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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: NINI 尼尼臺中店團體宴客合適嗎? 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。KoDō 和牛燒肉春節期間適合來嗎? 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。一笈壽司公司聚餐適合嗎? 下一餐,不妨從這10家開始。TANG Zhan 湯棧年節期間價格會變嗎? 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。三希樓值得推薦嗎? 如果你有私心愛店,也歡迎留言分享,印月餐廳整體體驗如何? 你的推薦,可能讓我下一趟美食旅程變得更精彩。一頭牛日式燒肉份量足夠嗎? Mitochondrial DNA (mtDNA), inherited only from the mother, contains 16,569 nucleotides that can mutate. Some mutations can cause mitochondrial diseases. Researchers found that mutant mtDNA buildup in eggs leads to mitochondrial disease transmission, suggesting new prevention strategies A research article published in the journal Science Advances describes a mechanism that helps explain how certain kinds of genetic disorders known as mitochondrial diseases are transmitted from mother to child. The study it reports could serve as the basis for novel strategies to ensure that future generations are not affected by such diseases. Existing treatments are palliative, aimed at improving quality of life for the patient or delaying progression of the disease. The Role of Mitochondria and mtDNA Mutations Mitochondria are organelles that generate most of the chemical energy needed by cells. Mitochondrial DNA (mtDNA) contains 16,569 nucleotides subject to mutation. Some of these mutations can lead to the development of mitochondrial diseases. Whereas nuclear DNA (the famous double helix, which encodes most of the genome) is inherited from both parents, mtDNA is inherited solely from the mother. At birth, a female infant’s ovaries already contain all the eggs she will ever have. During the reproductive cycles that begin at puberty, some of these immature eggs develop under the influence of hormones, leading to ovulation and potentially to fertilization. Immature mouse egg at a stage prior to ovulation, with mitochondria stained red. Credit: Marcos Roberto Chiaratti The study shows for the first time that mutant mtDNA builds up in the final stages of egg formation. The researchers conducted experiments in mice, reporting that the proportion of mutant molecules increased as the eggs matured, that these mutants can impair the functioning of mitochondria, and that they are responsible for the development of disease. At most 90% of the mtDNA was subject to mutation, the researchers discovered. The existence of an upper limit is important to an understanding of how mutant mtDNA is transmitted and can cause disease. Mechanisms of Mutant mtDNA Transmission When mutant and wild-type mtDNA coexist in a cell (heteroplasmy), the effects of mutant mtDNA may be masked, facilitating transmission to offspring. “Until now, no one knew if this buildup occurred, but our study proved it does. Now that we understand where and how it occurs, it’s possible to work out ways of avoiding it,” said Marcos Roberto Chiaratti, a professor in the Department of Genetics and Evolution at the Federal University of São Carlos (UFSCar) in the state of São Paulo, Brazil. Chiaratti and graduate student Carolina Habermann Macabelli are among the authors of the article. The study was supported by FAPESP via two projects (17/04372-0 and 16/07868-4). Chiaratti also received a Newton Advanced Fellowship from the UK’s Academy of Medical Sciences. He collaborates with the group led by Patrick Francis Chinnery, last author of the article. Chinnery is Professor of Neurology at the University of Cambridge, and Wellcome Trust Principal Research Fellow for its MRC Mitochondrial Biology Unit. “The most effective treatment entails identifying the mutation in the mother in order to prevent inheritance by the children. This is the context for our research, which aims to verify which mutations are transmitted and analyze the mechanism involved. The study of mitochondrial disease in Brazil is still very incipient,” Chiaratti said. Symptoms and Prevalence of Mitochondrial Disease The symptoms of mitochondrial disease vary according to the mutation, the number of damaged cells, and the tissue affected. The most common include weak muscles, loss of motor coordination, cognitive impairment, brain degeneration, and kidney or heart failure. Such hereditary metabolic diseases can appear at any age, but the earlier the mutation manifests itself, the more likely it is to lead to severe symptoms and even death. Diagnosis is difficult, typically requiring genetic and molecular testing, and statistics on prevalence are therefore deficient. According to estimates, diseases caused by mtDNA mutations affect at least one in every 5,000 people worldwide. However, the frequency of pathogenic mtDNA mutations is about one in 200. The mutation m.3243A>G, which causes MELAS syndrome (Mitochondrial Encephalopathy, Lactic Acidosis, and Stroke-like episodes), occurs in some 80% of adults with pathogenic heteroplasmic mutations. The researchers studied genetically modified mice with two types of mitochondrial genome: the wild type, which does not cause disease, and the pathogenic mutation m.5024C>T, similar to m.5650G>A, a pathogenic mutation present in humans. Analysis of 1,167 mother-pup pairs detected a strong tendency for females with low levels of m.5024C>T to transmit higher levels of the mutation to their offspring. In females with high levels of the mutation, however, the opposite tendency was detected, pointing to purifying selection against high levels of the mutation (over 90%). Analysis of Heteroplasmy and Positive Selection Analysis of mouse oocytes (immature eggs) at different stages of development showed rising levels