Web cookies (also called HTTP cookies, browser cookies, or simply cookies) are small pieces of data that websites store on your device (computer, phone, etc.) through your web browser. They are used to remember information about you and your interactions with the site.
Purpose of Cookies:
Session Management:
Keeping you logged in
Remembering items in a shopping cart
Saving language or theme preferences
Personalization:
Tailoring content or ads based on your previous activity
Tracking & Analytics:
Monitoring browsing behavior for analytics or marketing purposes
Types of Cookies:
Session Cookies:
Temporary; deleted when you close your browser
Used for things like keeping you logged in during a single session
Persistent Cookies:
Stored on your device until they expire or are manually deleted
Used for remembering login credentials, settings, etc.
First-Party Cookies:
Set by the website you're visiting directly
Third-Party Cookies:
Set by other domains (usually advertisers) embedded in the website
Commonly used for tracking across multiple sites
Authentication cookies are a special type of web cookie used to identify and verify a user after they log in to a website or web application.
What They Do:
Once you log in to a site, the server creates an authentication cookie and sends it to your browser. This cookie:
Proves to the website that you're logged in
Prevents you from having to log in again on every page you visit
Can persist across sessions if you select "Remember me"
What's Inside an Authentication Cookie?
Typically, it contains:
A unique session ID (not your actual password)
Optional metadata (e.g., expiration time, security flags)
Analytics cookies are cookies used to collect data about how visitors interact with a website. Their primary purpose is to help website owners understand and improve user experience by analyzing things like:
How users navigate the site
Which pages are most/least visited
How long users stay on each page
What device, browser, or location the user is from
What They Track:
Some examples of data analytics cookies may collect:
Page views and time spent on pages
Click paths (how users move from page to page)
Bounce rate (users who leave without interacting)
User demographics (location, language, device)
Referring websites (how users arrived at the site)
Here’s how you can disable cookies in common browsers:
1. Google Chrome
Open Chrome and click the three vertical dots in the top-right corner.
Go to Settings > Privacy and security > Cookies and other site data.
Choose your preferred option:
Block all cookies (not recommended, can break most websites).
Block third-party cookies (can block ads and tracking cookies).
2. Mozilla Firefox
Open Firefox and click the three horizontal lines in the top-right corner.
Go to Settings > Privacy & Security.
Under the Enhanced Tracking Protection section, choose Strict to block most cookies or Custom to manually choose which cookies to block.
3. Safari
Open Safari and click Safari in the top-left corner of the screen.
Go to Preferences > Privacy.
Check Block all cookies to stop all cookies, or select options to block third-party cookies.
4. Microsoft Edge
Open Edge and click the three horizontal dots in the top-right corner.
Go to Settings > Privacy, search, and services > Cookies and site permissions.
Select your cookie settings from there, including blocking all cookies or blocking third-party cookies.
5. On Mobile (iOS/Android)
For Safari on iOS: Go to Settings > Safari > Privacy & Security > Block All Cookies.
For Chrome on Android: Open the app, tap the three dots, go to Settings > Privacy and security > Cookies.
Be Aware:
Disabling cookies can make your online experience more difficult. Some websites may not load properly, or you may be logged out frequently. Also, certain features may not work as expected.
Liu, Q., Huang, B., Guiberson, N., Chen, S., Zhu, D., Ma, G., Ma, X., Crittenden, J.R., Yu, J., Graybiel, A, M., Dawson, T.M., Dawson, V.L., Xiong, Y. (2024) CalDAG-GEFI acts as a Guanine Nucleotide Exchange Factor for LRRK2 to regulate LRRK2 function and neurodegeneration. Science Advances(Accepted )
Xiong, Y.,Yu, J. (2024) LRRK2 in Parkinson’s disease: Upstream regulation and Therapeutic targeting.Trends Mol. Med.Aug 16:S1471-4914(24)00189-8. doi: 10.1016/j.molmed.2024.07.003
Liu, Q., Zhu, D., Li, N., Chen, S., Hu, L., Yu, J., Xiong, Y. (2023) Regulation of LRRK2 mRNA stability by ATIC and its substrate AICAR through ARE-mediated mRNA decay in Parkinson’s disease. TheEMBO Journal e113410 doi:10.15252/embj.2022113410
Hu, L., Brichalli, W., Li, N., Chen, S., Cheng, Y., Liu, Q., Xiong, Y.*, Yu, J.*. (2022) Myotubularin functions through actomyosin to interact with the Hippo pathway. EMBO Reports e55851 (*corresponding author).
