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文章數：89 |
 TANG Zhan 湯棧長輩會喜歡嗎？》公益路最值得吃的10家餐廳｜實訪整理 |
| 心情隨筆｜心情日記 2026/04/18 20:11:07 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
身為一個熱愛美食、喜歡在城市裡挖掘驚喜的人，臺中公益路一直是我最常出沒的地方之一。這條路可說是「臺中人的美食戰場」，從精緻西餐到創意火鍋，從日式丼飯到義式早午餐，每走幾步，就會有完全不同的特色料理餐廳。 這次我特別花了一整個月，實際造訪了公益路上十間口碑不錯的餐廳。有的是網友熱推的打卡名店，也有隱藏在巷弄裡的小驚喜。我以環境氛圍、口味表現、價格CP值與再訪意願為基準，整理出這篇實測評比。希望能幫正在猶豫去哪裡吃飯的你，找到那一間「吃完會想再來」的餐廳。 評比標準與整理方向
這次我走訪的10家餐廳橫跨不同料理類型，從高質感牛排館到巷弄系早午餐，每一間都有自己獨特的風格。為了讓整體比較更客觀，我依照以下四大面向進行評比，並搭配實際用餐體驗來打分。
整體而言，我希望這份評比不只是「哪家好吃」，而是幫你在不同情境下（約會、家庭聚餐、朋友小聚、商業午餐）都能快速找到合適的選擇。畢竟，美食不只是味覺的滿足，更是一段段與朋友共享的生活記憶。 10間臺中公益路餐廳評比懶人包公益路向來是臺中人聚餐的首選地段，從火鍋、燒肉到中式料理與早午餐，每走幾步就有驚喜。以下是我實際造訪過的10間代表性餐廳清單，橫跨平價、創意、高級各路風格。
一頭牛日式燒肉｜炭香濃郁的和牛饗宴，約會聚餐首選
走在公益路上，很難不被 一頭牛日式燒肉 的木質外觀吸引。低調卻不失質感的門面，搭配昏黃燈光與暖色調的內裝，讓人一進門就感受到濃濃的日式職人氛圍。店內空間不大，但桌距規劃得宜，每桌皆設有獨立排煙設備，烤肉時完全不怕滿身油煙味。 餐點特色
一頭牛的靈魂，絕對是他們招牌的「三國和牛拼盤」。 用餐體驗整體節奏掌握得非常好。店員會在你剛想烤下一片肉時貼心遞上夾子、幫忙換烤網，讓人完全不用分心。整場用餐過程就像一場表演，從視覺、嗅覺到味覺都被滿足。 綜合評分
地址：408臺中市南屯區公益路二段162號電話：04-23206800 小結語一頭牛日式燒肉不僅是「吃肉的地方」，更像是一場五感盛宴。從進門那一刻到最後一道甜點，都能感受到他們對細節的用心。 TANG Zhan 湯棧｜文青系火鍋代表，麻香湯底與視覺美感並重
在公益路這條美食戰線上，TANG Zhan 湯棧 是讓人一眼就會想走進去的那一種。 餐點特色
湯棧最有名的當然是它的「麻香鍋」。 用餐體驗整體氛圍比一般火鍋店更有質感。 綜合評分
地址：408臺中市南屯區公益路二段248號電話：04-22580617 官網：https://www.facebook.com/TangZhan.tw/ 小結語TANG Zhan 湯棧 把傳統火鍋做出新的樣貌保留臺式鍋物的溫度，又結合現代風格與細節服務，讓吃鍋這件事變得更有品味。 如果你想找一間兼具「好吃、好拍、好放鬆」的火鍋店，湯棧會是公益路上最有風格的選擇之一。 NINI 尼尼臺中店｜明亮寬敞的義式早午餐天堂
如果說前兩間是肉食愛好者的天堂，那 NINI 尼尼臺中店 絕對是想放鬆、聊聊天的好地方。餐廳外觀以白色系與大片玻璃窗為主，陽光灑進室內，讓人一踏入就有種度假般的輕盈感。假日早午餐時段特別熱鬧，建議提早訂位。 餐點特色
NINI 的菜單融合義式與臺灣人口味，選擇多樣且份量十足。主打的 松露燉飯 濃郁卻不膩口，米芯保留微Q口感；而 香蒜海鮮義大利麵 則以新鮮白蝦、花枝與淡菜搭配微辣蒜香，口感層次豐富。 用餐體驗店內氣氛輕鬆不拘謹，無論是一個人帶電腦工作、或朋友聚餐，都能找到舒服角落。餐點上桌速度穩定，服務人員態度親切、補水與收盤都非常主動。整體節奏讓人覺得「時間變慢了」，很適合想遠離忙碌日常的人。 綜合評分
地址：40861臺中市南屯區公益路二段18號電話：04-23288498 小結語NINI 尼尼臺中店是一間能讓人放下手機、慢慢吃飯的餐廳。餐點不追求浮誇，而是以「剛剛好」的份量與風味，陪伴每個平凡午後。如果你在找一間能邊吃邊聊天、拍照也漂亮的早午餐店，NINI 會是你在公益路上最不費力的幸福選擇。 加分100%浜中特選昆布鍋物｜平價卻用心的湯頭系火鍋，家庭聚餐好選擇
在公益路這條高質感餐廳林立的戰場上，加分100%浜中特選昆布鍋物 走的是截然不同的路線。它沒有浮誇的裝潢、也沒有高價位的套餐，但靠著實在的湯頭與親切的服務，默默吸引許多回頭客。每到用餐時間，總能看到家庭或情侶三兩成群地圍著鍋邊聊天。 餐點特色
主打 北海道浜中昆布湯底，湯頭清澈卻不單薄，越煮越能喝出海藻與柴魚的自然香氣。 用餐體驗整體氛圍偏家庭取向，桌距寬敞、座位舒適，帶小孩來也不覺擁擠。店員態度親切，補湯、收盤都很勤快，給人一種「被照顧著」的安心感。 綜合評分
地址：403臺中市西區公益路288號電話：0910855180 小結語加分100%浜中特選昆布鍋物是一間「不浮誇、但會讓人想再訪」的火鍋店。它不追求豪華擺盤，而是用最簡單的湯頭與新鮮食材，傳遞出家常卻不平凡的溫度。 印月餐廳｜中式料理的藝術演繹，宴客與家庭聚會首選
說到臺中公益路的中式料理代表，印月餐廳 絕對是榜上有名。這間開業多年的餐廳以「中菜西吃」的概念聞名，把傳統中式料理以現代手法重新詮釋。從建築外觀到餐具擺設，每個細節都散發著低調的典雅氣息。 餐點特色
印月最令人印象深刻的是他們將傳統中菜融入創意手法。 用餐體驗服務方面完全對得起餐廳的高級定位。從入座、點餐到上菜節奏，都拿捏得恰如其分。每道菜都會有服務人員細心介紹食材與吃法，讓人感受到「被款待」的尊榮感。 綜合評分
地址：408臺中市南屯區公益路二段818號電話：0422511155 小結語印月餐廳是一間「不只吃飯，更像品味生活」的地方。 KoDō 和牛燒肉｜極致職人精神，專為儀式感與頂級味覺而生
若要形容 KoDō 和牛燒肉 的用餐體驗，一句話足以總結——「像在欣賞一場關於肉的表演」。 餐點特色
這裡主打 日本A5和牛冷藏肉，以「精切厚燒」的方式呈現。 用餐體驗KoDō 的最大特色是「儀式感」。 綜合評分
地址：403臺中市西區公益路260號電話：0423220312 官網：https://www.facebook.com/kodo2018/ 小結語KoDō 和牛燒肉不是日常餐廳，而是一場體驗。 永心鳳茶｜在茶香裡用餐的優雅時光，臺味早午餐的新詮釋
走進 永心鳳茶公益店，彷彿進入一間有氣質的茶館。 餐點特色
永心鳳茶的餐點結合中式靈魂與西式擺盤，無論是「炸雞腿飯」還是「紅玉紅茶拿鐵」，都能讓人感受到熟悉卻不平凡的味道。 用餐體驗店內服務人員態度溫和，對茶品介紹詳盡。上餐節奏剛好，不急不徐。 綜合評分
地址：40360臺中市西區公益路68號三樓(勤美誠品)電話：0423221118 小結語永心鳳茶讓人重新定義「臺味」。 三希樓｜老饕級江浙功夫菜，穩重又帶人情味的中式饗宴
位於公益路上的 三希樓 是許多臺中老饕的口袋名單。 餐點特色
三希樓的菜色以 江浙與港式料理 為主，兼顧傳統與現代風味。 用餐體驗三希樓的服務給人一種老派但貼心的感覺。 綜合評分
地址：408臺中市南屯區公益路二段95號電話：0423202322 官網：https://www.sanxilou.com.tw/ 小結語三希樓是一間「吃得出功夫」的餐廳。 一笈壽司｜低調奢華的無菜單日料，職人手藝詮釋旬味極致
