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 一頭牛日式燒肉員工聚會夠氣派嗎？》台中公益路餐廳排行榜｜10家熱門店家解析 |
| 興趣嗜好｜偶像追星 2026/04/22 10:58:30 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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： 茶六燒肉堂有雷嗎？ 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。茶六燒肉堂肉質如何？ 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。印月餐廳第一次來要點什麼？ 下一餐，不妨從這10家開始。加分100%浜中特選昆布鍋物甜點好吃嗎？ 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。茶六燒肉堂適合約會嗎？ 如果你有私心愛店，也歡迎留言分享，印月餐廳年節期間價格會變嗎？ 你的推薦，可能讓我下一趟美食旅程變得更精彩。KoDō 和牛燒肉節慶時段會不會太難訂位？ The study site in Puerto Morelos, Mexico (Caribbean Sea), where the researchers collected Siderastrea radians. Credit: Sergio Guendulain-García Researchers tease apart contributions of symbiotic bacteria and algae to corals’ heat tolerance and identify genes involved in stress response. The microbiomes of corals — which comprise bacteria, fungi, and viruses — play an important role in the ability of corals to tolerate rising ocean temperatures, according to new research led by Penn State. The team also identified several genes within certain corals and the symbiotic photosynthetic algae that live inside their tissues that may play a role in their response to heat stress. The findings could inform current coral reef conservation efforts, for example, by highlighting the potential benefits of amending coral reefs with microbes found to bolster corals’ heat-stress responses. “Prolonged exposure to heat can cause ‘bleaching’ in which photosymbionts (symbiotic algae) are jettisoned from the coral animal, causing the animal to die,” said Monica Medina, professor of biology, Penn State. “We found that when some corals become heat stressed, their microbiomes can protect them from bleaching. In addition, we can now pinpoint specific genes in coral animals and their photosymbionts that may be involved in this thermal stress response.” Orbicella faveolata, Puerto Morelos, Mexico (Caribbean Sea). Credit: Monica Medina, Penn State Viridiana Avila-Magaña, a former student at Penn State and currently a postdoctoral fellow at Colorado University Boulder, noted, “Previous studies on the molecular mechanisms underlying corals’ heat-stress tolerance have tended to focus on just the animal or the photosymbiont, but we now know that the entire holobiont — the coral animal, photosymbiont and microbiome — is involved in the stress response.” In their study, which published today (September 30, 2021) in Nature Communications, the researchers focused on three species of coral — the mountainous star coral (Orbicella faveolata), the knobby brain coral (Pseudodiploria clivosa) and the shallow water starlet coral (Siderastrea radians) — which are known to differ in their sensitivities to heat stress. Collected near Puerto Morelos, Mexico, each coral species harbors a unique set of photosymbionts and microbiomes. The team’s goal was to investigate the varying metabolic contributions of each of the holobiont members to the corals’ overall stress tolerance and to identify differences in gene-expression patterns related to these metabolic activities. Siderastrea radians, Puerto Morelos, Mexico (Caribbean Sea). Credit: Monica Medina, Penn State Medina explained that metabolism is the process of converting food into energy. For corals, she said, this process is heavily driven by the photosymbionts, which, through photosynthesis, provide the coral animals with at least 90% of their energy requirements. But, until now, the contributions of the microbiomes were not well understood. “We know that heat stress resulting from climate change can disrupt coral metabolism and result in bleaching,” said Medina. “Therefore, it is important to understand the different contributions of the holobiont members and how these metabolic activities change in response heat stress.” The researchers performed a controlled heat-stress experiment in which they maintained the three coral species in a tank for nine days at 93˚F (34 ˚C), which is 11 degrees (6 ˚C) warmer than the average temperature normally experienced by these corals. The scientists sequenced the RNA of the coral holobionts — including the coral animals, the photosymbionts, and the members of the microbiomes — after the nine-day period and a control group not exposed to the heat stress, with a goal of detecting changes in gene expression that affect the heat-stress response of the holobiont. Specifically, they used the gene expression data to estimate the metabolic activities of each of the holobiont members. Next, the team used a type of phylogenetic ANOVA technique, called the Expression Variance and Evolution Model, to examine changes in gene expression related to heat stress that have occurred over evolutionary time. “In collaboration with professor Rori Rohlfs from San Francisco State University, who is a coauthor in this study, we developed a method based on a phylogenetic ANOVA that allowed us to track genes that have already diverged in expression across species in response to any given stimuli — in our case heat stress,” said Viridiana Avila-Magaña. “This approach becomes particularly relevant for coral reef research given the recent debates on adaptive potential of different coral holobionts under the threats of climate change. With this approach in mind, we were able to understand why different corals have unique physiological responses to heat stress, and how the evolution of gene expression shaped their different susceptibilities.” Avila-Magaña explained that corals have experienced episodes of elevated temperatures through evolutionary time and understanding how gene expression has evolved in response to those events can inform corals’ responses to present-day and future warming events. “Our