Swiss-Prot Turns 30 Anniversary Brochure, 2016 2 Table of Contents
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Naringenin Regulates FKBP4/NR3C1/TMEM173 Signaling Pathway in Autophagy and Proliferation of Breast Cancer and Tumor-Infltrating Dendritic Cell Maturation
Naringenin Regulates FKBP4/NR3C1/TMEM173 Signaling Pathway in Autophagy and Proliferation of Breast Cancer and Tumor-Inltrating Dendritic Cell Maturation Hanchu Xiong ( [email protected] ) Zhejiang Provincial People's Hospital https://orcid.org/0000-0001-6075-6895 Zihan Chen First Hospital of Zhejiang Province: Zhejiang University School of Medicine First Aliated Hospital Baihua Lin Zhejiang Provincial People's Hospital Cong Chen Zhejiang University School of Medicine Sir Run Run Shaw Hospital Zhaoqing Li Zhejiang University School of Medicine Sir Run Run Shaw Hospital Yongshi Jia Zhejiang Provincial People's Hospital Linbo Wang Zhejiang University School of Medicine Sir Run Run Shaw Hospital Jichun Zhou Zhejiang University School of Medicine Sir Run Run Shaw Hospital Research Keywords: FKBP4, TMEM173, Autophagy, Exosome, Dendritic cell, Breast cancer Posted Date: July 7th, 2021 DOI: https://doi.org/10.21203/rs.3.rs-659646/v1 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Page 1/38 Abstract Background TMEM173 is a pattern recognition receptor detecting cytoplasmic nucleic acids and transmits cGAS related signals that activate host innate immune responses. It has also been found to be involved in tumor immunity and tumorigenesis. Methods Bc-GenExMiner, PROMO and STRING database were used for analyzing clinical features and interplays of FKBP4, TMEM173 and NR3C1. Transient transfection, western blotting, quantitative real-time PCR, luciferase reporter assay, immunouorescence and nuclear and cytoplasmic fractionation were used for regulation of FKBP4, TMEM173 and NR3C1. Both knockdown and overexpression of FKBP4, TMEM173 and NR3C1 were used to analyze effects on autophagy and proliferation of breast cancer (BC) cells. -
Supplementary Table S4. FGA Co-Expressed Gene List in LUAD
Supplementary Table S4. FGA co-expressed gene list in LUAD tumors Symbol R Locus Description FGG 0.919 4q28 fibrinogen gamma chain FGL1 0.635 8p22 fibrinogen-like 1 SLC7A2 0.536 8p22 solute carrier family 7 (cationic amino acid transporter, y+ system), member 2 DUSP4 0.521 8p12-p11 dual specificity phosphatase 4 HAL 0.51 12q22-q24.1histidine ammonia-lyase PDE4D 0.499 5q12 phosphodiesterase 4D, cAMP-specific FURIN 0.497 15q26.1 furin (paired basic amino acid cleaving enzyme) CPS1 0.49 2q35 carbamoyl-phosphate synthase 1, mitochondrial TESC 0.478 12q24.22 tescalcin INHA 0.465 2q35 inhibin, alpha S100P 0.461 4p16 S100 calcium binding protein P VPS37A 0.447 8p22 vacuolar protein sorting 37 homolog A (S. cerevisiae) SLC16A14 0.447 2q36.3 solute carrier family 16, member 14 PPARGC1A 0.443 4p15.1 peroxisome proliferator-activated receptor gamma, coactivator 1 alpha SIK1 0.435 21q22.3 salt-inducible kinase 1 IRS2 0.434 13q34 insulin receptor substrate 2 RND1 0.433 12q12 Rho family GTPase 1 HGD 0.433 3q13.33 homogentisate 1,2-dioxygenase PTP4A1 0.432 6q12 protein tyrosine phosphatase type IVA, member 1 C8orf4 0.428 8p11.2 chromosome 8 open reading frame 4 DDC 0.427 7p12.2 dopa decarboxylase (aromatic L-amino acid decarboxylase) TACC2 0.427 10q26 transforming, acidic coiled-coil containing protein 2 MUC13 0.422 3q21.2 mucin 13, cell surface associated C5 0.412 9q33-q34 complement component 5 NR4A2 0.412 2q22-q23 nuclear receptor subfamily 4, group A, member 2 EYS 0.411 6q12 eyes shut homolog (Drosophila) GPX2 0.406 14q24.1 glutathione peroxidase -
The Hominoid-Specific Gene TBC1D3 Promotes Generation of Basal Neural