在熱鬧的公益路上，一笈壽司 低調得幾乎不顯眼。 餐點特色
一笈壽司採 Omakase（無菜單料理） 形式，每一餐都由主廚根據當日食材設計。 用餐體驗整場用餐約90分鐘，節奏緩慢但沉穩。 綜合評分
地址：408臺中市南屯區公益路二段25號電話：0423206368 官網：https://www.facebook.com/YIJI.sushi/ 小結語一笈壽司是一間真正讓人「放慢呼吸」的餐廳。 茶六燒肉堂｜人氣爆棚的和牛燒肉聖地，肉香與幸福感同時滿分
若要票選公益路上「最難訂位」的餐廳，茶六燒肉堂 絕對名列前茅。 餐點特色
茶六主打 和牛燒肉套餐，價格約落在 $700–$1000 間，份量與品質兼具。 用餐體驗茶六的服務效率相當高。店員親切、換網勤快、補水速度快，整場用餐流程流暢無壓力。 綜合評分
地址：403臺中市西區公益路268號電話：0423281167 官網：https://inline.app/booking/-L93VSXuz8o86ahWDRg0:inline-live-karuizawa/-LUYUEIOYwa7GCUpAFWA 小結語茶六燒肉堂用「穩定品質＋輕奢氛圍」抓住了臺中年輕族群的心。 吃完10家公益路餐廳後的心得與結語吃完這十家餐廳後，臺中公益路不只是一條美食街，而是一段生活風景線。 有的餐廳講究細膩與儀式感，像 一頭牛日式燒肉 與 一笈壽司，讓人感受到食材最純粹的美好 有的則以親切與溫度打動人心，像 加分昆布鍋物、永心鳳茶，讓人明白吃飯不只是為了飽足，而是一種被照顧的幸福。 而像茶六燒肉堂、TANG Zhan 湯棧 這類人氣名店，則用穩定的品質與熱絡的氛圍，成為許多臺中人心中「想吃肉就去那裡」的代名詞。 這十家店，構成了公益路最動人的縮影 有華麗的，也有溫柔的；有傳統的，也有創新的。 每一家都在自己的風格裡發光，讓人吃到的不只是料理，而是一種生活的溫度與節奏。 對我而言，這不僅是一場美食旅程，更是一趟關於「臺中味道」的回憶之旅。 FAQ：關於臺中公益路美食常見問題Q1：公益路哪一區的餐廳最集中？ Q2：需要提前訂位嗎？ 最後的話若要用一句話形容這趟美食之旅，我會說： 一頭牛日式燒肉適合辦尾牙嗎？ 如果你也和我一樣喜歡用味蕾探索一座城市，那就把這篇公益路美食攻略收藏起來吧。TANG Zhan 湯棧適合聚餐嗎？ 無論是約會、慶生、家庭聚餐，或只是想犒賞一下辛苦的自己——這條路上永遠會有一間剛剛好的餐廳在等你。一頭牛日式燒肉有提供尾牙方案嗎？ 下一餐，不妨從這10家開始。茶六燒肉堂口味偏臺式還是日式？ 打開手機、約上朋友，讓公益路成為你生活裡最容易抵達的小確幸。一笈壽司年末聚餐推薦嗎？ 如果你有私心愛店，也歡迎留言分享，NINI 尼尼臺中店適合多人分享嗎？ 你的推薦，可能讓我下一趟美食旅程變得更精彩。KoDō 和牛燒肉好吃嗎？ Scientists have introduced CluMPS, a novel molecular tool that simplifies the detection of tiny protein clusters implicated in diseases like Alzheimer’s. This technique allows for easy visualization with standard lab microscopes, overcoming the limitations of light microscopy and facilitating drug efficacy assessment and new treatment discoveries. The development of CluMPS, represents a significant step forward in understanding protein function and disease treatment. The bright white spots represent tiny clusters of proteins detected by CluMPS. Credit: Thomas R. Mumford Researchers bring the smallest protein clusters into focus. Penn Engineers have pioneered a new way to visualize the smallest protein clusters, skirting the physical limitations of light-powered microscopes and opening new avenues for detecting the proteins implicated in diseases like Alzheimer’s and testing new treatments. In a paper in Cell Systems, Lukasz Bugaj, Assistant Professor in Bioengineering, describes the creation of CluMPS, or Clusters Magnified by Phase Separation, a molecular tool that activates by forming conspicuous blobs in the presence of target protein clusters as small as just a few nanometers. In essence, CluMPS functions like an on/off switch that responds to the presence of clusters of the protein it is programmed to detect. Normally, says Bugaj, detecting such clusters requires laborious techniques. “With CluMPS, you don’t need anything beyond the standard lab microscope.” The tool fuses with the target protein to form condensates orders of magnitude larger than the protein clusters themselves that resemble the colorful blobs in a lava lamp. “We think the simplicity of the approach is one of its main benefits,” says Bugaj. “You don’t need specialized skills or equipment to quickly see whether there are small clusters in your cells.” Potential in Disease Treatment and Drug Discovery For treating diseases like Alzheimer’s, ALS, and even cancer, being able to detect protein clusters