corpus callosum, in which phospho-FAK and phospho-JNK were distributed at reduced levels.

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Article Synopsis
  • Chronic stress, whether psychological, chemical, or physical, significantly alters liver physiology, but the specific mechanisms are not well understood.
  • A study using mice exposed to chronic restraint stress identified over 235 genes with altered expression, particularly those related to lipid metabolism and detoxification.
  • These findings indicate that chronic stress can change liver gene expression similarly to how diets, environmental chemicals, and drugs do.
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Mice lacking JIP1, a scaffold protein that organizes JNK pathway components, were constructed independently by two groups. The proposed in vivo function, however, remains contradictory; One study reported that targeted disruption of the jip1 caused embryonic death due to the requirement of JIP1 for fertilized eggs (Thompson et al. [2001] J.

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