1 The hominoid-specific gene TBC1D3 promotes generation of basal neural 2 progenitors and induces cortical folding in mice 3 4 Xiang-Chun Ju1,3,9, Qiong-Qiong Hou1,3,9, Ai-Li Sheng1, Kong-Yan Wu1, Yang Zhou8, 5 Ying Jin8, Tieqiao Wen7, Zhengang Yang6, Xiaoqun Wang2,5, Zhen-Ge Luo1,2,3,4 6 7 1Institute of Neuroscience, State Key Laboratory of Neuroscience, Shanghai Institutes for 8 Biological Sciences, Chinese Academy of Sciences, Shanghai, China. 9 2CAS Center for Excellence in Brain Science and Intelligence Technology, Shanghai, 10 China. 11 3Chinese Academy of Sciences University, Beijing, China. 12 4ShanghaiTech University, Shanghai, China 13 5Institute of Biophysics, Chinese Academy of Sciences, Beijing, China. 14 6Institutes of Brain Science, State Key Laboratory of Medical Neurobiology, Fudan 15 University, Shanghai, China. 16 7School of Life Sciences, Shanghai University, Shanghai, China. 17 8The Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese 18 Academy of Sciences, Shanghai, China. 19 9Co-first author 20 Correspondence should be addressed to Z.G.L ([email protected]) 21 22 Author contributions 23 X.-C.J and Q.-Q. H performed most experiments, analyzed data and wrote the paper. 24 A.-L.S helped with in situ hybridization. K.-Y.W assisted with imaging analysis. T.W 25 helped with the construction of nestin promoter construct. Y. Z and Y. J helped with 26 ReNeuron cell culture and analysis. Z.Y provided human fetal samples and assisted with 1 27 immunohistochemistry analysis. X.W provided help with live-imaging analysis. Z.-G.L 28 supervised the whole study, designed the research, analyzed data and wrote the paper. -
Comparative Transcriptome Profiling of the Human and Mouse Dorsal Root Ganglia: an RNA-Seq-Based Resource for Pain and Sensory Neuroscience Research
bioRxiv preprint doi: https://doi.org/10.1101/165431; this version posted October 13, 2017. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Title: Comparative transcriptome profiling of the human and mouse dorsal root ganglia: An RNA-seq-based resource for pain and sensory neuroscience research Short Title: Human and mouse DRG comparative transcriptomics Pradipta Ray 1, 2 #, Andrew Torck 1 , Lilyana Quigley 1, Andi Wangzhou 1, Matthew Neiman 1, Chandranshu Rao 1, Tiffany Lam 1, Ji-Young Kim 1, Tae Hoon Kim 2, Michael Q. Zhang 2, Gregory Dussor 1 and Theodore J. Price 1, # 1 The University of Texas at Dallas, School of Behavioral and Brain Sciences 2 The University of Texas at Dallas, Department of Biological Sciences # Corresponding authors Theodore J Price Pradipta Ray School of Behavioral and Brain Sciences School of Behavioral and Brain Sciences The University of Texas at Dallas The University of Texas at Dallas BSB 14.102G BSB 10.608 800 W Campbell Rd 800 W Campbell Rd Richardson TX 75080 Richardson TX 75080 972-883-4311 972-883-7262 [email protected] [email protected] Number of pages: 27 Number of figures: 9 Number of tables: 8 Supplementary Figures: 4 Supplementary Files: 6 Word count: Abstract = 219; Introduction = 457; Discussion = 1094 Conflict of interest: The authors declare no conflicts of interest Patient anonymity and informed consent: Informed consent for human tissue sources were obtained by Anabios, Inc. (San Diego, CA). Human studies: This work was approved by The University of Texas at Dallas Institutional Review Board (MR 15-237). -
FKBP4 Is a Malignant Indicator in Luminal a Subtype of Breast Cancer
Journal of Cancer 2020, Vol. 11 1727 Ivyspring International Publisher Journal of Cancer 2020; 11(7): 1727-1736. doi: 10.7150/jca.40982 Research Paper FKBP4 is a malignant indicator in luminal A subtype of breast cancer Hanchu Xiong1,2*, Zihan Chen3*, Wenwen Zheng2, Jing Sun2, Qingshuang Fu4, Rongyue Teng1, Jida Chen1, Shuduo Xie1, Linbo Wang1, Xiao-Fang Yu2, Jichun Zhou1 1. Department of Surgical Oncology, Sir Run Run Shaw Hospital, Zhejiang University, Hangzhou, 310016, China. 2. Cancer Institute, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310016, China. 3. Surgical Intensive Care Unit, First Affiliated Hospital, Zhejiang University, Hangzhou, Zhejiang, 310016, China. 