A cancer drug that unlocks the anti-inflammatory power of the immune system could help to reduce the risk of future heart attacks,according to research part-funded by the British Heart Foundation.By repurposing an existing drug,researchers hope it could soon become part of routine treatment for patients after aheart attack.The findings will be presented at the European Society of Cardiology Congress in London by Dr Rouchelle Sriranjan,NIHR Clinical Lecturer in Cardiology at the University of Cambridge.High levels of inflammation in blood vessels are linked to an increased risk of heart disease and heart attacks.After aheart attack,the body’s immune response can aggravate existing inflammation,causing more harm and increasing risk even further.However,NICE guidelines don’t currently recommend the use of any anti-inflammatory drugs to reduce future risk.Now,a team of researchers,led by Dr Joseph Cheriyan from Cambridge University Hospitals NHS Foundation Trust,have found that low doses of an anti-inflammatory drug called aldesleukin,injected under the skin of patients after aheart attack,significantly reduces inflammation in arteries.The researchers are currently following up patients to investigate the longer-term impact of this fall in inflammation.To date,in the two and ahalf years after their treatment,there have been no major adverse cardiac events in the group that received aldesleukin,compared to seven in the group that received the placebo.Professor Ziad Mallat,BHF Professor of Cardiovascular Medicine at the University of Cambridge who developed the trial,said:“We associate inflammation with healing–an inbuilt response that protects us from infection and injury.But it’s now clear that inflammation is aculprit in many cardiovascular conditions.“Early signs from our ongoing trial suggest that people treated with aldesleukin may have better long-term outcomes,including fewer heart attacks.If these findings are repeated in alarger trial,we’re hopeful that aldesleukin could become part of routine care after aheart attack within five to 10 years.”Aldesleukin is already used to treat kidney cancer,as high doses stimulate the immune system to attack cancer cells.The Cambridge team previously found that doses one thousand times lower than those used in cancer treatment increased the number of regulatory Tcells–a type of anti-inflammatory white blood cell–in patients’blood compared to aplacebo.In the current trial at Addenbrooke‘s and Royal Papworth hospitals in Cambridge,60 patients admitted to hospital with aheart attack or unstable angina received either low dose aldesleukin or placebo.Patients received an injection once aday for the first five days,then once per week over the next seven weeks.Neither the participants nor their doctors knew whether they had received the drug or placebo.At the end of treatment,Positron Emission Tomography(PET)scans showed that inflammation in the artery involved in patients’heart attack or angina was significantly lower in the group treated with aldesleukin,compared to those who received the placebo.The anti-inflammatory effect of aldesleukin appeared even more striking in the most inflamed arteries,leading to alarger reduction in inflammation levels in these vessels and abigger difference between the two groups by the end of the study.Dr Sonya Babu-Narayan,Associate Medical Director at the British Heart Foundation and consultant cardiologist said:“Thanks to research,we have an array of effective treatments to help people avoid heart attacks and strokes and save lives.But,even after successful heart attack treatment,unwanted inflammation in the coronary arteries can remain,which can lead to life-threatening complications.