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 發報日期 : 2021/07/19 發行期數:266 
 
 
 

最新消息

 
 
 
 
新書展示
 
 
展期:2021-07-19 ~ 2021-07-26
 
 
 
 
 
 

資料庫介紹

 
 
 
 
HSTalks新片上架
 
 
HSTalks the Biomedical & Life Sciences 七月份新片上架囉!
 
 
 
 
 
 
 
資料庫試用
 
 
敬請把握Wiley Digital Textbooks 1147本電子教科書最後試用期限,7/31/2021 到期
 
 
 
 
 
 

影音服務

 
 
 
 
健康講座錄影分享
 
 
題目:「提升免疫,吃出健康」應用篇
主講人:中研院生醫所潘文涵研究員
 
 
 
 
 
 
 
110年度科技部研究人員學術倫理增能工作坊線上演講(分享)
 
 
講題:談抄襲與自我抄襲
講者:分生所孫以瀚特聘研究員
 
 
 
 
 
 
 
新增課程之影音及講義,歡迎線上瀏覽
 
 
4/14 IPA分析軟體讀書會(in Chinese)

4/22 RNA-seq資料分析介紹(In English)
 
 
 
 
 
 

Blog

 
 
 
 
Scientific Laboratory Protocol and Method Resources
 
 
LSL provides links to online resources of laboratory protocols and methods that are used primarily in the life sciences.
 
 
 
 
 
 

生命組演講公告

 
 
 
 
7/26 生醫所演講
 
 
講題:The role of Akt-CBAP-TSC2-Rheb signalosome in growth factor signaling—Part II
主講者:Dr. 嚴仲陽
時間:07/26 (週一) 11:00 - 12:00
地點:Webex only
 
 
 
 
 
 
 
7/30 植微所演講
 
 
講題:Type 2C Protein phosphatases and their target proteins that regulate growth during drought stress
主講者:Dr. Paul Verslues
時間:2021-07-30 11:00
地點:presented virtually or physically depends on CECC's announcement
 
 
 
 
 
 

研討會資訊

 
 
 
 
資服處線上課程
 
 
以Python實現人工智慧的入門款學習報名中
 
 
 
 
 
 

生命組研究成果重要發現

 
 
 
 
通過定向進化提高β-葡萄糖苷酶 D2-BGL的糖化效率和在嗜甲醇酵母菌中的重組酵素產量
 
 
β-葡萄糖苷酶在水解纖維低聚物和纖維二糖為葡萄糖的過程中發揮重要角色。 植微所所賀端華博士和他的研究團隊發現,從真菌Chaetomella raphigera中發現的 β-葡萄糖苷酶 D2-BGL 具有高基質親和力,混合Trichoderma reesei纖維素分解酶使用時,D2-BGL可以有效地水解酸處理後的木質纖維素生物質(Kao et al. 2019 Biotechnology for Biofuels)。
 
 
 
 
 
 
 
 
鑑定 MaWRKY40 和 MaDLO1 作為追踪香蕉中水楊酸介導的免疫反應的有效標記基因
 
 
追踪免疫標記基因表現,為研究植物免疫之重要方法。在植物免疫調節中,水楊酸(salicylic acid, SA)是植物對抗生物營養性及半生物營養性病原菌之關鍵植物免疫反應荷爾蒙。因此,穩定的SA反應標記基因,為研究植物對抗病原菌之重要基礎。然而,已發表的 SA 反應標記基因,在不同的香蕉栽培品種,或不同的組織中,其被SA之誘導表現,並不一致。因此,我們在台灣重要的栽培種-北蕉(AAA基因組)上,以SA 處理後,進行轉錄體分析,發現MaWRKY40、MaWRKY70 、和MaDLO1基因,在 SA 處理後,被強烈誘導,且在不同基因組類型(AA與ABB 基因組)的香蕉葉和根中, MaWRKY40、MaWRKY70 、和MaDLO1基因也都穩定的被SA的誘導。
 
 
 
 
 
 
 
A GalNAc/Gal-specific lectin modulates immune responses via toll-like receptor 4 independently of carbohydrate-binding ability
 
 
Toll-like receptor 4 (TLR4) recognizes various protein ligands; however, the protein-TLR4 binding model is unclear. Here we demonstrate a Crenomytilus grayanus lectin (CGL)-TLR4/MD2 model to show that CGL interacts with a TLR4/myeloid differentiation factor 2 (MD2) complex independently of sugar-binding properties. CGL could suppress lipopolysaccharide-induced immune responses significantly, suggesting that TLR4 itself has potential as a therapeutic target.
 