this small promises to be a foundational advancement, allowing researchers to determine whether or not drugs actually eliminate disease-causing clusters of a target protein in a cell. “You need a very clear signal,” says Bugaj, to know whether or not a treatment worked. “It’s very obvious when you have a gigantic cluster, but if you have small clusters, it is much harder. Now we can amplify that signal and see which drugs actually dissolve the clusters.” The red and cyan dots represent clusters of proteins detected by CluMPS. Credit: Thomas R. Mumford In addition to providing new avenues for drug discovery, CluMPS will permit researchers to understand the functioning of proteins in new ways, leading to a deeper, more sophisticated rendering of cells themselves. “There’s an entire landscape of protein clustering that’s happening at the small scale, that’s important, but we just don’t know about it yet,” says Bugaj. Overcoming Technical Challenges One of the challenges that CluMPS overcomes is that lightwaves themselves are larger than the smallest protein clusters, making it very hard to see such clusters without specialized techniques. “The wavelength of blue light is about 400 nanometers,” says Bugaj. “You can’t actually resolve the location of anything smaller than half that wavelength with a conventional microscope,” rendering protein clusters tens of nanometers wide all but invisible. To develop CluMPS, Bugaj, and his lab partnered with Elizabeth Rhoades, Professor of Chemistry at Penn Arts & Sciences, whose lab helped validate that CluMPS did indeed detect target protein clusters instead of generating false positives. “It was a really rewarding collaboration for us,” says Rhoades, “because it allowed us to apply the methods commonly used by our lab to help validate this powerful new tool in living cells. It was exciting to see how well we could differentiate between clusters and the single proteins.” Thomas R. Mumford, a doctoral student in the Bugaj Lab and the paper’s lead author, played a key role in brainstorming and performing the necessary experiments. “It was crucial to characterize how underlying features of protein clusters interacted with CluMPS to trigger condensation,” says Mumford, to enable future users of the technology to understand precisely how it works. “The burden was on us to demonstrate that we were in fact detecting small clusters,” adds Bugaj. “One of the most rewarding aspects was working with Tom and the Rhoades lab to think of new types of experiments that would convincingly make the point.” Reference: “Simple visualization of submicroscopic protein clusters with a phase-separation-based fluorescent reporter” by Thomas R. Mumford, Diarmid Rae, Emily Brackhahn, Abbas Idris, David Gonzalez-Martinez, Ayush Aditya Pal, Michael C. Chung, Juan Guan, Elizabeth Rhoades and Lukasz J. Bugaj, 8 February 2024, Cell Systems. DOI: 10.1016/j.cels.2024.01.005 This study was conducted at the University of Pennsylvania School of Engineering and Applied science and supported by grants from The National Institutes of Health awarded to Bugaj (R35GM138211) and to collaborator Juan Guan (R35GM146877). Additional co-authors