Zobrazeno 1 - 10
of 71
pro vyhledávání: '"Valerie P. Castle"'
Publikováno v:
Cerebrovascular Diseases Extra, Vol 5, Iss 2, Pp 52-54 (2015)
Externí odkaz:
https://doaj.org/article/a71e4b71f6e84b9da4da30fa9d9aa088
Autor:
Chitra Subramanian, Jason A. Jarzembowski, Anthony W. Opipari, Jr, Valerie P. Castle, Roland P.S. Kwok
Publikováno v:
Neoplasia: An International Journal for Oncology Research, Vol 13, Iss 8, Pp 726-734 (2011)
Ku70 was first characterized as a nuclear factor that binds DNA double-strand breaks in nonhomolog end-joining DNA repair. However, recent studies have shown that Ku70 is also found in the cytoplasm and binds Bax, preventing Bax-induced cell death. W
Externí odkaz:
https://doaj.org/article/4e10ef98375f4129975c15ac748ec97b
Autor:
Chitra Subramanian, Jason A. Jarzembowski, Anthony W. Opipari, Jr., Valerie P. Castle, Roland P.S. Kwok
Publikováno v:
Neoplasia: An International Journal for Oncology Research, Vol 9, Iss 6, Pp 495-503 (2007)
The cytotoxic mechanism of the histone deacetylase inhibitor (HDACI) Trichostatin A (TSA) was explored in a neuroblastoma (NB) model. TSA induces cell death in neuroblastic-type NB cells by increasing the acetylation of Ku70, a Bax-binding protein. K
Externí odkaz:
https://doaj.org/article/e6bc134d5bd141a480523bfa6b1ee43c
Autor:
Michael B. Armstrong, Xin Bian, Yihong Liu, Chitra Subramanian, Anthony B. Ratanaproeksa, Feng Shao, Victor C. Yu, Roland P.S. Kwok, Anthony W. Opipari, Jr., Valerie P. Castle
Publikováno v:
Neoplasia: An International Journal for Oncology Research, Vol 8, Iss 11, Pp 967-977 (2006)
Neuroblastic (N) type neuroblastoma (NB) is the predominant cell type in NB tumors. Previously, we determined that activated nuclear factor κB (NF-κB) is required for doxorubicin and etoposide to kill N-type NB cells. This study was undertaken to d
Externí odkaz:
https://doaj.org/article/f466702252ff403c9931c8e2ba219e47
Autor:
Xiaoxiang Zhu, Katharina Wimmer, Rork Kuick, Barbara J. Lamb, Stephanie Motyka, Rama Jasty, Valerie P. Castle, Samir M. Hanash
Publikováno v:
Neoplasia: An International Journal for Oncology Research, Vol 4, Iss 5, Pp 432-439 (2002)
The human p73 gene is a homolog of p53, which has been localized to chromosome 1p36 in a region that is frequently deleted in neuroblastoma. Transfection of the p73 gene into neuroblastoma cells that lack detectable p73 protein has been shown to resu
Externí odkaz:
https://doaj.org/article/ecd52189fd1843aeb20c7e2e7ea671b5
Autor:
Rama Jasty, Cynthia {ptvan} Golen, Huey-Jen Lin, Gabe Solomon, Kathleen Heidelberger, Peter Polverini, Anthony Opipari, Eva Feldman, Valerie P. Castle
Publikováno v:
Neoplasia: An International Journal for Oncology Research, Vol 3, Iss 4, Pp 304-313 (2001)
The bcl-2 and c-myc oncogenes cooperate to transform multiple cell types. In the pediatric malignancy NB2, Bcl2 is highly expressed. In tumors with a poor prognosis, N-Myc, a protein homologous to c-Myc, is overexpressed as a result of gene amplifica
Externí odkaz:
https://doaj.org/article/11a5a4c0fdc24af0bc43249561a0a972
Supplemental Table 1: represents heterogeneity of NB tumors
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::26ad2c7e9201918e8340ab120ab620f7
https://doi.org/10.1158/1541-7786.22516995.v1
https://doi.org/10.1158/1541-7786.22516995.v1
Legend for Supplemental Figures
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::2431bda87755915974f8183cf1596b7c
https://doi.org/10.1158/1541-7786.22517004
https://doi.org/10.1158/1541-7786.22517004
Supplemental Figure 4: Representative immunoblot demonstrating PARP1 cleavage in IMR32 cells in response to Lig3 siRNA knockdown.
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::2f1ebc0b7d91f705f7d4275376a98d25
https://doi.org/10.1158/1541-7786.22517007.v1
https://doi.org/10.1158/1541-7786.22517007.v1
Autor:
Angela C. Weyand, Yi-Mi Wu, Rajen Mody, Nathanael G. Bailey, Gregory A. Yanik, Valerie P. Castle
Publikováno v:
Pediatric Blood & Cancer. 63:164-167
We report a 4-year-old female who presented with severe hypereosinophilia (215.7 K/μl) and end-organ dysfunction. Extensive evaluation including whole exome sequencing was performed, revealing no causative mutation. Initial treatment with corticoste