4. Rui An Hospital of Traditional Chinese Medicine, Wenzhou, 325200, China. * These authors contributed equally Corresponding authors: Xiao-Fang Yu, E-mail: [email protected]; Jichun Zhou, E-mail: [email protected] © The author(s). This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions. Received: 2019.10.08; Accepted: 2019.12.20; Published: 2020.01.16 Abstract Purpose: FKBP4 is a member of the immunophilin protein family, which plays a role in immunoregulation and basic cellular processes involving protein folding and trafficking associated with HSP90. However, the relationship between abnormal expression of FKBP4 and clinical outcome in luminal A subtype breast cancer (LABC) patients remains to be elucidated. Methods: Oncomine, bc-GenExMiner and HPA database were used for data mining and analyzing FKBP4 and its co-expressed genes. GEPIA database was used for screening co-expressed genes of FKBP4. -
TITLE PAGE Exome Sequencing Identifies Variants in FKBP4 That Are
TITLE PAGE Exome sequencing identifies variants in FKBP4 that are associated with recurrent fetal loss in humans Authors: Charalambos Demetriou1*, Estelle Chanudet2, GOSgene2, Agnel Joseph3, Maya Topf3, Anna C. Thomas1, Maria Bitner-Glindzicz1, Lesley Regan4, Philip Stanier1, Gudrun E. Moore1 Affiliations: 1Genetics and Genomic Medicine, UCL Great Ormond Street Institute of Child Health, University College London, London, UK. 2Centre for Translational Omics - GOSgene, UCL Great Ormond Street Institute of Child Health, University College London, London, UK. 3Institute of Structural and Molecular Biology, Birkbeck College, London, UK. 4Department of Obstetrics and Gynaecology, St. Mary's Campus, Imperial College London, London, UK. Philip Stanier and Gudrun Moore contributed equally. *Corresponding author: Charalambos Demetriou Address: UCL Great Ormond Street Institute of Child Health 30 Guilford Street, Lonodn, WC1N 1EH Tel: 0044796 081 3545 Fax: 0044207 905 2832 Email address: [email protected] 1 ABSTRACT Recurrent pregnancy loss (RPL) is defined as two or more consecutive miscarriages and affects an estimated 1.5% of couples trying to conceive. RPL has been attributed to genetic, endocrine, immune and thrombophilic disorders, But many cases remain unexplained. We investigated a Bangladeshi family where the proband experienced 29 consecutive pregnancy losses with no successful pregnancies from three different marriages. Whole exome sequencing identified rare genetic variants in several candidate genes. These were further investigated in Asian and White European RPL cohorts, and in Bangladeshi controls. FKBP4, encoding the immunophilin FK506 binding protein 4, was identified as a plausible candidate, with three further novel variants identified in Asian patients. None were found in European patients or controls. -
Alternatively Activated NUSAP1 Promotes Tumor Growth and Indicates Poor Prognosis in Hepatocellular Carcinoma
247 Original Article Alternatively activated NUSAP1 promotes tumor growth and indicates poor prognosis in hepatocellular carcinoma Chao Shi1#, Hui Xu2#, Junyu Liu3, Yuanbin Zhong4, Xinping Zhang2, Xiaoqin Tong2, Lunli Zhang4, Xiaopeng Li4, Libin Deng5,6 1Department of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang 330006, China; 2Jiangxi Provincial Key Laboratory of Preventive Medicine, School of Public Health, Nanchang University, Nanchang 330006, China; 3Queen Mary School, Medical College of Nanchang University, Nanchang 330031, China; 4Department of Infectious Diseases & Key Laboratory of Liver Regenerative Medicine of Jiangxi Province, The First Affiliated Hospital of Nanchang University, Nanchang 330006, China;5 College of Basic Medical Science, Nanchang University, Nanchang 330031, China; 6Institute of Translational Medicine, Nanchang University, Nanchang 330031, China Contributions: (I) Conception and design: L Deng; (II) Administrative support: L Deng; (III) Provision of study materials or patients: C