include Diarmid Rae, Abbas Idris, David Gonzalez-Martinez and Ayush Aditya Pal at Penn Engineering; Emily Brackhahn at Penn; and Michael C. Chung and Juan Guan at the University of Florida. Green rhodopsin proteins inside the blue cell walls help these yeast grow faster when exposed to light. Credit: Anthony Burnetti, Georgia Institute of Technology Yeast is often known for its ability to ferment carbohydrates into products such as bread and beer, typically requiring a dark environment. Exposure to light in these situations can disrupt or spoil the fermentation process. However, a recent study published in Current Biology by researchers from the School of Biological Sciences at Georgia Tech presents a groundbreaking development: they have engineered one of the first strains of yeast that may be happier with the lights on. “We were frankly shocked by how simple it was to turn the yeast into phototrophs (organisms that can harness and use energy from light),” says Anthony Burnetti, a research scientist working in Associate Professor William Ratcliff’s laboratory and corresponding author of the study. “All we needed to do was move a single gene, and they grew 2% faster in the light than in the dark. Without any fine-tuning or careful coaxing, it just worked.” Easily equipping the yeast with such an evolutionarily important trait could mean big things for our understanding of how this trait originated — and how it can be used to study things like biofuel production, evolution, and cellular aging. Biology Ph.D. student Autumn Peterson, the study’s lead author, looks at yeast cells with Research Scientist Anthony Burnetti, the study’s corresponding author, in the lab. Credit: Audra Davidson, Georgia Institute of Technology Looking for an energy boost The research was inspired by the group’s past work investigating the evolution of multicellular life. The group published their first report on their Multicellularity Long-Term Evolution Experiment (MuLTEE) in Nature last year, uncovering how their single-celled model organism, “snowflake yeast,” was able to evolve multicellularity over 3,000 generations. Throughout these evolution experiments, one major limitation for multicellular evolution appeared: energy. “Oxygen has a hard time diffusing deep into tissues, and you get tissues without the ability to get energy as a result,” says Burnetti. “I was looking for ways to get around this oxygen-based energy limitation.” One way to give organisms an energy boost without using oxygen is through light. However, the ability to turn light into usable energy can be complicated from an evolutionary standpoint. For example, the molecular machinery that allows plants to use light for energy involves a host of genes and proteins that are hard to synthesize and transfer to other organisms — both in the lab and naturally through evolution. Luckily, plants are not the only organisms that can convert light to energy. Keeping it simple A simpler way for organisms to use light is with rhodopsins: proteins that can convert light into energy without additional cellular machinery. “Rhodopsins are found all over the tree of life and apparently are acquired by organisms