更新于：2024-05-01

S100B

S100 calcium binding protein B

更新于：2024-05-01

基本信息

别名

Protein S100-B、S-100 protein beta chain、S-100 protein subunit beta

+ [4]

简介

Small zinc- and- and calcium-binding protein that is highly expressed in astrocytes and constitutes one of the most abundant soluble proteins in brain (PubMed:6487634, PubMed:20950652). Weakly binds calcium but binds zinc very tightly-distinct binding sites with different affinities exist for both ions on each monomer (PubMed:6487634, PubMed:20950652). Physiological concentrations of potassium ion antagonize the binding of both divalent cations, especially affecting high-affinity calcium-binding sites (By similarity). Acts as a neurotrophic factor that promotes astrocytosis and axonal proliferation (By similarity). Involved in innervation of thermogenic adipose tissue by acting as an adipocyte-derived neurotrophic factor that promotes sympathetic innervation of adipose tissue (By similarity). Binds to and initiates the activation of STK38 by releasing autoinhibitory intramolecular interactions within the kinase (By similarity). Interaction with AGER after myocardial infarction may play a role in myocyte apoptosis by activating ERK1/2 and p53/TP53 signaling (By similarity). Could assist ATAD3A cytoplasmic processing, preventing aggregation and favoring mitochondrial localization (PubMed:20351179). May mediate calcium-dependent regulation on many physiological processes by interacting with other proteins, such as TPR-containing proteins, and modulating their activity (PubMed:22399290).

关联

100 项与 S100B 相关的临床结果

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0 项与 S100B 相关的专利（医药）

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4,529

项与 S100B 相关的文献（医药）

2024-12-01·Pharmaceutical biology

Berberine decreases S100B generation to regulate gut vascular barrier permeability in mice with burn injury.

Article

作者: Aiwen Feng ; Shaosheng Su ; Cheng Li ; Yutian Kang ; Jiasheng Qiu ; Jun Zhou

Context: Berberine (BBR) can regulate enteric glial cells (EGCs) and the gut vascular barrier (GVB).Objective: To explore whether BBR regulates GVB permeability via the S100B pathway.Materials and methods: GVB hyperpermeability in C57BL/6J mice was induced by burns or S100B enema. BBR (25 or 50 mg/kg/d, 3 d) was gavaged preburn. S100B monoclonal antibody (S100BmAb) was i.v. injected postburn. Mouse intestinal microvascular endothelial cells (MIMECs) were treated with S100B, S100B plus BBR, or Z-IETD-FMK. GVB permeability was assayed by FITC-dextran, S100B by ELISA, caspase-8, β-catenin, occludin and PV-1 by immunoblot.Results: Burns elevated S100B in serum and in colonic mucosa to a peak (147.00 ± 4.95 ng/mL and 160.30 ± 8.50 ng/mg, respectively) at 36 h postburn, but BBR decreased burns-induced S100B in serum (126.20 ± 6.30 or 90.60 ± 3.78 ng/mL) and in mucosa (125.80 ± 12.40 or 91.20 ± 8.54 ng/mg). Burns raised GVB permeability (serum FITC-dextran 111.40 ± 8.56 pg/mL) at 48 h postburn, but BBR reduced GVB permeability (serum FITC-dextran 89.20 ± 6.98 or 68.60 ± 5.50 ng/mL). S100B enema (1 μM) aggravated burns-raised GVB permeability (142.80 ± 8.07 pg/mL) and PV-1, but the effect of S100B was antagonized by BBR. Z-IETD-FMK (5 μM) increased S100B-induced permeability to FITC-dextran (205.80 ± 9.70 to 263.80 ± 11.04 AUs) while reducing β-catenin in MIMECs. BBR (5 μM) reduced S100B-induced permeability (104.20 ± 9.65 AUs) and increased caspase-8, β-catenin and occludin.Discussion and conclusion: BBR decreases burns-induced GVB hyperpermeability via modulating S100B/caspase-8/β-catenin pathway and may involve EGCs.

2024-02-23·Artificial organs

Selective brain perfusion improves the neurological outcomes after extracorporeal cardiopulmonary resuscitation in a rat model.