“A treatment to reduce inflammation after aheart attack could be agame-changer.It would help doctors to interrupt the dangerous feedback loop that exacerbates inflammation and drives up risk.This research is an important step towards that treatment becoming areality.”The study was predominantly funded by the Medical Research Council,with significant support from the BHF and National Institute for Health and Care Research Cambridge Biomedical Research Centre(NIHR-BRC).Originally published by the British Heart Foundation. 查看详细>>

Bacterial cells can“remember”brief,temporary changes to their bodies and immediate surroundings,a new Northwestern University and University of Texas-Southwestern study has found.And,although these changes are not encoded in the cell’s genetics,the cell still passes memories of them to its offspring—for multiple generations.Not only does this discovery challenge long-held assumptions of how the simplest organisms transmit and inherit physical traits,it also could be leveraged for new medical applications.For example,researchers could circumvent antibiotic resistance by subtly tweaking apathogenic bacterium to render its offspring more sensitive to treatment for generations.The study was published today(Aug.28)in the journal Science Advances.“A central assumption in bacterial biology is that heritable physical characteristics are determined primarily by DNA,”said Northwestern’s Adilson Motter,the study’s senior author.“But,from the perspective of complex systems,we know that information also can be stored at the level of the network of regulatory relationships among genes.We wanted to explore whether there are characteristics transmitted from parents to offspring that are not encoded in DNA,but rather in the regulatory network itself.We found that temporary changes to gene regulation imprint lasting changes within the network that are passed on to the offspring.In other words,the echoes of changes affecting their parents persist in the regulatory network while the DNA remains unchanged.”Motter is the Charles E.and Emma H.Morrison Professor of Physics at Northwestern’s Weinberg College of Arts and Sciences and director of the Center for Network Dynamics.The study’s co-first authors are postdoctoral fellow Thomas Wytock and graduate student Yi Zhao,who are both members of Motter’s laboratory.The study also involves acollaboration with Kimberly Reynolds,a systems biologist at the University of Texas Southwestern Medical Center. 查看详细>>

轴手性羰基化合物不仅广泛存在于天然产物、生物活性分子、药物和材料中，也是一类具有优势结构的手性配体或有机催化剂，在不对称催化中具有广阔的应用前景。但是这类结构的合成往往需要繁琐的步骤，一定程度上限制了它们的进一步发展。尽管近年来不对称催化合成轴手性化合物的方法得到了空前发展，但通过不对称羰基化反应直接合成轴手性羰基化合物仍有待发展。催化羰基化反应是合成羰基化合物最高效的方法，自19世纪30年代首次实现以来，羰基化已经成为均相催化领域工业应用规模最大的反应，通过该技术每年生产超过千万吨大宗和精细化学品。相比之下，不对称羰基化反应的发展则相对滞后，主要存在以下挑战：（1）高压CO与手性配体竞争配位，削弱了配体的手性控制能力；（2）酰基金属物种的转化能垒高，且往往是反应的决速步，需要较高的温度；（3）产生的手性羰基化合物在反应体系中易消旋化。尽管如此，在过去的几十年里仍有许多不对称羰基化反应被开发出来，但底物范围大多局限于降冰片烯、苯乙烯、环丙烯等活化的烯烃，且反应主要构筑具有中心手性的羰基化合物，利用不对称羰基化反应合成轴手性羰基化合物的方法仍有待开发。近日，上海交通大学变革性分子前沿科学中心刘家旺课题组，利用手性钯催化剂，通过底物动态动力学不对称转化的策略，发展了外消旋联杂芳基三氟甲磺酸酯与CO以及胺类亲核试剂的不对称胺羰化反应，实现了轴手性酰胺的高效、高对映选择性合成。详细的机理研究表明：酰胺产物的杂环氮原子与NH结构之间的分子内氢键作用会加速产物的轴旋转，从而导致产物的对映选择性显著下降，而碳酸铯的使用破坏了这种分子内氢键，是反应取得高对映选择性的关键。此外，合成的部分酰胺产物可以直接作为手性三齿配体应用到铜催化的不对称自由基反应中，展示了其作为手性配体的应用潜力。 查看详细>>