of m.5024C>T over wild-type mtDNA. This suggests mutant mtDNA is preferentially replicated during oocyte maturation, regardless of the cellular cycle, as eggs do not undergo cell division until ovulation. The researchers tested several mathematical models, and the one that best explained the phenomenon pointed to a replicative advantage favoring mutant mtDNA and purifying selection that prevents the mutation from reaching high levels. They first measured heteroplasmy in 42 females and 1,167 descendants. Next, they measured levels of mutant mtDNA in eggs at different stages of development and compared them with levels of mutation in different organs at different ages. They found evidence that the results applied to mice bearing another pathogenic mutation (m.3875delC tRNA) and to humans, as indicated by analysis of 236 mother-child pairs. This pointed to positive selection when the mutation was transmitted from mothers with low heteroplasmy levels and purifying selection against high heteroplasmy levels (over 90%). They concluded that positive selection resulted from a preference for replication of the mutant over the wild-type molecule. “This preferential replication enabled the level of mutation to reach the 90% ceiling, above which the negative effect of mutations is too great and other mechanisms appear to act on the egg to prevent them from reaching 100%,” Chiaratti said. He plans to travel to the UK soon to conduct new experiments. A possible next step would be to proceed to the pharmacological treatment stage with the aim of combating levels of mtDNA mutation so as to prevent transmission of disease. “Once we understand how the buildup in mutations leading to mitochondrial disease occurs during the final stage of egg formation, we’re in a position to produce eggs in vitro and manipulate them, pharmacologically as well as genetically, in order to reduce mutation levels, lowering the probability that a child will develop the disease,” he said. Reference: “Mitochondrial DNA heteroplasmy is modulated during oocyte development propagating mutation transmission” by Haixin Zhang, Marco Esposito, Mikael G. Pezet, Juvid Aryaman, Wei Wei, Florian Klimm, Claudia Calabrese, Stephen P. Burr, Carolina H. Macabelli, Carlo Viscomi, Mitinori Saitou, Marcos R. Chiaratti, James B. Stewart, Nick Jones and Patrick F. Chinnery, 8 December 2021, Science Advances. DOI: 10.1126/sciadv.abi5657 In the future, the researchers hope to identify the common targets of the cold and hot circuits in order to learn how each might impact sleep. A Study on Fruit Flies Revealed a Brain Circuit That Promotes Midday Napping on Hot Days You might find yourself falling asleep in the middle of the day on the hottest summer days. It’s customary to arrange “siestas” and close shops at the hottest times of the day in some parts of the world. In fact, biology—not just culture—might be the cause of this. Human behavior is impacted by temperature across the board, including eating and activity levels as well as sleep-wake cycles. In the summer, we may have trouble falling asleep, and in the winter, we might take longer to get out of bed. However, the relationship between sensory neurons and the neurons that control this cycle is not well known. Neurobiologists at Northwestern University have uncovered a few hints as to what is going on. According to a new study that was just published in Current Biology, fruit flies are biologically programmed to nap in the middle of the day. The new paper, which is a follow-up to their 2020 Biology publication that discovered a brain thermometer that is exclusively active in cold conditions, investigates a similar “thermometer” circuit for hot temperatures. Flies are pre-programmed to take a midday siesta. Credit: Gallio Lab/Northwestern University “Changes in temperature have a strong effect on behavior in both humans and animals, and offer animals a cue that is time to adapt to the changing seasons,” said Marco Gallio, associate professor of neurobiology at the Weinberg College of Arts and Sciences. “The effect of temperature on sleep can be quite extreme, with some animals deciding to sleep off an entire season — think of a hibernating bear — but the specific brain circuits that mediate the interaction between temperature and sleep centers remain largely unmapped.” The study’s lead author, Gallio, noted that fruit flies are a particularly useful model for investigating important questions like “why do we sleep” and “what does sleep do for the brain” because they don’t try to disrupt instinct in the same way that people do, for instance when they stay up all night studying. They also make it possible for researchers to investigate how biological pathways are influenced by external cues like light and temperature. Cells That Stay on Longer The paper is the first to identify “absolute heat” receptors in fly heads, which respond to temperatures above about 77 degrees Fahrenheit — the fly’s favorite temperature. As it turns out, the common laboratory fruit fly (Drosophila) has colonized nearly the entire planet by forming a close association with humans. Not surprisingly, its favorite temperature also matches that of many humans. Just as they expected based on the results of their previous paper on cold temperature, researchers found that brain neurons receiving information about heat are part of the broader system that regulates sleep. When the hot circuit, which runs parallel to the cold circuit, is active, the target cells that promote midday sleep stay on longer. This results in an increase in midday sleep that keeps flies away from the hottest part of the day. The study