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Sökning: L773:1674 800X OR L773:1674 8018

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1.
  • Cheng, Yirui, et al. (författare)
  • NDFIP1 limits cellular TAZ accumulation via exosomal sorting to inhibit NSCLC proliferation
  • 2023
  • Ingår i: Protein & Cell. - : Springer Nature. - 1674-800X .- 1674-8018. ; 14:2, s. 123-136
  • Tidskriftsartikel (refereegranskat)abstract
    • NDFIP1 has been previously reported as a tumor suppressor in multiple solid tumors, but the function of NDFIP1 in NSCLC and the underlying mechanism are still unknown. Besides, the WW domain containing proteins can be recognized by NDFIP1, resulted in the loading of the target proteins into exosomes. However, whether WW domain-containing transcription regulator 1 (WWTR1, also known as TAZ) can be packaged into exosomes by NDFIP1 and if so, whether the release of this oncogenic protein via exosomes has an effect on tumor development has not been investigated to any extent. Here, we first found that NDFIP1 was low expressed in NSCLC samples and cell lines, which is associated with shorter OS. Then, we confirmed the interaction between TAZ and NDFIP1, and the existence of TAZ in exosomes, which requires NDFIP1. Critically, knockout of NDFIP1 led to TAZ accumulation with no change in its mRNA level and degradation rate. And the cellular TAZ level could be altered by exosome secretion. Furthermore, NDFIP1 inhibited proliferation in vitro and in vivo, and silencing TAZ eliminated the increase of proliferation caused by NDFIP1 knockout. Moreover, TAZ was negatively correlated with NDFIP1 in subcutaneous xenograft model and clinical samples, and the serum exosomal TAZ level was lower in NSCLC patients. In summary, our data uncover a new tumor suppressor, NDFIP1 in NSCLC, and a new exosome-related regulatory mechanism of TAZ.
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  • Lu, B, et al. (författare)
  • Regulation of HMGB1 release by inflammasomes
  • 2013
  • Ingår i: Protein & cell. - : Oxford University Press (OUP). - 1674-8018 .- 1674-800X. ; 4:3, s. 163-167
  • Tidskriftsartikel (refereegranskat)
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5.
  • Luo, Yunyun, et al. (författare)
  • The minor collagens in articular cartilage
  • 2017
  • Ingår i: Protein and Cell. - : Oxford University Press (OUP). - 1674-800X .- 1674-8018. ; 8:8, s. 560-572
  • Tidskriftsartikel (refereegranskat)abstract
    • Articular cartilage is a connective tissue consisting of a specialized extracellular matrix (ECM) that dominates the bulk of its wet and dry weight. Type II collagen and aggrecan are the main ECM proteins in cartilage. However, little attention has been paid to less abundant molecular components, especially minor collagens, including type IV, VI, IX, X, XI, XII, XIII, and XIV, etc. Although accounting for only a small fraction of the mature matrix, these minor collagens not only play essential structural roles in the mechanical properties, organization, and shape of articular cartilage, but also fulfil specific biological functions. Genetic studies of these minor collagens have revealed that they are associated with multiple connective tissue diseases, especially degenerative joint disease. The progressive destruction of cartilage involves the degradation of matrix constituents including these minor collagens. The generation and release of fragmented molecules could generate novel biochemical markers with the capacity to monitor disease progression, facilitate drug development and add to the existing toolbox for in vitro studies, preclinical research and clinical trials.
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  • Resultat 1-6 av 6

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