Article

作者: Ru-Wen Chang ; Man-Chen Hsu ; Tzong-Shyuan Lee ; Yih-Sharng Chen ; Chih-Hsien Wang

BACKGROUND:

The major concern in patients who have suffered from cardiac arrest (CA) and undergone successful extracorporeal cardiopulmonary resuscitation (E-CPR) is poor neurological outcomes. In this study, we aimed to introduce a rat model of selective brain perfusion (SBP) during E-CPR to improve the neurological outcome after CA.

METHODS:

The rats underwent 7 min of untreated asphyxial CA and then were resuscitated with E-CPR for 30 min. The right external jugular vein and right femoral artery were separately cannulated to the E-CPR outflow and inflow. The right common carotid artery was cannulated from the proximal to the distal side for SBP. Subsequently, rats were removed from E-CPR, wounds were closed, and 90 min of intensive care were provided. Neurological deficit scores were tested after 4 h of recovery when the rats were mechanical ventilation-free. S100 calcium-binding protein B (S100B) and glial fibrillary acidic protein (GFAP) were detected through immunohistochemistry (IHC) of brain tissue.

RESULTS:

The rats that received SBP while resuscitated by E-CPR showed markedly better neurological performances after 4-h recovery than those resuscitated by E-CPR only. The IHC staining of GFAP and S100B in the hippocampus was low in the rats receiving SBP during E-CPR, but only GFAP showed significant differences.

CONCLUSIONS:

We successfully developed a novel and reproducible rat model of SBP while resuscitated by E-CPR to ameliorate the neurological performances after CA. This achievement might have opportunities for studying how to improve the neurological outcome in the clinical condition.

2024-02-22·Current medical research and opinion

Combining biomarkers of BNIP3 L, S100B, NSE and accessible measures to prediction sepsis-associated encephalopathy: a prospective observational study.

Article

作者: Nannan Zhang ; Keliang Xie ; Fei Yang ; Yunying Wang ; Xinhao Yang ; Lina Zhao

BACKGROUND:

Accurate identification of delirium in sepsis patients is crucial for guiding clinical diagnosis and treatment. However, there are no accurate biomarkers and indicators at present. We aimed to identify which combinations of cognitive impairment-related biomarkers and other easily accessible assessments best predict delirium in sepsis patients.

METHODS:

101 sepsis patients were enrolled in a prospective study cohort. S100B, NSE, and BNIP3 L biomarkers were detected in plasma and cerebrospinal fluid and patients' optic nerve sheath diameter (ONSD). The optimal biomarkers identified by Logistic regression are combined with other factors such as ONSD to filter out the perfect model to predict delirium in sepsis patients through Logistic regression, Naïve Bayes, decision tree, and neural network models.

MAIN RESULTS:

Among all biomarkers, compared with BNIP3 L (AUC 0.706, 95% CI 0.597-0.815) and NSE (0.711, 95% CI 0.609-0.813) in cerebrospinal fluid, plasma S100B (AUC 0.729, 95% CI 0.626-0.832) had the best discrimination performance for delirium in sepsis patients. Logistic regression analysis showed that the combination of cerebrospinal fluid BNIP3 L with plasma S100B, ONSD, neutrophils, and age provided the best discrimination to cognitive impairment in sepsis patients (accuracy:0.901, specificity: 0.923, sensitivity:0.911), which was better than Naïve Bayes, decision tree and neural network models. Neutrophils, ONSD, and cerebrospinal fluid BNIP3 L were consistently the major contributors in a few models.

CONCLUSIONS:

The Logistic regression showed that combination model was strongly correlated with cognitive dysfunction in sepsis patients.