goal with this research was to determine if there have been lineage-specific innovations to heat stress in corals and their algal photosymbionts, as well as whether all members, including bacterial communities, differentially contribute to holobiont robustness,” she said. The gene-expression data revealed that the three coral holobionts did, indeed, differ in their responses and metabolic capabilities under high temperature stress. The team also found that the members of each holobiont had unique responses that influenced the holobiont’s overall ability to cope with thermal stress. “We have uncovered more genes associated with a thermal stress response in coral holobionts than previous studies, and we also show that changes in the expression of these genes arose over evolutionary time,” said Medina. Interestingly, the scientists concluded that the greater thermal tolerance observed in some coral holobionts, such as the starlet coral, may be due, in part, to a higher number and diversity of thermally tolerant microbes in their microbiomes, which provides redundancy in key metabolic pathways that are protective against heat stress. “We found that some corals harbor a stable and diverse microbiome translating to a vast array of metabolic capabilities that we have shown remain active during the thermal challenge,” said Avila-Magaña. “By contrast, we found that less thermally tolerant species had reduced bacterial activity and diversity.” Medina noted that the results stress the importance of comparative approaches across a wide range of species to better understand the diverse responses of corals to increasing sea surface temperatures. Medina and Avila-Magaña said, “Corals have been highly impacted by climate change, and the methods we developed in our study represent an excellent tool for scientists trying to understand the adaptive potential of populations and species.” Reference: “Elucidating gene expression adaptation of phylogenetically divergent coral holobionts under heat stress” by Viridiana Avila-Magaña, Bishoy Kamel, Michael DeSalvo, Kelly Gómez-Campo, Susana Enríquez, Hiroaki Kitano, Rori V. Rohlfs, Roberto Iglesias-Prieto and Mónica Medina, 30 September 2021, Nature Communications. DOI: 10.1038/s41467-021-25950-4 Other authors on the paper include Susana Enríquez, professor, Universidad Nacional Autónoma de México; Bishoy Kamel, research assistant professor of biology, University of New Mexico and the Joint Genome Institute, Michael DeSalvo, University of California Merced; Roberto Iglesias-Prieto, professor of biology, Penn State; Kelly Gómez-Campo, graduate student in biology, Penn State; Hiroaki Kitano, professor, Systems Biology Institute Japan; and Rori Rohlfs, assistant professor of biology, San Francisco State University. The National Science Foundation and the Joint Genome Institute (Department of Energy) supported this research. Researchers have identified fructose as a central factor in obesity, linking its function as a “survival switch” to weight gain and metabolic issues. The study shows fructose increases food intake, damages mitochondria, and can lead to diseases like diabetes and fatty liver disease New research suggests that fructose plays a pivotal role in obesity by lowering energy metabolism and increasing fat storage, similar to how animals prepare for hibernation. University of Colorado Anschutz Medical Campus researchers have officially identified a central conduit to obesity: fructose. While fructose’s contribution to obesity is well-known, a study recently published in Philosophical Transactions aggregates a large amount of work to make a full argument for how fructose drives obesity and diseases such as diabetes and fatty liver disease. “This is an in-depth review on a hypothesis that puts nature at the center of weight gain, examining how fructose works differently than other nutrients by lowering active energy,” says Richard Johnson, MD, professor at the University of Colorado School of Medicine and study lead author. “We determine a recently discovered function of fructose in survival that stores fuel in case resources become scarce. This is known as the ‘survival switch,’” he says. Fructose is the source of sweetness in fruit but is primarily consumed in Western society as table sugar and high fructose corn syrup, much different than the nutrition ingested by our ancestors ahead of lean winter months. Johnson and researchers posited that fructose works differently than other nutrients by lowering active energy, and damaging mitochondria. Fructose’s Impact on Energy and Metabolism Study results show that fructose stimulates food intake and lowers resting energy metabolism, much like an animal preparing to hibernate. Further, results show that the administration of fructose can lead to weight gain, insulin resistance, elevated blood pressure, and fatty liver among a host of other metabolic-related issues. “This work puts together in one place the full argument for how a particular carbohydrate, fructose, might have a central role in driving obesity and diabetes,” says Johnson. “This is a very exciting, new hypothesis that unites other hypotheses to point to the specific role fructose plays in the onset of obesity. And we can trace it back to our ancestors, as well as learn from hibernating animals, exactly how fructose causes this ‘switch’ within us.” Reference: “The fructose survival hypothesis for obesity” by Richard J. Johnson, Miguel A. Lanaspa, L. Gabriela Sanchez-Lozada, Dean Tolan, Takahiko Nakagawa, Takuji Ishimoto, Ana Andres-Hernando, Bernardo Rodriguez-Iturbe and Peter Stenvinkel, 24 July 2023, Philosophical Transactions of the Royal Society B Biological Sciences. DOI: 10.1098/rstb.2022.0230 An international team