Liu, Q., Bautista-Gomez, J., Higgins, D.A., Yu, J. *, Xiong, Y.* (2021) LRRK2 regulates an AP2M1 phosphorylation cycle to mediate endocytosis and dopaminergic neurodegeneration. Sci. Signal. 14(693): eabg3555 (*corresponding author)
Xiong, Y.*, Yu, J.* (2020) Linking the leucine-rich repeat kinase 2 (LRRK2) gene, animal models and Parkinson’s disease. The Neuroscience of Parkinson’s disease: Volume 2:Genetics, Neurology, Behavior, and Diet in Parkinson’s Disease (Elsevier, ISBN: 9780128159507). (Book chapter, *corresponding author)
Li, N., Liu, Q., Xiong, Y*, Yu, J.*. (2019) Headcase and Unkempt regulate tissue growth and cell cycle progression in response to nutrient restriction. Cell Reports, 26,733-747 (*corresponding author)
Xiong, Y.*, Yu, J.* (2018) Modeling Parkinson’s disease in Drosophila: What have we learned for dominant traits? Front Neurol.Apr 9; 9:228. (*corresponding author)
Yu, J., Pan, D. (2018). Validating upstream regulators of Yorkie activity in Hippo signaling through scalloped-based genetic epistasis. Development 145(4): dev157545.
Maoxu Ge, Hong Liu, Yixuan Zhang, Naren Li, Shuangshuang Zhao, Wuli Zhao, Yongzhan Zhen, Jianzhong Yu, Hongwei He, Rongguang Shao (2017). The anti-hepatic fibrosis effects of dihydrotanshinone I are mediated by disrupting the yes-associated protein and transcriptional enhancer factor D2 complexand stimulating autophagy. British Journal of Pharmacology 174(10):1147-1160.
Chan P, Han X, Zheng B, DeRan M, Yu J, Jarugumilli GK, Deng H, Pan D, Luo X, Wu X (2016). Autopalmitoylation of TEAD proteins regulates transcriptional output of the Hippo pathway. Nat Chem Biol. 12(4):282-9
Liu B, Zheng Y, Yin F, Yu J, Silverman N, Pan D (2016). Toll Receptor-Mediated Hippo Signaling Controls Innate Immunity in Drosophila. Cell 164(3):406-19.
Deng H, Wang W, Yu J, Zheng Y, Qing Y, Pan D (2015). Spectrin regulates Hippo signaling by modulating cortical actomyosin activity. Elife 31: 4. doi: 10.7554/eLife.06567.
Yin F, Yu J, Zheng Y, Chen Q, Zhang N, Pan D (2013). Spatial organization of Hippo signaling at the plasma membrane mediated by the tumor suppressor Merlin/NF2. Cell 154(6):1342-55.
Ni L, Li S, Yu J, Min J, Brautigam CA, Tomchick DR, Pan D, Luo X (2013). Structural basis for autoactivation of human Mst2 kinase and its regulation by RASSF5. Structure 21(10):1757-68.
Koontz LM, Liu-Chittenden Y, Yin F, Zheng Y, Yu J, Huang B, Chen Q, Wu S, Pan D (2013). The Hippo effector Yorkie controls normal tissue growth by antagonizing scalloped-mediated default repression. Developmental Cell 25(4):388-401.
Ling C, Zheng Y, Yin F, Yu J, Huang J, Hong Y, Wu S, Pan D (2010). The apical transmembrane protein Crumbs functions as a tumor suppressor that regulates Hippo signaling by binding to Expanded. Proc. Natl. Acad. Sci. USA, 107(23):10532-7
Tian W, Yu J, Tomchick D, Pan D, Luo X (2010). Structural and Functional Analysis of the YAP-binding Domain of Human TEAD2. Proc. Natl. Acad. Sci. USA, 107(16):7293-8
Yu J, Zheng Y, Dong J, Klusza S, Deng WM, Pan D (2010). Kibra functions as a tumor suppressor protein that regulates hippo signaling in conjunction with Merlin and expanded. Developmental Cell 18(2):288-99.
Alarcón C, Zaromytidou AI, Xi Q, Gao S, Yu J, Fujisawa S, Barlas A, Miller AN, Manova-Todorova K, Macias MJ, Sapkota G, Pan D, Massagué J (2009). Nuclear CDKs drive Smad transcriptional activation and turnover in BMP and TGF-beta pathways. Cell 139(4):757-69.
Yu J, Poulton J, Huang YC, Deng WM (2008). The Hippo Pathway Promotes Notch Signaling in Regulation of Cell Differentiation, Proliferation, and Oocyte Polarity. PLoS ONE. 3(3): e1761.