项与 S100B 相关的新闻（医药）

2023-11-08

·生物谷

Nat. Commun. | 邱义福团队发现YAP/TAZ调控脂肪组织交感神经分布

肥胖是现代社会的重大健康问题，不但与糖尿病、非酒精性脂肪肝、动脉粥样硬化等一系列代谢疾病有关，还会加速癌症、衰老的发生发展。因其可改善肥胖和相关疾病，褐色和米色脂肪的生成和调控机制是代谢研究的焦点。不同于褐色脂肪，米色脂肪由白色脂肪在寒冷暴露或其他条件刺激下经由“褐色化”而成，其细胞内产热程序被激活。脂肪组织内交感神经的分布对米色脂肪的发生及正常功能的发挥具有重要的作用；当交感神经激活后，其末梢释放儿茶酚胺类物质作用于脂肪（前体）细胞表面受体，从而激活一系列下游信号、调控米色脂肪的生成和功能。已有研究报道，寒冷刺激可诱导脂肪组织内交感神经增多，并且在肥胖或衰老情况下脂肪组织内的交感神经分布及功能都出现异常，然而尚不清楚如何调控脂肪组织内的交感神经分布。2023年11月4日，北京大学未来技术学院/北大-清华生命科学联合中心邱义福团队在Nature Communications发表题为Transcriptional repression of beige fat innervation via a YAP/TAZ-S100B axis的研究论文[1]。该论文报道了YAP/TAZ蛋白通过调控PRDM16-C/EBPβ复合体的形成从而影响神经营养因子S100B的表达，进而调控白色脂肪在不同生理病理情况下的交感神经分布。作者首先从调控米色脂肪生成的关键因子——PRDM16入手，通过质谱分析鉴定出YAP/TAZ可能与PRDM16在米色脂肪细胞中互作；过表达及内源免疫共沉淀证实PRDM16通过第二锌指结构域（ZF2）与YAP/TAZ互作。为了探究该互作在脂肪细胞中的生物学功能，作者构建了脂肪细胞特异性Yap/Taz基因敲除小鼠（YT-AKO）。转录组测序分析结果显示，相比于对照小鼠，基因敲除鼠的皮下脂肪组织（scWAT）产热程序被激活、产热基因表达显著上升；同时YT-AKO小鼠的耗氧增加，寒冷耐受性增强。值得一提的是，YAP/TAZ的缺失并不影响褐色脂肪组织中产热基因的表达。出乎意料的是，在体外培养的米色脂肪细胞中敲除Yap/Taz基因后，产热相关基因的表达并不受影响，暗示YAP/TAZ可能通过重塑脂肪组织微环境而调控米色脂肪的发生。脂肪组织透明化及三维成像结果显示，YT-AKO小鼠的scWAT中交感神经的分布显著增加，表明YAP/TAZ的缺失可能通过增加脂肪组织内交感神经的分布而促进米色脂肪的生成。为了探究YAP/TAZ调控神经分布的机制，作者通过分析转录组测序结果发现神经营养因子——S100B在YAP/TAZ缺失后的scWAT中表达量显著上升，且展现为脂肪细胞自主性效应。后续通过一系列过表达和敲除实验，作者证实S100B介导YAP/TAZ缺失引起的scWAT交感神经分布增加及产热增强。为回答YAP/TAZ如何调控S100B表达，作者通过分析ChIP-Seq数据及敲除实验发现：转录共调控因子PRDM16可以结合S100b基因启动子并调控其表达。