 
 
 
 
 
 
Differential effects of SUMO1 and SUMO2 on circadian protein PER2 stability and function
 
 
Posttranslational modification (PTM) of core circadian clock proteins, including Period2 (PER2), is required for proper circadian regulation. PER2 function is regulated by casein kinase 1 (CK1)-mediated phosphorylation and ubiquitination but little is known about other PER2 PTMs or their interaction with PER2 phosphorylation. We found that PER2 can be SUMOylated by both SUMO1 and SUMO2; however, SUMO1 versus SUMO2 conjugation had different effects on PER2 turnover and transcriptional suppressor function. SUMO2 conjugation facilitated PER2 interaction with β-TrCP leading to PER2 proteasomal degradation. In contrast, SUMO1 conjugation, mediated by E3 SUMO-protein ligase RanBP2, enhanced CK1-mediated PER2 S662 phosphorylation, inhibited PER2 degradation and increased PER2 transcriptional suppressor function. PER2 K736 was critical for both SUMO1- and SUMO2-conjugation. A PER2 K736R mutation was sufficient to alter PER2 protein oscillation and reduce PER2-mediated transcriptional suppression. Together, our data revealed that SUMO1 versus SUMO2 conjugation acts as a determinant of PER2 stability and function and thereby affects the circadian regulatory system and the expression of clock-controlled genes.
 
 
 
 
 
 
 
Genetically encoded multivalent liquid glycan array displayed on M13 bacteriophage
 
 
The central dogma of biology does not allow for the study of glycans using DNA sequencing. We report a liquid glycan array (LiGA) platform comprising a library of DNA 'barcoded' M13 virions that display 30-1,500 copies of glycans per phage. A LiGA is synthesized by acylation of the phage pVIII protein with a dibenzocyclooctyne, followed by ligation of azido-modified glycans. Pulldown of the LiGA with lectins followed by deep sequencing of the barcodes in the bound phage decodes the optimal structure and density of the recognized glycans. The LiGA is target agnostic and can measure the glycan-binding profile of lectins, such as CD22, on cells in vitro and immune cells in a live mouse. From a mixture of multivalent glycan probes, LiGAs identify the glycoconjugates with optimal avidity necessary for binding to lectins on living cells in vitro and in vivo.
 
 
 
 
 
 
 
TIFA protein expression is associated with pulmonary arterial hypertension
 
 
Tumor necrosis factor receptor-associated factor-interacting protein with a forkhead-associated domain (TIFA), a key regulator of inflammation, may be involved in the pathogenesis of pulmonary arterial hypertension (PAH). A total of 48 PAH patients (age 50.1 ± 13.1 years, 22.9% men), 25 hypertensive subjects, and 26 healthy controls were enrolled. TIFA protein expression in peripheral blood mononuclear cells (PBMCs) and plasma interleukin (IL)-1β and tumor necrosis factor (TNF)-α were measured. Pulmonary arterial hemodynamics were derived from right heart catheterization. PAH patients had the highest expression of TIFA, TNF-α, and IL-1β. TIFA protein expression was significantly associated with IL-1β (r = 0.94; P < 0.001), TNF-α (r = 0.93; P < 0.001), mean pulmonary artery pressure (r = 0.41; P = 0.006), and pulmonary vascular resistance (r = 0.41; P = 0.007). TIFA protein expression could independently predict the presence of PAH (odds ratio [95% confidence interval per-0.1 standard deviation]: 1.72 [1.37-2.16]; P < 0.001) and outperformed echocardiographic estimation. Ex vivo silencing of TIFA protein expression in PBMCs led to the suppression of the cellular expression of IL-1β and TNF-α. IL-1β and TNF-α mediated 80.4% and 56.6% of the causal relationship between TIFA and PAH, respectively, supporting the idea that TIFA protein is involved in the pathogenesis of PAH.
 
 
 
 
 
 
 
 
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