Citrix, 告別了…… 單國璽樞機, human protein atlas

由 sufang 在 五, 08/29/2014 - 08:56 發表 Pre-published Important message
Citrix is at http://faq.nhri.org.tw ,  進入 ”用戶端軟體存取平台系統 “


告別了…… 單國璽樞機 感念他
以及舅舅 2012/08/23

The Human Protein Atlas: http://www.proteinatlas.org/

2014/09/02 Journal Club

The role of insulin-like growth factor binding protein-3 in the breast cancer cell response to DNA-damaging agents (PubMed Link) (pdf 按我下載)

NICR LIN LAB

由 sufang 在 四, 08/21/2014 - 09:57 發表 Pre-published Temp

Head and neck cancers, including oral cancer and nasopharyngeal carcinoma (NPC), are caused by known extrinsic factors and develop within pre-neoplastic fields of genetically or epigenetically altered cells. In Taiwan, betel quid chewing in oral cancer and Epstein-Barr virus (EBV) infection in NPC are thought to be unique etiologies that promote tumor progression. My lab have been directed our efforts on two main projects: To identify overexpressed protein tyrosine kinases (PTKs) in oral caner cells. To elucidate the role of EBV lytic cycle replication in NPC pathogenesis. For the first project we hypothesized that by knowing what protein tyrosine kinases (PTKs) that drive oral cancer cell survive, would provide rational molecularly targeted therapies for oral cancer. For the second project we specifically asked what are the host factors that restrict EBV lytic cycle replication in nasopharyngeal cells. Research Activities & Accomplishment Role of collagen receptor DDR1 in oral cancer pathogenesis: DDR1-mediated cell survival DDR1-mediated collective cancer cell migration FGFR3 gene fusions in head and neck cancer: Prevalence of FGFR3-TACC3 gene fusion in oral cancer Oncogenic role of FGFR3-TACC3 gene fusion in oral cancer cells EBV Rta interferes with CTCF binding in both host and viral genomes: Rta expression enhances DNA methylation in cellular CpG islands Rta expression disrupts the bindings of CTCF in EBV genome 舊貨不刪: Dr. Lin's laboratory is directed at understanding the reactivation mechanism of two human herpesviruses: Epstein-Barr virus (EBV) and Kaposi's sarcoma associated herpesvirus (KSHV). During their infections, the conversion of an EBV or KSHV latent genome into a lytic replicating one is defined as reactivation. In single-gene systems, several EBV and KSHV encoded latent proteins are oncogenic, indicating that these latent proteins are crucial to EBV and KSHV pathogenesis. Recently, emerging evidence indicates that repeated lytic reactivation may also play a role in EBV and KSHV tumorigenesis. To delineate the molecular processes of EBV and KSHV lytic reactivations, we established a doxycycline inducible system in HEK293 cells that produces a nearly permissive replication phenotype for both EBV and KSHV. Because this system is homogeneous and robust, it is now feasible to elucidate host and viral factors that contribute to regulate the EBV and KSHV reactivations. For more details, please visit Here. Dr. Lin’s second research interest is focused on identifying oncogenic protein tyrosine kinases (PTK) that are involved in oral cancers. Precise molecular classification of cancer subtypes coupled with target inhibition of altered PTK activity has been clinically proven in chronic myelogenous leukemia (ABL), gastrointestinal stromal tumors (c-KIT), ERBB2 positive breast cancer (ERBB2), and a portion of advanced non-small-cell lung cancer (mutated EGFR). A prerequisite to the success of these role models is to precisely uncover the dys-regulated or activated PTK in the cancer cells. To this end, Dr. Lin’s lab has recently identified four PTKs over-expressed in Taiwanese oral squamous cell carcinoma cells. There pathologic relevance in oral cancer progression are under investigations. For more details, please explore Here. Research Activities & Accomplishment Overexpression of DDR1 in oral cancer cells Protein phosphorylation of KSHV RTA/ORF50 is involved in KSHV lytic reactivation Suppressive regulation of KSHV RTA/ORF50 with O-GlcNAcylation Roles of OSCC-specific PTKs in oral cancer pathogenesis

Start: 08/21/2014

Timezone: Asia/Taipei

EBV and KSHV EBV infection HOK

20140812 lab meeting_YCK
由 ingrid 在 二, 08/19/2014 - 10:48 發表 EBV and KSHV EBV infection HOK Ingrid LabMeeting YCK

2014/08/05 關於FGFR3 IHC

由 maruko 在 二, 08/05/2014 - 09:34 發表  Older Posts   FGFR3   IHC 整理FGFR3已發表文章中使用Santa Cruz的anti-FGFR3(B9) 的條件及染色情形(圖片1-4)(圖片5為DDR1染在細胞核及染在細胞質) 1.後來發現  原參考論文2013 J Pathol中的CC1 buffer為偏鹼的條件(PH=8) (之前疏忽了 抱歉!!)   所以 使用PH=6的buffer應該是較不恰當(non-specific較高) 因此會請小夏詢價 買CC1 buffer再做做看 應該就可知道答案了 2. 雖然大多FGFR3都染在細胞質或膜上 但不能排除FGFR3 fusion可能出在核中   Start: 08/05/2014 Timezone: Asia/Taipei 發送此內容 Transfer this content to remote ELN server Bookmark/Search this post with       ‹ 2014/11/04 Epigenetic Talks Bing Ren2011/06/28 To ship RNA sample without dry ice › 增加新的回應   行事曆