was enabled by a 10-year initiative that produced the first completed map of neural connections in an animal (a fly), called the connectome. With the connectome, researchers have access to a computer system that tells them all possible brain connections for each of the fly’s ~100,000 brain cells. However, even with this extremely detailed road map, researchers still need to figure out how information in the brain goes from point A to B. This paper helps fill that gap. The different circuits for hot versus cold temperatures make sense to Gallio because “hot and cold temperatures can have quite different effects on physiology and behavior,” he said. This separation may also reflect evolutionary processes based on the heat and cold cycles of the Earth. For example, the possibility that brain centers for sleep may be directly targeted in humans by a specific sensory circuit is now open to be investigated based on this work. Next Steps Next, Gallio’s team hopes to figure out the common targets of the cold and hot circuit, to discover how each can influence sleep. “We identified one neuron that could be a site of integration for the effects of hot and cold temperatures on sleep and activity in Drosophila,” said Michael Alpert, the paper’s first author and a post-doctoral researcher in the Gallio lab. “This would be the start of interesting follow-up studies.” Gallio added that the team is interested in looking at the long-term effects of temperature on behavior and physiology to understand the impact of global warming, looking at how adaptable species are to change. “People may choose to take an afternoon nap on a hot day, and in some parts of the world this is a cultural norm, but what do you choose and what is programmed into you?” Gallio said. “Of course, it’s not culture in flies, so there actually might be a very strong underlying biological mechanism that is overlooked in humans.” Reference: “A thermometer circuit for hot temperature adjusts Drosophila behavior to persistent heat” by Michael H. Alpert, Hamin Gil, Alessia Para and Marco Gallio, 17 August 2022, Current Biology. DOI: 10.1016/j.cub.2022.07.060 The study was funded by the National Institutes of Health. The contracted and extended states of Spirostomum cells. Chinese scientists have discovered the molecular basis for the ultrafast contraction of Spirostomum, a genus of millimeter-scale single-celled protists known for their incredibly rapid movement, using a high-quality genome obtained from RNAi. Credit: Image by IHB Scientists have discovered the molecular basis for the ultrafast contraction of Spirostomum, a genus of millimeter-scale single-celled protists known for their incredibly rapid movement. Using a high-quality genome obtained from RNAi, the researchers found that the contractile structure, a mesh-like contractile fibrillar system, was composed of two giant proteins and two Ca2+ binding proteins. This study is significant for understanding the molecular mechanism of ultrafast cell contraction and provides a blueprint for the design and construction of ultrafast contractile micromachines. In his famous letter to the Royal Society dated October 9, 1676, Antonie van Leeuwenhoek described a single-celled eukaryote (Vorticella) and its fascinating ultrafast cell contraction as the first set of discoveries. This kind of ultrafast cell contraction triggered by a Ca2+-dependent mechanism is distinct from the adenosine triphosphate (ATP)-dependent mechanisms found in actin-myosin and dynein/kinesin-tubulin systems. Spirostomum, is a genus of millimeter-scale single-celled protists that are known for their incredibly rapid movement like Vorticella. They are capable of some of the fastest movement in the biological world due to their ultrafast contraction. Despite much research, however, the molecular mechanism behind this type of ultrafast cell contraction has long been a mystery. Recently, a research group led by Prof. MIAO Wei from the Institute of Hydrobiology (IHB) of the Chinese Academy of Sciences has unlocked this mystery by describing the molecular basis behind the ultrafast contraction of Spirostomum. The team’s research was published in Science Advances. In this study, the researchers obtained a high-quality genome of Spirostomum using a genome assembly pipeline they had previously established. They found that the contractile structure, a mesh-like contractile fibrillar system, was composed of two giant proteins and two Ca2+ binding proteins. Using RNAi, they validated the functions of the giant proteins. Super-resolution imaging showed that the mesh-like contractile fibrillar system couples with the microtube cytoskeleton, mitochondria and endoplasmic reticulum (ER) and fits well with the biological and physical need for repetitive ultrafast contraction and extension of the Spirostomum cell. “Actually, our research offers a valuable reference for investigating non-model protists, covering aspects from the genome to molecular studies,” said Prof. MIAO. This study is highly significant for understanding the molecular mechanism of ultrafast cell contraction and provides a good blueprint for the biomimicry, design, and construction of ultrafast contractile micromachines. Reference: “Giant proteins in a giant cell: Molecular basis of ultrafast Ca2+-dependent cell contraction” by Jing Zhang, Weiwei Qin, Che Hu, Siyu Gu, Xiaocui Chai, Mingkun Yang, Fang Zhou, Xueyan Wang, Kai Chen, Guanxiong Yan, Guangying Wang, Chuanqi Jiang, Alan Warren, Jie Xiong and Wei Miao, 22 February 2023, Science Advances. DOI: 10.1126/sciadv.add6550 RRG455KLJIEVEWWF |
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