研究院簡介

南京大學(xué)現(xiàn)代生物研究院，簡稱"現(xiàn)代生物院"(institute of modern biology, nanjing university; imb)，聚焦于創(chuàng)新型生物醫(yī)學(xué)前沿基礎(chǔ)研究，鼓勵和支持開拓性、系統(tǒng)性的科學(xué)探索，致力成為擁有學(xué)者型研究環(huán)境的國際一流生物醫(yī)學(xué)研究中心?，F(xiàn)代生物院林安寧實驗室現(xiàn)面向國內(nèi)外公開招聘實驗技術(shù)員。

pi簡介：

林安寧教授1990年在美國阿拉巴馬州立大學(xué)伯明翰分校(uab)獲博士學(xué)位。1991年在美國加州大學(xué)圣地亞哥分校(ucsd)從事博士后研究。1996年在美國阿拉巴馬州立大學(xué)伯明翰分校任準聘助理教授。1999年在美國芝加哥大學(xué)任準聘助理教授，2002年晉升為終身副教授，2006年晉升為終身正教授。2009年回國任中科院上海生化與細胞所所長，課題組長，博士生導(dǎo)師，終身正教授,國家特聘教授。2014年回美國芝加哥大學(xué)任終身正教授。2020年回國任南京大學(xué)現(xiàn)代生物研究院創(chuàng)院院長，博士生導(dǎo)師，終身正教授，南京大學(xué)醫(yī)學(xué)院附屬鼓樓醫(yī)院特聘教授。

林安寧教授是jnk-c-jun信號轉(zhuǎn)導(dǎo)通路的主要發(fā)現(xiàn)者之一，在cell，nature、science，molecular cell、pnas等著名國際期刊發(fā)表80余篇研究論文，論文總引用數(shù)超過20,000次。林安寧教授長期以來研究細胞信號轉(zhuǎn)導(dǎo)網(wǎng)絡(luò)的分子機理及其調(diào)控異常在疾病中的作用，其在美國的研究工作長期受到nih經(jīng)費支持。在2009到2014年期間，林安寧教授曾擔(dān)任科技部重大研究計劃項目首席科學(xué)家，其研究工作也得到基金委重點項目支持。目前擔(dān)任molecular and cellular biology和cell research編委。

研究方向：

1.細胞信號轉(zhuǎn)導(dǎo)網(wǎng)絡(luò)異常在炎癥、神經(jīng)退行性疾病和癌癥中的作用

2.生物人工智能

代表性論文：

zhang, w., zhangyuan, y., wang, f., jin, k., shen, h., zhang, l., yuan, x., wang, j., zhang, h., yu, w., huang, r., xu, x., yin, y., zhong, g., lin, a*., sun, b*. (2021). the zinc finger protein miz1 suppresses liver tumorigenesis by restricting hepatocyte-driven macrophage activation and inflammation. immunity. doi: https://doi.org/10.1016/j.immuni.2021.04.027

zhang, l., qian, y., li, j., zhou, x., xu, h., yan, j., xiang, j., yuan, x., sun, b., sisodia, s., jiang, y., cao, x., jing, n., lin, a*. (2021). bad-mediated neuronal apoptosis and neuroinflammation contribute to alzheimer's disease pathology. iscience. doi: https://doi.org/10.1016/j.isci.2021.102942

li, j., zhang l., zheng, y., shao, r., liang, q., yu w., wang, h., zou, w., wang, d., xiang, j., lin, a*. (2020). bad inactivation exacerbates rheumatoid arthritis pathology by promoting survival of sublining macrophages. elife 9: e56309.

yan, j., zhang, h., xiang, j., zhao, y., yuan, x., sun, b., and lin, a*. (2018). the bh3-only protein bad mediates tnfalpha cytotoxicity despite concurrent activation of ikk and nf-kappab in septic shock. cell res 28, 701-718.

yan, j., xiang, j., lin, y., ma, j., zhang, j., zhang, h., sun, j., danial, n.n., liu, j., and lin, a*. (2013). inactivation of bad by ikk inhibits tnfalpha-induced apoptosis independently of nf-kappab activation. cell 152, 304-315.

liu, j., yan, j., jiang, s., wen, j., chen, l., zhao, y., and lin, a*. (2012). site-specific ubiquitination is required for relieving the transcription factor miz1-mediated suppression on tnf-alpha-induced jnk activation and inflammation. proc natl acad sci 109, 191-196.

liu, j., zhao, y., eilers, m., and lin, a*. (2009). miz1 is a signal- and pathway-specific modulator or regulator (smor) that suppresses tnf-alpha-induced jnk1 activation. proc natl acad sci 106, 18279-18284.

liu, j., yang, d., minemoto, y., leitges, m., rosner, m.r., and lin, a*. (2006). nf-kappab is required for uv-induced jnk activation via induction of pkcdelta. mol cell 21, 467-480.

yu, c., minemoto, y., zhang, j., liu, j., tang, f., bui, t.n., xiang, j., and lin, a*. (2004). jnk suppresses apoptosis via phosphorylation of the proapoptotic bcl-2 family protein bad. mol cell 13, 329-340.

tang, g., minemoto, y., dibling, b., purcell, n.h., li, z., karin, m., and lin, a*. (2001). inhibition of jnk activation through nf-kappab target genes. nature 414, 313-317.