进一步，通过转录因子预测软件、结合米色脂肪内PRDM16的互作质谱结果以及体外过表达验证实验，作者发现PRDM16与转录因子C/EBPβ协同促进S100B的表达，且该促进作用可被YAP/TAZ所抑制。有研究显示PRDM16可通过其ZF2结构域与C/EBPβ发生互作，作者据此推测YAP/TAZ可能与C/EBPβ竞争结合PRDM16的ZF2结构域，从而阻碍PRDM16-C/EBPβ复合体的形成。免疫共沉淀及CUT&Tag实验证实了该猜想，并且YAP/TAZ的缺失可以促进scWAT中PRDM16-C/EBPβ复合体的形成。作者进一步发现去甲肾上腺素（NE）可以通过NE-cAMP-PKA信号通路促进米色脂肪细胞S100B的表达。该信号通路能够诱导YAP/TAZ蛋白的磷酸化及出核降解，从而解除其对PRDM16的抑制，促进细胞核内PRDM16-C/EBPβ复合体的形成。作者发现寒冷刺激可激活该通路从而诱导scWAT中S100B的表达和交感神经分布的增加，当外源表达不能被磷酸化的TAZ突变体（TAZ4SA）后，寒冷刺激既不能诱导S100B的表达也不能增加交感神经的分布。内脏白色脂肪是一类惰性脂肪组织，很难诱导褐色化且有碍机体代谢健康，有研究显示内脏白色脂肪中交感神经的分布较少，这可能是其难以褐色化的原因之一。作者发现YAP/TAZ在内脏白色脂肪中高表达且活性最强，而YAP/TAZ的缺失则可以显著增加脂肪中交感神经的分布并促进寒冷诱导的褐色化。最后，作者通过高脂诱导的肥胖小鼠及年老相关的肥胖小鼠两种模型，发现YAP/TAZ在脂肪细胞中的缺失能够显著抵抗肥胖的发生，促进皮下和内脏白色脂肪的交感神经分布及褐色化，改善小鼠的葡萄糖代谢。另外，通过AAV局部注射肥胖小鼠的内脏脂肪组织实现外源表达S100B也可以改善小鼠的代谢。总之，该研究发现了YAP/TAZ可通过阻碍脂肪细胞内PRDM16-C/EBPβ复合体的形成而抑制神经营养因子——S100B的表达，进而抑制脂肪组织内交感神经的分布；而寒冷刺激可通过NE-cAMP-PKA信号通路诱导YAP/TAZ的磷酸化，解除其与PRDM16的结合从而促进PRDM16-C/EBPβ复合体形成，进而诱导S100B的表达并促进交感神经的分布（图一）。此外，干预YAP/TAZ-S100B通路可以改善饮食诱导或年老相关的肥胖及代谢紊乱，为肥胖的预防和治疗提供了新的线索和策略。邱义福实验室之前报道，抑制YAP/TAZ可减轻脂肪组织纤维化、改善胰岛素敏感性及葡萄糖耐受性（BioArtMED: Nat Commun | 邱义福团队发现Hippo通路控制脂肪组织纤维化）。这两项研究综合表明，靶标Hippo通路，有望“一石两鸟”：通过抑制YAP/TAZ，一方面抑制肥胖诱导的脂肪纤维化，另一方面促进白色脂肪的米色化，从而改善肥胖和相应的代谢失调。图一：YAP/TAZ调控皮下脂肪组织交感神经分布的机制模式图。本文仅用于学术分享，转载请注明出处。若有侵权，请联系微信：bioonSir 删除或修改！