Shi, H Xu, X Zhang, X Tong; (IV) Collection and assembly of data: C Shi, H Xu, Y Zhong, X Zhang, X Tong, L Zhang, X Li; (V) Data analysis and interpretation: H Xu, J Liu, Y Zhong, X Zhang; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors. #These authors contributed equally to this work. Correspondence to: Libin Deng, PhD. Institute of Translational Medicine, Nanchang University, Nanchang 330031, China. Email: [email protected]. Background: Hepatocellular carcinoma (HCC) is one of the most common malignancies with high mortality. The key genes involved in initiation and development of HCC is not entirely clear. Methods: We performed a meta-analysis of available transcriptome data from 6 independent HCC datasets [5 datasets from the Gene Expression Omnibus (GEO) and 1 dataset from The Cancer Genome Atlas (TCGA)]. -
FKBP4 Integrates FKBP4/Hsp90/IKK with FKBP4/Hsp70/Rela Complex To
Zong et al. Cell Death and Disease (2021) 12:602 https://doi.org/10.1038/s41419-021-03857-8 Cell Death & Disease ARTICLE Open Access FKBP4 integrates FKBP4/Hsp90/IKK with FKBP4/ Hsp70/RelA complex to promote lung adenocarcinoma progression via IKK/NF-κB signaling Shuai Zong1, Yulian Jiao1,XinLiu1,WenliMu1, Xiaotian Yuan1,YunyunQu1,2,YuXia1,ShuangLiu1,HuanxinSun1, Laicheng Wang1,BinCui1,XiaowenLiu1,PingLi3 and Yueran Zhao 1,4,5 Abstract FKBP4 belongs to the family of immunophilins, which serve as a regulator for steroid receptor activity. Thus, FKBP4 has been recognized to play a critical role in several hormone-dependent cancers, including breast and prostate cancer. However, there is still no research to address the role of FKBP4 on lung adenocarcinoma (LUAD) progression. We found that FKBP4 expression was elevated in LUAD samples and predicted significantly shorter overall survival based on TCGA and our cohort of LUAD patients. Furthermore, FKBP4 robustly increased the proliferation, metastasis, and invasion of LUAD in vitro and vivo. Mechanistic studies revealed the interaction between FKBP4 and IKK kinase complex. We found that FKBP4 potentiated IKK kinase activity by interacting with Hsp90 and IKK subunits and promoting Hsp90/IKK association. Also, FKBP4 promotes the binding of IKKγ to IKKβ, which supported the facilitation role in IKK complex assembly. We further identified that FKBP4 TPR domains are essential for FKBP4/IKK interaction 1234567890():,; 1234567890():,; 1234567890():,; 1234567890():,; since its association with Hsp90 is required. In addition, FKBP4 PPIase domains are involved in FKBP4/IKKγ interaction. Interestingly, the association between FKBP4 and Hsp70/RelA favors the transport of RelA toward the nucleus. -
Identifying the Proteins to Which Small-Molecule Probes and Drugs Bind in Cells
Identifying the proteins to which small-molecule probes and drugs bind in cells Shao-En Onga,1, Monica Schenonea, Adam A. Margolinb, Xiaoyu Lic, Kathy Doa, Mary K. Doudd, D. R. Mania,b, Letian Kuaie, Xiang Wangd, John L. Woodf, Nicola J. Tollidayc, Angela N. Koehlerd, Lisa A. Marcaurellec, Todd R. Golubb, Robert J. Gouldd, Stuart L. Schreiberd,1, and Steven A. Carra,1 aProteomics Platform, bCancer Biology Program, cChemical Biology Platform, dChemical Biology Program, and eStanley Center for Psychiatric Research, The Broad Institute of MIT and Harvard, 7 Cambridge Center, Cambridge, MA 02142; and fChemistry Department, Colorado State University, Fort Collins, CO 80523 Contributed by Stuart L. Schreiber, January 15, 2009 (sent for review December 21, 2008) Most small-molecule probes and drugs alter cell circuitry by interact- known (the ‘‘target I.D. problem’’). It could provide strong clues to ing with 1 or more proteins. A complete understanding of the the mechanisms used by SMs to achieve their recognized actions interacting proteins and their associated protein complexes, whether and it could suggest potential unrecognized actions. the compounds are discovered by cell-based phenotypic or