obtaining genes from each other over evolutionary time,” says Autumn Peterson, a biology Ph.D. student working with Ratcliff and lead author of the study. This type of genetic exchange is called horizontal gene transfer and involves sharing genetic information between organisms that aren’t closely related. Horizontal gene transfer can cause seemingly big evolutionary jumps in a short time, like how bacteria are quickly able to develop resistance to certain antibiotics. This can happen with all kinds of genetic information and is particularly common with rhodopsin proteins. Georgia Tech biology researchers who worked on the study include (from left to right) School of Biological Sciences Assistant Professor William Ratcliff, Center for Microbial Dynamics and Infection grant writer Carina Baskett, biology Ph.D. student Autumn Peterson (lead author), and Research Scientist Anthony Burnetti (corresponding author). Credit: Audra Davidson, Georgia Institute of Technology “In the process of figuring out a way to get rhodopsins into multi-celled yeast,” explains Burnetti, “we found we could learn about horizontal transfer of rhodopsins that has occurred across evolution in the past by transferring it into regular, single-celled yeast where it has never been before.” To see if they could outfit a single-celled organism with solar-powered rhodopsin, researchers added a rhodopsin gene synthesized from a parasitic fungus to common baker’s yeast. This specific gene is coded for a form of rhodopsin that would be inserted into the cell’s vacuole, a part of the cell that, like mitochondria, can turn chemical gradients made by proteins like rhodopsin into energy. Equipped with vacuolar rhodopsin, the yeast grew roughly 2% faster when lit — a huge benefit in terms of evolution. “Here we have a single gene, and we’re just yanking it across contexts into a lineage that’s never been a phototroph before, and it just works,” says Burnetti. “This says that it really is that easy for this kind of a system, at least sometimes, to do its job in a new organism.” This simplicity provides key evolutionary insights and says a lot about “the ease with which rhodopsins have been able to spread across so many lineages and why that may be so,” explains Peterson, who Peterson recently received a Howard Hughes Medical Institute (HHMI) Gilliam Fellowship for her work. Carina Baskett, grant writer for Georgia Tech’s Center for Microbial Dynamics and Infection, also worked on the study. Because vacuolar function may contribute to cellular aging, the group has also initiated collaborations to study how rhodopsins may be able to reduce aging effects in the yeast. Other researchers are already starting to use similar new, solar-powered yeast to study advancing bioproduction, which could mark big improvements for things like synthesizing biofuels. Ratcliff and his group, however, are mostly keen to explore how this added benefit could impact the single-celled yeast’s journey to a multicellular organism. “We have this beautiful model system of simple multicellularity,” says Burnetti, referring to the long-running Multicellularity Long-Term Evolution Experiment (MuLTEE). “We want to