has identified the structures and crucial functions of FLVCR1 and FLVCR2 proteins, which transport key molecules affecting cellular health. This research enhances understanding of rare genetic disorders linked to these proteins and opens avenues for new therapeutic developments. FLVCR proteins (green, blue) sitting in the cellular membrane (purple). These proteins transport the cellular building blocks ethanolamine and choline across the membrane. Credit: Ella Maru Studio The dynamic structure of FLVCR proteins and their role in nutrient transport within our cells have been revealed. It is known that malfunctions of the proteins FLVCR1 and FLVCR2 lead to rare hereditary diseases in humans that cause motor, sensory and neurological disorders. However, the biochemical mechanisms behind this and the physiological functions of the FLVCR proteins have been unclear to date. An interdisciplinary team of researchers from Frankfurt am Main, Singapore and the USA has now deciphered the FLVCR proteins’ 3D structures and their cellular functions. The researchers have shown that the proteins transport the cellular building blocks choline and ethanolamine. Their findings contribute significantly to understanding the pathogenesis of rare diseases and developing new therapies. In hospital TV series such as Scrubs or Dr. House, medical doctors search for correct diagnoses and possible treatments for patients with sometimes puzzling or strange symptoms. In reality, this process often takes years for those affected by rare diseases. In many cases, there is no effective medication and therapeutic options are limited. Approximately 6-8% of the world’s population suffers from a rare disease. That’s around 500 million people, even though each of the over 7000 different diseases only affects around one in 2000 people. Since these diseases are so rare, medical and scientific knowledge about them is limited. There are only a few experts worldwide and social awareness is lacking. Unraveling the structure and function of proteins to understand diseases and develop therapies An international team of researchers led by Schara Safarian, project group leader at the Max Planck Institute of Biophysics as well as independent group leader at the Fraunhofer Institute for Translational Medicine and Pharmacology ITMP, and the Institute of Clinical Pharmacology at Goethe University Frankfurt, has now investigated the structure and cellular function of two proteins, FLVCR1 and FLVCR2, which play a causal role in a number of rare hereditary diseases. The scientists have published their findings in the prestigious journal Nature. Malfunctions of FLVCR1 and FLVCR2 due to gene mutations cause rare diseases, some of which result in severe visual, mobility, and sensory disorders – such as posterior column ataxia with retinitis pigmentosa, Fowler’s syndrome or sensory and autonomic neuropathies. The latter can, for example, lead to a complete loss of pain sensation. “In many diseases, including the rare ones, cellular structures in our body are altered and this leads to malfunctions in biochemical processes,” says Schara Safarian. “In order to understand the development of such diseases and develop therapies, we need to know how these proteins are structured at the molecular level and what functions they perform in healthy cells.” FLVCR1 and FLVCR2 transport the cellular building blocks choline and ethanolamine The scientists have discovered that FLVCR 1 and FLVCR2 transport the molecules choline and ethanolamine across the membranes of our cells. “Choline and ethanolamine are essential for important bodily functions. They support the growth, regeneration, and stability of our cells, for example in muscles, internal organs, and the brain,” explains Safarian. “Furthermore, choline is involved in fat metabolism and detoxification by the liver. Our body also needs it to produce the neurotransmitter acetylcholine which is crucial for our nervous system and is needed by our brain to control the organs. So, you can imagine that malfunctions of the FLVCR proteins can cause severe neurological and muscular disorders.” The researchers used microscopic, biochemical, and computer-assisted methods to investigate the FLVCR proteins. “We shock-froze the proteins and then observed them under an electron microscope,” explains Di Wu, a researcher at the Max Planck Institute of Biophysics and co-author of the study. “An electron beam penetrates the frozen sample and the interaction of the electrons with the material creates an image.” The researchers take many individual images and process them and combine them computationally to obtain high-resolution 3D structures of proteins. In this way, they were able to decipher the structures of FLVCR1 and FLVCR2 and see how they change in the presence of ethanolamine and choline. Computer simulations confirmed and visualized how the FLVCR proteins interact with ethanolamine and choline, and dynamically change their structure to enable nutrient transport. Safarian summarizes: “Our findings pave the way for understanding the development and progression of rare diseases associated with the FLVCR proteins. In the future, patients may be able to benefit from new therapies that restore their life quality.” Reference: “Molecular mechanism of choline and ethanolamine transport in humans” by Keiken Ri, Tsai-Hsuan Weng, Ainara Claveras Cabezudo, Wiebke Jösting, Yu Zhang, Andre Bazzone, Nancy C. P. Leong, Sonja Welsch, Raymond T. Doty, Gonca Gursu, Tiffany Jia Ying Lim, Sarah Luise Schmidt, Janis L. Abkowitz, Gerhard Hummer, Di Wu, Long N. Nguyen and Schara Safarian, 22 May 2024, Nature. DOI: 10.1038/s41586-024-07444-7 RRG455KLJIEVEWWF |
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