024年8月7日，生研院汪方炜实验室在《美国国家科学院院刊》（PNAS）发表了题为Molecular mechanism and functional significance of Wapl interaction with the Cohesin complex的研究论文，揭示了黏连蛋白功能的重要调控机制。黏连蛋白（Cohesin）是一个在进化上高度保守的环状结构复合体，参与调控一系列基于DNA和染色质的重要生物学过程（图1）。黏连蛋白可以拓扑联结两个DNA分子，通过介导姐妹染色单体粘连（sister chromatid cohesion）调控染色体分离、DNA复制和同源重组DNA修复，进而维护基因组的稳定性。黏连蛋白还可以拓扑结合单个DNA分子，通过形成染色质环（chromatin loop）调控基因组三维构象和基因转录。黏连蛋白的突变常见于癌细胞中，与癌症等疾病的发生发展密切相关。024年8月7日，生研院汪方炜实验室在《美国国家科学院院刊》（PNAS）发表了题为Molecular mechanism and functional significance of Wapl interaction with the Cohesin complex的研究论文，揭示了黏连蛋白功能的重要调控机制。黏连蛋白（Cohesin）是一个在进化上高度保守的环状结构复合体，参与调控一系列基于DNA和染色质的重要生物学过程（图1）。黏连蛋白可以拓扑联结两个DNA分子，通过介导姐妹染色单体粘连（sister chromatid cohesion）调控染色体分离、DNA复制和同源重组DNA修复，进而维护基因组的稳定性。黏连蛋白还可以拓扑结合单个DNA分子，通过形成染色质环（chromatin loop）调控基因组三维构象和基因转录。黏连蛋白的突变常见于癌细胞中，与癌症等疾病的发生发展密切相关。本项研究利用一系列体内外蛋白互作实验，以及基于AlphaFold2的人工智能蛋白质结构分析，发现Wapl分别通过FGF基序和YNARHWN基序结合黏连蛋白核心亚基Scc1与SA2互作界面的不同区域（图3）。破坏FGF基序或YNARHWN基序与Scc1-SA2界面的结合，仅部分减弱Wapl与Scc1-SA2界面的结合，并部分削弱Wapl从染色体上移除黏连蛋白的能力。当FGF基序和YNARHWN基序被同时突变后，Wapl几乎不能结合黏连蛋白核心亚基，导致黏连蛋白异常紧密地结合DNA，进而阻碍有丝分裂期姐妹染色单体粘连的及时解除，造成染色体分离错误。此外，FGF基序和YNARHWN基序的叠加突变还会导致细胞分裂间期染色质异常凝缩，提示了基因组三维构象的改变。以上结果说明，Wapl通过两个独立的结构模块同时结合黏连蛋白核心亚基Scc1与SA2的互作界面，赋予Wapl从染色质上移除黏连蛋白的最大活性，从而确保了有丝分裂期染色体精确分离，以及分裂间期细胞中基因组的正常三维结构。有丝分裂期染色体着丝粒区的黏连蛋白不能被Wapl移除。那么，Wapl的活性在着丝粒区又是如何被拮抗的呢？先前的研究表明，Sgo1在保护着丝粒区黏连蛋白中发挥重要作用。本研究发现，类似于Wapl的FGF基序与Scc1-SA2的相互作用，Sgo1利用其YNF基序结合Scc1-SA2界面。当YNF基序被突变为不能结合Scc1-SA2界面的ANA后，Sgo1保护黏连蛋白的活性大幅下降。有意思的是，Sgo1的YNF基序只能与Wapl的FGF基序竞争结合Scc1-SA2界面，而不能与Wapl的YNARHWN基序竞争。以上结果提示，着丝粒区可能存在一个含有YNARHWN基序的蛋白，该蛋白与Sgo1以及内层动粒蛋白CENP-U（包含一个可以结合Scc1-SA2界面的FDF基序）协同作用，充分抑制了Wapl与着丝粒区黏连蛋白核心亚基的结合。综上所述，这项研究揭示了Wapl结合黏连蛋白复合体核心亚基的分子基础和功能，为受黏连蛋白调控的染色体行为和生物学功能研究提供了新的见解，并为黏连蛋白突变促进癌变的转化研究奠定了重要基础。 查看详细>>

中国科学技术大学高能核物理团队与兰州近代物理研究所合作，在RHIC-STAR国际合作重离子碰撞实验中首次发现了一种新反物质超核——反超氢-4核，这是迄今实验上发现的最重的反物质超核。研究成果以“Observation of the antimatter hypernucleus anti-hyperhydrogen-4”为题，于8月21日在线发表于《自然》杂志上。这是STAR实验继发现反超氚核、反氦4核以来在反物质探索领域的又一次重大突破。反物质和普通物质的不对称性是现代物理学的一个基本问题。我们生活的世界和现今的宇宙中为何绝大多数的物质都是正物质？这仍然是一个谜。1931年安德森正电子的发现证实了狄拉克方程反物质的猜想。此后科学家们相继发现了反质子、反中子，反氘核等等。越重结构越复杂的反物质，在自然界中的产率就越低，且呈指数下降，每增加一个反核子（质量数A+1），其产率就下降约1000倍，这导致在实验上发现发物质极其困难。人们猜想在宇宙“大爆炸”的初期，极端高温高密度的条件下，可能存在与正物质等量的反物质，但由于绝大多数正物质与反物质发生湮灭，并且随着宇宙膨胀温度降低，约百亿分之一的正物质存活下来，演变为现今的世界。运行在美国布鲁克海文国家实验室的相对论重离子加速器RHIC可以将两束重原子核（例如金核）加速到每核子100GeV的能量，并使其对撞，从而可以在碰撞瞬间产生几万亿度的高温火球，被人们称为“小爆炸”，以此模拟宇宙“大爆炸”初期的环境，为发现反物质创造了良好的条件。反超氢-4核由一个反质子、两个反中子和一个反Lambda超子组成。研究团队在相对论重离子加速器RHIC的STAR实验上，在66亿个重离子对撞事例中找到了约16个反超氢-4核，并首次测量了其寿命，发现与普通超氢-4核的寿命在误差范围内一致，进一步验证了正反物质在寿命这一内禀属性上的对称性。反超氢-4核是目前实验上观测到的最重的反物质超核。它的发现和性质研究，使人类在反物质及正反物质对称性的探索方面又迈出了重要一步。中国科大高能核物理团队张一飞教授、博士生李东升作为该论文的主要作者参与了相关物理分析，在发展基于卡尔曼滤波方法的粒子衰变拓扑重建关键技术、粒子重建效率计算方面作出了重要贡献。团队主导研制的基于MRPC技术的飞行时间探测器TOF，极大拓展了STAR实验上带电粒子的鉴别能力，也为此次反超氢-4核的发现提供了末态衰变产物鉴别的关键作用。值得一提的是，中国科大高能核物理团队在第一个反物质超核——反超氚的发现中也作出了重要贡献，相关成果发表SCIENCE,328(2010)5974上。相比反超氚，反超氢4仅仅多了一个反中子，实验上的寻找难度就增大了很多，又经十四年才得以发现。此外，近年来团队还在超氚核与超氢-4核的寿命测量中作出了重要工作，相关成果发表在Phys.Rev.Lett.128(2022)202301上。RHIC-STAR是基于美国布鲁克海文国家实验室相对论重离子对撞机（RHIC）上STAR实验的大型国际合作组，由来自14个国家74个单位的700多位科研人员组成。该项研究受到了国家自然科学基金委、科技部等单位的经费资助。 查看详细>>

While amosquito bite is often no more than atemporary bother,in many parts of the world it can be scary.One mosquito species,Aedes aegypti,spreads the viruses that cause over 100,000,000 cases of dengue,yellow fever,Zika and other diseases every year.Another,Anopheles gambiae,spreads the parasite that causes malaria.The World Health Organization estimates that malaria alone causes more than 400,000 deaths every year.Indeed,their capacity to transmit disease has earned mosquitoes the title of deadliest animal.Male mosquitoes are harmless,but females need blood for egg development.It’s no surprise that there’s over 