give it phototrophy and see how it changes its evolution.” Reference: “Transforming yeast into a facultative photoheterotroph via expression of vacuolar rhodopsin” by Autumn Peterson, Carina Baskett, William C. Ratcliff and Anthony Burnetti, 12 January 2024, Current Biology. DOI: 10.1016/j.cub.2023.12.044 The study was funded by the National Science Foundation and the David and Lucile Packard Foundation. Proteins labeled with colored tags fill the main compartment — but not the nuclei (blue) — of human cervical cancer cells. Green cells contain the protein TRPV2, red cells contain STING, and yellow and orange cells contain a mixture of both. The proteins are part of a newly discovered DNA-protection pathway that potentially could be targeted to improve cancer therapies, according to researchers at Washington University School of Medicine in St. Louis. Credit: Lingzhen Kong/Washington University Researchers Uncover a Previously Unknown Method of Genome Protection During Replication The safeguarding of cellular genomes is of utmost importance as any damage can result in cancer or cell death. The genome, consisting of the complete set of DNA, is at its most vulnerable stage during replication prior to cell division. This makes the genomes of cancer cells, which undergo constant division, constantly in jeopardy. A new signaling pathway utilized by cells to protect their DNA during replication has been uncovered by researchers at Washington University School of Medicine. The findings, published in Molecular Cell, indicate that targeting this pathway could enhance the effectiveness of cancer treatments. “A cell that can’t protect its genome is going to die,” said senior author Zhongsheng You, Ph.D., a professor of cell biology & physiology. “This entire pathway we found exists to protect the genome so the cell can survive in the face of replication stress. By combining inhibitors of this pathway with chemotherapy drugs that target the DNA replication process, we potentially could make such drugs more effective.” Replication Stress and Its Role in Cancer Replication stress occurs when the cell’s DNA duplication machinery runs into problems copying the genome. Certain stretches of DNA are inherently difficult to copy, because they contain many repeated sequences. Factors that damage the DNA, such as radiation and toxic molecules, also cause replication stress, as does the activation of cancer-causing genes. Dozens of cancer drugs, including widely used medications such as cisplatin and doxorubicin, work by damaging the DNA and increasing replication stress. You studies how cells protect their genomes while they are being duplicated. Early in his career, he worked on the ATR-Chk1 genome-protection pathway — a pathway that controls the cell-division cycle and prevents stalled replication machinery from failing entirely and causing breaks in the DNA. For the past eight years, he and his team painstakingly have been piecing together another previously unknown genome-protection pathway. With this new study, the final piece of the puzzle has clicked into place. Unveiling the Exo1-Driven Defense Mechanism The process they discovered goes like this: When