Zobrazeno 1 - 10
of 63
pro vyhledávání: '"Xiujie Xie"'
Autor:
Curtis B. Read, Anika N. Ali, Daniel J. Stephenson, H. Patrick Macknight, Kenneth D. Maus, Chelsea L. Cockburn, Minjung Kim, Xiujie Xie, Jason A. Carlyon, Charles E. Chalfant
Publikováno v:
mBio, Vol 15, Iss 4 (2024)
ABSTRACTMany intracellular pathogens structurally disrupt the Golgi apparatus as an evolutionarily conserved promicrobial strategy. Yet, the host factors and signaling processes involved are often poorly understood, particularly for Anaplasma phagocy
Externí odkaz:
https://doaj.org/article/10e5f04be2dd4e119229141c954aa4ba
Publikováno v:
Cell Death Discovery, Vol 9, Iss 1, Pp 1-11 (2023)
Abstract Neointimal hyperplasia (IH) is a common vascular pathology that typically manifests in in-stent restenosis and bypass vein graft failure. Smooth muscle cell (SMC) phenotypic switching is central to IH, both regulated by some microRNAs, yet t
Externí odkaz:
https://doaj.org/article/0995f48040b245f3a1e278c0598d7b3d
Publikováno v:
Cell Death Discovery, Vol 7, Iss 1, Pp 1-9 (2021)
Abstract Endothelial cell (EC) and smooth muscle cell (SMC) are major cell types adjacent in the vascular wall. Recent progress indicates that their communication is crucial for vascular homeostasis and pathogenesis. In particular, dysfunctional (pro
Externí odkaz:
https://doaj.org/article/a474cb47b6624d54be799f152e285a6c
Publikováno v:
Atherosclerosis Plus, Vol 44, Iss , Pp 31-42 (2021)
Background: Vascular smooth muscle cell (SMC) apoptosis is involved in major cardiovascular diseases. Smad2 is a transcription factor implicated in aortic aneurysm. The molecular mediators of Smad2-driven SMC apoptosis are not well defined. Here we h
Externí odkaz:
https://doaj.org/article/bd1c150c014c4f97a908b6935c939720
Publikováno v:
Cell Death Discovery, Vol 8, Iss 1, Pp 1-1 (2022)
Externí odkaz:
https://doaj.org/article/d9136af2af9a4cc4ac57a871eed4e669
Publikováno v:
iScience, Vol 19, Iss , Pp 872-882 (2019)
Summary: Vascular smooth muscle cell (VSMC) proliferation promotes intimal hyperplasia (IH) in occluding vascular diseases. Here we identified a positive role of ALDH1A3 (an aldehyde dehydrogenase) in this pro-IH process. The expression of ALDH1A3, b
Externí odkaz:
https://doaj.org/article/5b152a1b77f640e9ae0dd193d80c5848
Autor:
W. Quinn O’Neill, Xiujie Xie, Shanying Gui, Heping Yu, Jacqueline Davenport, Thomas Cartwright, Marta Storl-Desmond, Esther Ryu, Ernest R. Chan, Shufen Cao, Pingfu Fu, Theodoros N. Teknos, Quintin Pan
Publikováno v:
Cancers, Vol 14, Iss 2, p 282 (2022)
Human papillomavirus-associated head and neck squamous cell carcinoma (HPV+ HNSCC) is recognized as a distinct disease with unique etiology and clinical features. Current standard of care therapeutic modalities are identical for HPV+ and HPV− HNSCC
Externí odkaz:
https://doaj.org/article/3fbda51acdc147f1900a29feca9b5fba
Publikováno v:
Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, Vol 9, Iss 8 (2020)
Background Vascular smooth muscle cell phenotypic change and consequential intimal hyperplasia (IH) cause arterial stenosis and posttreatment restenosis. Smad3 is a master transcription factor, yet its underlying functional mechanisms in this disease
Externí odkaz:
https://doaj.org/article/d1868cb3d57f4377aeed9111879b6da1
Autor:
Quintin Pan, Anna K. Mapp, Theodoros N. Teknos, Xiujie Xie, James C. Lang, Jharna Datta, Longzhu Piao, Manchao Zhang
Supplemental Figure 1. Restoration of miR-124 in CAL27 enhances the anti-tumor efficacy of afatinib.
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::82e7d60842ce6b18268bbff1f6420547
https://doi.org/10.1158/1535-7163.22502308
https://doi.org/10.1158/1535-7163.22502308
Autor:
Quintin Pan, Anna K. Mapp, Theodoros N. Teknos, Xiujie Xie, James C. Lang, Jharna Datta, Longzhu Piao, Manchao Zhang
Supplemental Figure Legend
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::b0ff798b0b609366ce7eca973c5f8824
https://doi.org/10.1158/1535-7163.22502311.v1
https://doi.org/10.1158/1535-7163.22502311.v1