100 years of rigorous research on how they find their hosts.Over that time,scientists have discovered there is no one single cue that these insects rely on.Instead,they integrate information from many different senses across various distances.A team led by researchers at UC Santa Barbara has added another sense to the mosquito’s documented repertoire:infrared detection.Infrared radiation from asource roughly the temperature of human skin doubled the insects’overall host-seeking behavior when combined with CO2 and human odor.The mosquitoes overwhelmingly navigated toward this infrared source while host seeking.The researchers also discovered where this infrared detector is located and how it works on amorphological and biochemical level.The results are detailed in the journal Nature.“The mosquito we study,Aedes aegypti,is exceptionally skilled at finding human hosts,”said co-lead author Nicolas DeBeaubien,a former graduate student and postdoctoral researcher at UCSB in Professor Craig Montell’s laboratory.“This work sheds new light on how they achieve this.” 查看详细>>

近日，中国科学技术大学地球和空间科学学院王文忠特任教授与多位学者合作，通过第一性原理计算与机器学习相结合的方法，发现位于地球核幔边界高速区域的超低速区是由超离子态铁氢化物形成，相关成果以“Superionic iron hydride shapes ultralow-velocity zones at Earth’s core–mantle boundary”为题通过直投方式发表在美国国家科学院院刊《Proceedings of the National Academy of Sciences》。地球核幔边界(CMB)是地球内部成分差异最大的边界层，是地核与地幔物质和能量交换的重要场所。近二十年的地震学研究发现，在CMB上方存在不同尺度的低速异常体，如位于非洲和太平洋板块下方的大型低剪切波速省(LLSVP)，以及位于LLSVP内部和周围的超低速区(ULVZ)。理解这些低速异常体的特征和成因对理解核幔边界的动力学演化过程具有重要意义。ULVZ通常有数百公里宽，数十公里厚，相比于周围地幔其具有明显的低波速和高密度特征，因此能够长期稳定在CMB。传统观点认为ULVZ的成因主要分为两种：温度异常和成分异常。对于温度较高的区域(如LLSVP内部)，部分熔融可能是ULVZ的主要成因。然而，最近的地震学研究发现，ULVZ不仅存在于低速区域，在一些高速区域(如俯冲板片附近或内部)也探测到了ULVZ，无法通过简单的部分熔融来解释，需要成分异常来解释。板片俯冲是将地表水输送到地球深部的重要途径。在下地幔底部，俯冲板片脱水与液态外核发生反应生成FeHx，且这种物质能够与下地幔的主要矿物相共存。然而，由于缺乏对FeHx的波速、密度、熔点等物理性质的约束，目前尚不清楚这一物质能否是形成ULVZ的潜在成因。研究团队采用“第一性原理计算+机器学习“的方法对FeHx在核幔边界条件下的稳定性和热弹性性质开展了研究。结果表明，在核幔边界的温压条件下，FeHx能够以超离子态的形式稳定存在(图1a)：Fe原子在其晶格平衡位置附近振动，类似于固体，而H原子能够像流体一样在晶格间扩散。由于扩散导致的剪切软化效应，超离子态FeHx具有极低的波速，其VP和VS分别比正常地幔低34%和63%，密度比正常地幔高50%（图1b），与ULVZ的地震学特征吻合，表明超离子态FeHx可能是ULVZ的一种重要成因，尤其能形成在高速区内形成的ULVZ。这种ULVZ的形成主要通过两种机制：一方面，俯冲板片深部脱水与铁核反应形成FeHx；另一方面，俯冲板片作为较冷区域能够促进液态外核中的FeHx析出(图2)。这一研究揭示了水在地球核幔边界产生速度异常结构方面发挥了重要作用。 查看详细>>

Fibrotic hypersensitivity pneumonitis is achronic and progressive interstitial lung disease,caused by an immune response to inhaled foreign antigens or allergens.Researchers from Yale’s Section of Pulmonary,Critical Care and Sleep Medicine have used single-cell sequencing technology to provide the first high-resolution atlas of this disease,revealing apreviously unrecognized immune signature.Their findings were recently published in the American Journal of Respiratory and Critical Care Medicine.Fibrotic hypersensitivity pneumonitis belongs to acategory of diseases known as pulmonary fibrosis,which is characterized by inflammation and irreversible scarring in the lungs.Other diseases under this umbrella include idiopathic pulmonary fibrosis,which is when scarring occurs in the lungs for an unknown reason.Clinically,fibrotic hypersensitivity pneumonitis and idiopathic pulmonary fibrosis are hard to distinguish.“Patients with these diseases can present very similarly,”says study lead author Amy Zhao,an MD/PhD(genetics)student in the Kaminski lab at Yale.