the DNA-duplicating machinery stalls, a protein called Exo1 that normally follows behind the machinery gets a little out of hand. Exo1’s job is to perform quality control by cutting out incorrectly copied pieces of DNA, but when the machinery stops moving forward, Exo1 starts snipping away haphazardly, cleaving off bits of DNA that then make their way out of the nucleus and into the main part of the cell. DNA is not found outside the nucleus under normal conditions, so its presence in the main part of the cell sets off an alarm. Upon encountering a fragment of DNA, a sensor molecule triggers a cascade of molecular events, including the release of the calcium ion from a cellular organelle known as the endoplasmic reticulum, which in turn shuts down Exo1, preventing it from dicing up the genome any further until the problem with the machinery can be fixed. This newest study describes the discovery of DNA fragments as the warning signal that sets off the whole genome-protection response. The study was led by first author Shan Li, Ph.D., as a postdoctoral researcher and then a staff scientist in You’s lab. Li is now an assistant professor at Zhejiang University School of Medicine in Hangzhou, China. Co-author Lingzhen Kong, a graduate student, also made important contributions to the study. Over the years, You and colleagues have identified eight protein factors involved in this genome-protection pathway. Most of them already have inhibitors under development that could be repurposed for cancer studies. Implications for Cancer Treatments “Now that we have the pathway, we want to know whether it can be targeted for cancer treatment,” You said. “Lung, ovarian, and breast cancer are intrinsically under replication stress. Other cancers are put under replication stress by chemotherapy drugs. This pathway protects cells from replication stress, so if we could block the pathway, it might improve patients’ response to cancer therapies.” Several of the proteins in this pathway also play a role in other critical biological processes, including immunity, metabolism, and autophagy, the process by which cells break down their own unwanted materials. “One of the most exciting things about this pathway is how it intersects with so many other pathways,” You said. “I’ve been focusing on cancer, but much of this could also apply to autoimmune diseases. Two of the proteins we identified have been linked to chronic activation of the immune response and autoimmune disease. We want to understand the relationship between this replication-stress response pathway and the innate immune response pathway. The work we do is very basic, and it is so exciting to connect the dots between these fundamental processes and see how they relate to human health and disease.” Reference: “Cytosolic DNA sensing by cGAS/STING promotes TRPV2-mediated Ca2+ release to protect stressed replication forks” by Shan Li, Lingzhen Kong, Ying Meng, Chen Cheng, Delphine Sangotokun Lemacon, Zheng Yang, Ke Tan, Abigael Cheruiyot, Zhimin Lu and Zhongsheng You, 24 January 2023, Molecular Cell. DOI: 10.1016/j.molcel.2022.12.034 RRG455KLJIEVEWWF |
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