- (2001). news and views, nature 414, 265-266.

- (2001). highlights, nature reviews 2, 875.

- (2003). hot papers, the scientist 12,32-33.

tang, g., yang, j., minemoto, y., and lin, a*. (2001). blocking caspase-3-mediated proteolysis of ikkbeta suppresses tnf-alpha-induced apoptosis. mol cell 8, 1005-1016.

purcell, n.h., tang, g., yu, c., mercurio, f., didonato, j.a., and lin, a*. (2001). activation of nf-kappa b is required for hypertrophic growth of primary rat neonatal ventricular cardiomyocytes. proc natl acad sci 98, 6668-6673.

minden, a., lin, a., claret, f.x., abo, a., and karin, m. (1995). selective activation of the jnk signaling cascade and c-jun transcriptional activity by the small gtpases rac and cdc42hs. cell 81, 1147-1157.

lin, a., minden, a., martinetto, h., claret, f.x., lange-carter, c., mercurio, f., johnson, g.l., and karin, m. (1995). identification of a dual specificity kinase that activates the jun kinases and p38-mpk2. science 268, 286-290.

minden, a., lin, a., mcmahon, m., lange-carter, c., derijard, b., davis, r.j., johnson, g.l., and karin, m. (1994). differential activation of erk and jnk mitogen-activated protein kinases by raf-1 and mekk. science 266, 1719-1723.

hibi, m., lin, a., smeal, t., minden, a., and karin, m. (1993). identification of an oncoprotein- and uv-responsive protein kinase that binds and potentiates the c-jun activation domain. genes dev 7, 2135-2148.

lin, a., frost, j., deng, t., smeal, t., al-alawi, n., kikkawa, u., hunter, t., brenner, d., and karin, m. (1992). casein kinase ii is a negative regulator of c-jun dna binding and ap-1 activity. cell 70, 777-789.

代表性綜述：

lin, a. (2011). atia: a link between inflammation and hypoxia. mol cell 42, 557-558.

liu, j., and lin, a. (2007). wiring the cell signaling circuitry by the nf-kappa b and jnk1 crosstalk and its applications in human diseases. oncogene 26, 3267-3278.

lin, a. (2006). a five-year itch in tnf-alpha cytotoxicity: the time factor determines jnk action. dev cell 10, 277-278.

lin, a. (2006). regulation of apoptosis by the jnk signaling pathway. in anning lin eds., the jnk signaling pathway. tx: landers bioscience. 63-69.

liu, j., and lin, a. (2005). role of jnk activation in apoptosis: a double-edged sword. cell res 15, 36-42.

lin, a., and karin, m. (2003). nf-kappab in cancer: a marked target. semin cancer biol 13, 107-114.

lin, a. (2003). activation of the jnk signaling pathway: breaking the brake on apoptosis. bioessays 25, 17-24.

karin, m., and lin, a. (2002). nf-kappab at the crossroads of life and death. nat immunol 3, 221-227.

- one of the most cited papers in the field (3,092 citations), isi.

招聘崗位：實驗技術(shù)員

一、崗位職責(zé)

1、主要負責(zé)實驗室儀器設(shè)備、常用試劑耗材的采購，實驗室公共數(shù)據(jù)庫的管理和維護；

2、參與科研經(jīng)費管理，負責(zé)實驗室財務(wù)預(yù)算和報銷；

3、負責(zé)實驗室公共小鼠的基因型鑒定，以及更新各品系小鼠的繁殖籠；

4、與院各行政職能部門聯(lián)系，協(xié)助落實各項規(guī)章制度；

5、完成研究組長交辦的其他事宜。

二、崗位要求

1、應(yīng)聘者必須具有生物學(xué)相關(guān)專業(yè)本科及以上學(xué)歷，本科學(xué)歷應(yīng)聘者需具備兩年及以上實驗室工作經(jīng)驗；有實驗小鼠操作經(jīng)驗者優(yōu)先；

2、應(yīng)聘者必須具有責(zé)任心，工作細致認真，善于溝通交流，態(tài)度積極樂觀，且具備良好的組織協(xié)調(diào)能力與團隊合作精神；能熟練運用辦公相關(guān)軟件。

三、酬薪待遇

根據(jù)南京大學(xué)相關(guān)規(guī)定以及申請人工作能力，實驗室將提供在具有競爭力的薪酬待遇以及科研條件，享受五險一金及南京大學(xué)的相關(guān)福利。具體待遇面議。

四、報名方式

請應(yīng)聘者將個人簡歷及相關(guān)證明材料以pdf文件形式發(fā)送至電子郵箱929454496@qq.com。簡歷請注明"實驗室技術(shù)員-姓名-今日招聘網(wǎng)jrzp.com"，如："實驗室技術(shù)員-張三-今日招聘網(wǎng)jrzp.com"。應(yīng)聘材料將予以嚴格保密，不予退還。通過初審者，我們會盡快安排面試。

信息來源于網(wǎng)絡(luò)，如有變更請以原發(fā)布者為準。

來源鏈接：

https://imb.nju.edu.cn/rczp/syszp/20230530/i247318.html

[我要糾錯]