“They may have similar symptoms and radiographic imaging,so patients will sometimes have to undergo further workup using invasive biopsies,and therapeutic decisions may be delayed.”Utilizing single-cell sequencing,a technology that allows measuring of all the genes expressed in every cell in asample,Zhao and the Kaminski lab team analyzed over 500,000 peripheral blood mononuclear cells in patients with both diseases,as well as healthy controls.In the blood of patients with fibrotic hypersensitivity pneumonitis,they identified previously unreported populations of immune cells with the capacity to kill other cells,known as cytotoxic Tcells.These cells carried aspecific subpopulation of granzymes,enzymes that cause cell death and were relatively restricted to patients with fibrotic hypersensitivity pneumonitis.Additionally,the team identified immune changes common to both ailments,including elevated classical monocytes in the blood.“These findings may be helpful in the future for guiding diagnosis,”says Zhao.“For example,if apatient has elevated levels of cytotoxic Tcells,it suggests more likely that they have fibrotic hypersensitivity pneumonitis over idiopathic pulmonary fibrosis,but of course,more studies are required.”While there are currently two FDA-approved drugs and multiple other therapeutic trials for idiopathic pulmonary fibrosis,treatment options for fibrotic hypersensitivity pneumonitis are dramatically understudied.The principal investigator of this study,Naftali Kaminski,MD,Boehringer-Ingelheim Pharmaceuticals Professor of Medicine(pulmonary)and section chief of pulmonary,critical care,and sleep medicine,hopes that this study will spark specific therapeutic interventions for fibrotic hypersensitivity pneumonitis.“There are very few clinical trials directly focused on fibrotic hypersensitivity pneumonitis,”says Kaminski.“Our current treatment paradigm involves antigen avoidance and immunosuppression,which are helpful during the acute or non-fibrotic phase,but inadequate during the fibrotic phase.Since immunity is still active during this phase,it’s unlikely that only anti-fibrotics will help.By studying the immune system in these patients,we could develop novel targets that potentially limit the immune system from actively participating in lung scarring and fibrosis.” 查看详细>>

the growth of healthy tissues in the body depends on the development of new blood vessels,a process called angiogenesis,that enable proper blood flow,meaning nutrients and oxygen are delivered while toxic metabolic products are removed.But solid tumors grow faster than healthy tissues,resulting in deficiencies in oxygen and blood flow,which leads to accelerated formation of dysfunctional blood vessels.Malignant cells rapidly grow while antitumor immune cells quickly lose their viability and function.These events,cell biologist Serge Fuchs of the School of Veterinary Medicine says,promote generation of the immunosuppressive tumor microenvironment,which stimulates the spread and growth of tumors and confers resistance to antitumor therapies.Past research has shown how native C-type natriuretic peptide(CNP),a 22-amino acid peptide produced by endothelial cells and fibroblasts,stimulates growth of normal blood vessels and restores proper blood flow and oxygenation within tissues of rodent limbs that weren’t getting enough blood flow.Given the importance of CNP in angiogenesis,researchers reasoned that CNP would also play acritical role in regulating tumor vasculature.But therapeutic potential of CNP is severely hampered by its short half-life of less than three minutes,says Zhen Lu,a former senior research investigator in Fuchs’lab.Fuchs and Lu are part of an interdisciplinary,collaborative team which found that modifying CNP stimulated the formation of blood vessels,increased blood flow through tissue,reinvigorated antitumor immune responses,and slowed growth of tumors in an animal model.The results published in the journal Science Translational Medicine suggest that the treatment could alleviate hypoxia,or insufficient oxygen levels,in tumors.The team includes researchers from Kyushu University,the Higashiosaka City Medical Center,the Case Western Reserve University School of Medicine,and PharmaIN Corp.