临床结果

2023-04-26

·生物谷

举铁吧，头脑还能更聪明！Neuroscience新发现：锻炼肌肉有利于增强海马体功能，让大脑更健康！

你有多久没有运动了？在工作外不多的可支配时间里，生活、社交和家庭已然占据了绝大部分，而且似乎也丧失了幼年时一股脑的运动热情，即便我们知道长期坚持运动可以提高心肺、肌肉、骨骼等器官和组织的功能水平，还能缓解焦虑，甚至多种慢性疾病的发生......而且运动的益处也不止于此，近日，美国贝克曼高级科学技术研究所的Justin S. Rhodes和M. Taher A. Saif教授团队在Neuroscience上发表最新成果，该研究显示，锻炼在一定程度上能通过调节星形胶质细胞来增强海马体功能，进一步支持大脑健康。图片来源：doi: 10.1016/j.neuroscience.2023.01.028我们都知道，锻炼有利于大脑健康，目前的解释为，肌肉在收缩时会释放一些因子，这些因子进入体内循环并进入大脑，在大脑中增强海马体功能如神经发生和突触发生。那么，肌肉信号是如何通过海马细胞转导来调节大脑网络活动和突触发育的呢？起初，研究人员在一项小鼠后肢反复电收缩的实验中观察到海马体中新星形胶质细胞的数量增加，这意味着星形胶质细胞对肌肉因子敏感。同时，星形胶质细胞又在血脑屏障的形成中发挥着关键作用，可以将信号传递到大脑。因此，研究人员将收缩肌细胞和海马细胞分离出来进行体外实验。当肌肉细胞成熟时，它们开始自行收缩，将化学信号分子释放到培养基中。将这些含有信号分子的培养基（条件介质，CM）添加到海马神经元和星形胶质细胞的培养体系中，通过免疫荧光、钙成像等技术来观察细胞生长和神经元电信号活动。结果显示，加入含肌肉细胞信号分子的培养基后，海马体神经元表现出了更为频繁和更大强度的电信号，代表神经元迅速生长；几天后神经元形成成熟网络同步发射电信号，就如同大脑一样。此外，作者还发现，肌肉收缩是CM影响海马体所必需的，当使用BTS阻止肌肉收缩时，无论是在常规介质（RM）还是CM中，BTS似乎都直接消除了神经元的同步放电。图1. 肌肉收缩条件介质增加海马神经元活动。图片来源：doi: 10.1016/j.neuroscience.2023.01.028原代海马细胞培养一段时间会形成突触，研究发现，相比于RM，CM更能促进突触发育。对表达S100b（星形胶质细胞标记物）的细胞进行计数量化，从第2天到第9天，星形胶质细胞数量在RM中增加了9.0倍，在CM中增加了10.4倍，这表明来自收缩肌肉的肌肉调节介质诱导星形胶质细胞增殖。星形胶质细胞数量的增加可能通过加强特定突触或削弱其他突触来促进海马网络的成熟。当培养皿中出现新的成熟神经元时表示神经发生，通过对NeuN阳性细胞计数显示，RM和CM在第3天的神经元数量没有显著差异，但CM在第9天的神经元数量比RM多约40%，说明来自收缩肌肉的肌肉调节介质诱导神经发生。图2. 肌肉收缩条件介质加速海马神经元突触发育。图片来源：doi: 10.1016/j.neuroscience.2023.01.028星形胶质细胞作为大脑中接收血液信号的第一反应者，它是如何调节化学信号与海马神经元之间的关系的呢？研究人员从培养体系中去除星形胶质细胞，惊奇的发现神经元活动增强，表明CM增加星形胶质细胞的抑制功能来抵消CM对神经元活动的兴奋作用，从而促进了海马体的可塑性。简单来讲，星形胶质细胞可以阻止海马体本身参与运动反应的过度兴奋，避免神经元失控。图3. 星形胶质细胞释放抑制肌肉介质诱导的神经元活动的因子。图片来源：doi: 10.1016/j.neuroscience.2023.01.028简而言之，运动使肌肉细胞产生的化学信号分子能够让海马神经元兴奋，星形胶质细胞调节神经元活动防止过度兴奋，二者共同促进了大脑功能的健康平衡。另外，海马体是认知，学习和记忆的关键区域，这项研究也为开发认知障碍运动方案提供了新的思路，我们也期待着通过“药物+运动”的合理搭配，让更多的如阿尔兹海默症等认知障碍病患从中获益！天气变暖啦，一起出门动起来吧^_^参考文献：[1] Lee KY, Rhodes JS, Saif MTA. Astrocyte-mediated Transduction of Muscle Fiber Contractions Synchronizes Hippocampal Neuronal Network Development. Neuroscience. 2023 Apr 1; 515:25-36. doi: 10.1016/j.neuroscience.2023.01.028.[2] Ruegsegger GN, Booth FW. Health Benefits of Exercise. Cold Spring Harb Perspect Med. 2018 Jul 2;8(7): a029694. doi: 10.1101/cshperspect. a029694.撰文 | 白露编辑 | cici精彩推荐精彩推荐：1、警惕！BMC：我国学者调查44万人健康数据显示：每周1~3天食用腌菜，死亡风险提升0.32倍！2、长寿的秘密找到了！Nature Aging：我国学者分析300位百岁老人，发现肠道微生物群越像年轻人越健康长寿！3、健康“杀手”帕金森诊断新突破！Lancet子刊最新研究证实：α-突触核蛋白检测有望成为帕金森病筛查新选择4、Cancer Letters：于颖彦教授团队权威综述！从药物筛选到临床试验，类器官应用潜力巨大！5、核桃真的能补脑？《柳叶刀》子刊最新研究：坚持补充核桃可补脑增加预期寿命、降低多种疾病风险！

2022-10-04

·PRNewswire

BRAINBox Solutions Announces New U.S. Patent Allowance, Strengthening Biomarker Portfolio for Multi-Modal Mild Traumatic Brain Injury Test

