Publications by authors named "Kwang-Bo Joung"

Article Synopsis
  • Inherited or sporadic loss of a specific gene can lead to pulmonary lymphangioleiomyomatosis (LAM), a rare lung disease caused by tumor nodules that display characteristics of neural crest and smooth muscle cells.
  • The abnormal growth of these "LAM cells" is linked to increased activity of the mTORC1 protein, which is typically regulated by the TSC1-TSC2 protein complex; while rapamycin slows LAM progression, it does not eliminate the disease, suggesting other processes are involved.
  • Recent studies have identified G-protein coupled urotensin-II receptor (UT) signaling as a key player in LAM's cancer-related signaling, revealing that enhanced signaling through UT promotes harmful cell behaviors in
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Article Synopsis
  • Inactivation of mTORC1 enhances the nuclear levels of certain transcription factors involved in metabolism and cell death, particularly STAT1, which requires the mTORC1-associated protein KPNA1 for its nuclear import.
  • The study identifies a specific TOS motif in protein kinase C delta (PKCδ) that facilitates its interaction with mTORC1, suggesting that PKCδ's regulation is influenced by mTORC1 activity.
  • Disruption of this TOS motif leads to increased nuclear PKCδ levels, heightening STAT1 activity and apoptosis, indicating that mTORC1 plays a role in controlling the nuclear entry of PKCδ and consequently affects apoptosis signaling pathways.
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Lymphangioleiomyomatosis (LAM) is a destructive lung disease that can arise sporadically or in adults suffering from the tumor syndrome tuberous sclerosis complex (TSC). Microscopic tumors ('LAM nodules') in the lung interstitium arise from lymphatic invasion and metastasis. These consist of smooth muscle-like cells (LAM cells) that exhibit markers of neural crest differentiation and loss of the tumor suppressor protein 'tuberous sclerosis complex-2' (TSC2).

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Under conditions of reduced mitogen or nutritional substrate levels, the serine/threonine kinase target of rapamycin can augment the nuclear content of distinct transcription factors and promote the induction of stress response genes. In its latent (i.e.

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Target of rapamycin (TOR) is a highly conserved serine/threonine kinase that controls cell growth, primarily via regulation of protein synthesis. In Saccharomyces cerevisiae, TOR can also suppress the transcription of stress response genes by a mechanism involving Tap42, a serine/threonine phosphatase subunit, and the transcription factor Msn2. A physical association between mammalian TOR (mTOR) and the transcription factor signal transducer and activator of transcription-1 (STAT1) was recently identified in human cells, suggesting a similar role for mTOR in the transcription of interferon-gamma-stimulated genes.

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A cellobiohydrolase-encoding cDNA, Tvcel7a, from Trametes versicolor has been cloned and expressed in Aspergillus niger. The deduced amino acid sequence shows that Tvcel7a encodes a 456-amino acid polypeptide belonging to glycosyl hydrolase family 7. TvCel7a possesses a 19-amino acid secretion signal but does not possess a linker region nor a carbohydrate-binding domain.

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The distribution of IS231 has been analyzed in Bacillus thuringiensis serovars. A 723-bp HaeII conserved fragment from IS231M has been used as a probe against EcoRI-digested B. thuringiensis total DNA to yield serovar-specific hybridization profiles.

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