“It is asuccessful approach to target the immunosuppressive tumor microenvironment,which should lead to abreakthrough in treatment of alarge variety of solid tumors,”says Fuchs,a corresponding author on the paper. 查看详细>>

“It’s never been clear why skin needs this many proteins and their complicated expression pattern just to provide mechanical strength.People have been very interested in what else these proteins might do,and we’re finally starting to get answers,”said first author Benjamin Nanes,M.D.,Ph.D.,Assistant Professor of Dermatology and in the Lyda Hill Department of Bioinformatics at UT Southwestern.Dr.Nanes led the study under the mentorship of Gaudenz Danuser,Ph.D.,Chair and Professor of Bioinformatics and Professor of Cell Biology,who served as the study’s senior author.Dr.Nanes explained that skin gets its mechanical strength from keratin intermediate filaments(KIFs),rope-like proteins that crisscross the interior of skin cells and form connections between cells.This family of proteins includes 54 members,which the cells produce in different combinations depending on circumstances.For example,when skin becomes wounded,it increases the abundance of KIFs known as K6A,K6B,K6C,K16,and K17 in higher proportions than other KIFs.However,because the skin’s strength remains roughly the same despite different circumstances,the need for so many different members in the KIF family and the way changes in their relative abundance affect processes like wound healing have been unclear.Scientists often study the roles of specific proteins by mutating or deleting the gene responsible for making them.However,Dr.Nanes said,studying KIFs using this strategy would just weaken skin,making it impossible to separate their role in providing mechanical strength from other possible jobs they have.To avoid this drawback,he and his colleagues genetically engineered two batches of skin cells:one made more of the wound-associated KIF K6A and another made more of aKIF associated with intact skin,known as K5.After allowing these cells to grow into skin organoids that formed layers typical of natural skin,the researchers compared how the cells in each of these organoids behaved.They found that the cells with higher K6A migrated more readily than cells with higher K5,allowing them to better close wounds generated in the skin organoids.However,cellular migration depends on different proteins called myosin motors that generate the forces needed for traction.The operation of myosin motors is not directly connected to KIFs.Investigating further,the team showed that the relative abundance of K6A changed the operation of amolecular switch that activates myosin;more K6A triggered more myosin to turn on,which prompted cells to roam.Less K6A prevented these motors from starting.Although it is not completely clear why K6A is able to switch on myosin more effectively,Dr.Danuser speculated that different KIFs might serve as venues where molecules involved in cellular control can congregate and form the complexes necessary to switch certain activities on or off. 查看详细>>