Company Names Stephen Liu, M.D. to Board of Directors RICHMOND, Va., Oct. 4, 2022 /PRNewswire/ -- BRAINBox Solutions, Inc announced today that the U.S. Patent & Trademark Office (PTO) issued a notice of allowance for a patent covering methods for detection of mild traumatic brain injury (mTBI), also known as concussion, using Brain Derived Neurotrophic Factor (BDNF). BDNF is an important component of the biomarker panel in the multi-modal diagnostic prognostic and prognostic solutions the company is developing for mTBI. "BRAINBox's test is the first to integrate blood biomarkers with functional testing for both the diagnosis and prognosis of mild TBI," said Donna Edmonds, BRAINBox Solutions' Chief Executive Officer. "The new BDNF patent is an important addition to our broad, worldwide portfolio of patents covering biomarkers related to various aspects of diagnostic use. Incorporating BDNF into our TBI biomarker panels enhances the competitive advantage of our algorithms to generate an objective TBI score to help guide healthcare decision making." She noted that BRAINBox Solutions' current intellectual property portfolio includes 17 issued patents protecting a portfolio of more than 30 proprietary TBI biomarkers and 18 pending applications directed to other novel TBI biomarkers. The newly allowed patent is based on BRAINBox Solutions' discovery that a decrease in blood levels of BDNF alone are sensitive and specific in the detection of mild TBI. The claims in the new patent also protect the BDNF discovery alone, and in combination with other biomarkers, including GFAP, S100B, NSE, MT3, and NRGN. The new patent covers both diagnosis of TBI and patient monitoring post-injury, particularly for determining return to work or play. The company's pending patents also cover patient risk stratification based upon TBI symptoms and the correlation with specific neuroimaging features in CT and advanced MRI. In this context, the results of the TBI biomarker test may be used to justify a more definitive neuroimaging test such as MRI. The work underlying the discoveries in the company's patent portfolio established important relationships to guide clinical care decisions at multiple steps in the care pathways of TBI, and aid eligibility decisions in clinical trials for treatments for TBI. Stephen Liu, M.D., joins Board of Directors Separately, the company announced that Stephen Liu, M.D., a been appointed to the board of directors. Dr. Liu is a Partner at Uptick Health Advisors and IFG Health Fund, and he serves as an advisor to BioVentures Investors. "Stephen brings more than 25 years of experience as a physician-entrepreneur, academic orthopedic surgeon specializing in sports medicine and senior clinical advisor to several medical device companies and financial organizations in the U.S. and Asia," said Ms. Edmonds. "We welcome his insights and guidance as the BRAINBox TBI test nears final clinical development and commercialization." The BRAINBOX TBI test is currently undergoing a pivotal clinical trial, HeadSMARTII, in the U.S. and Europe designed to support applications for regulatory clearance and marketing. Stephen is Chairman/Founder of Forme®. Forme is a smart wearable technology company focused on posture and back health. He has served as a Senior Advisor to OPKO Health and a Senior Advisor to Landenburg Thalman. He also served as a Member of the Board of Directors of Cardo Medical, a publicly traded medical device company that was acquired by Arthrex and served as a clinical advisor to major MedTech companies including J&J and Stryker. Previously, Stephen was a faculty member at the UCLA School of Medicine and Director of the school's Bio-skill Laboratory. He and his team commercialized several medical device R&D projects which were later acquired. He has also co-authored seven books, published more than 40 peer reviewed articles and lectured in over 25 countries. Stephen holds a B.A. in Biology and Psychology and an M.D. from the University of Southern California. About BRAINBox Solutions BRAINBox Solutions is developing the first AI enabled, multi-modality approach for the diagnosis and prognosis of Mild Traumatic Brain Injury, commonly referred to as a concussion. The company seeks to establish a clinical best practice standard for the diagnosis and prognosis of concussion. The TBI product incorporates a panel of proprietary, patented blood biomarkers which can be detected in minutes on a point of care instrument or using standard laboratory systems, as well as neurocognitive testing, to provide a single system score. The company is led by key physician and scientific thought leaders in the field and an experienced, clinically focused management team. BrainBox has been granted Breakthrough Designation for Diagnosis and Prognosis of mTBI and is a recipient of grant funding from the NFL-GE Head Health Challenge, Virginia Catalyst and NIH, and is supported by initial funding from BioVentures Investors, the Lazlo Tauber Foundation, and subsequent funding from Genoa Ventures, Ambit Health Ventures, Astia Angels, Virginia Tech Innovation Fund and Seed Fund, as well as several Internationally recognized athletes and other Family Offices. For more information, contact: Donna Edmonds, CEO [email protected] 1‐804‐724‐0009 SOURCE BRAINBox Solutions, Inc.