target- Strategies for ‘‘target identification’’ have been developed that based screens, is extremely rare. Such a capability is expected to be rely on genetic (9), computational (10, 11) and biochemical (12) highly illuminating—providing strong clues to the mechanisms used principles. Although several key molecular targets have been iden- by small-molecules to achieve their recognized actions and suggest- tified through affinity chromatography (13–15), it has not been ing potential unrecognized actions. We describe a powerful method widely applied as a general solution to target identification for a combining quantitative proteomics (SILAC) with affinity enrichment number of reasons. -
TRNP1 Sequence, Function and Regulation Co-Evolve with Cortical Folding in Mammals
bioRxiv preprint doi: https://doi.org/10.1101/2021.02.05.429919; this version posted February 5, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-ND 4.0 International license. TRNP1 sequence, function and regulation co-evolve with cortical folding in mammals Zane Kliesmete1,§, Lucas E. Wange1,§, Beate Vieth1, Miriam Esgleas2,3, Jessica Radmer1, Matthias H¨ulsmann1,4, Johanna Geuder1, Daniel Richter1, Mari Ohnuki1, Magdalena G¨otz2,3,5, Ines Hellmann1,*,§, Wolfgang Enard1,*,§ 1 Anthropology and Human Genomics, Department of Biology II, Ludwig-Maximilians Universitaet, Munich, Germany 2 Department of Physiological Genomics, BioMedical Center - BMC, Ludwig-Maximilians Universitaet, Munich, Germany 3 Institute for Stem Cell Research, Helmholtz Zentrum Muenchen, German Research Center for Environmental Health, Neuherberg, Germany 4 current address: Department of Environmental Microbiology, Eawag, 8600 D¨ubendorf, Switzerland & Department of Environmental Systems Science, ETH Zurich, 8092 Z¨urich, Switzerland 5 SYNERGY, Excellence Cluster of Systems Neurology, BioMedical Center (BMC), Ludwig-Maximilians-Universitaet, Munich, Germany § equal author contribution * correspondence [email protected], [email protected] Abstract Genomes can be seen as notebooks of evolution that contain unique information on successful genetic experiments (Wright 2001). This allows to identify conserved genomic sequences (Zoonomia Consortium 2020) and is very useful e.g. for finding disease-associated variants (Kircher et al. 2014). Additional information from genome comparisons across species can be leveraged when considering phenotypic variance across species. Here, we exemplify this principle in a cross-species association study by testing whether structural or regulatory changes in TRNP1 correlate with changes in brain size and cortical folding in mammals. -
FKBP4 (Human) Recombinant Protein (Q01)
Produktinformation Diagnostik & molekulare Diagnostik Laborgeräte & Service Zellkultur & Verbrauchsmaterial Forschungsprodukte & Biochemikalien Weitere Information auf den folgenden Seiten! See the following pages for more information! Lieferung & Zahlungsart Lieferung: frei Haus Bestellung auf Rechnung SZABO-SCANDIC Lieferung: € 10,- HandelsgmbH & Co KG Erstbestellung Vorauskassa Quellenstraße 110, A-1100 Wien T. +43(0)1 489 3961-0 Zuschläge F. +43(0)1 489 3961-7 [email protected] • Mindermengenzuschlag www.szabo-scandic.com • Trockeneiszuschlag • Gefahrgutzuschlag linkedin.com/company/szaboscandic • Expressversand facebook.com/szaboscandic FKBP4 (Human) Recombinant protein is a cis-trans prolyl isomerase that binds to the Protein (Q01) immunosuppressants FK506 and rapamycin. It has high structural and functional similarity to FK506-binding Catalog Number: H00002288-Q01 protein 1A (FKBP1A), but unlike FKBP1A, this protein does not have immunosuppressant activity when Regulation Status: For research use only (RUO) complexed with FK506. It interacts with interferon regulatory factor-4 and plays an important role in Product Description: Human FKBP4 partial ORF ( immunoregulatory gene expression in B and T AAH07924, 301 a.a. - 410 a.a.) recombinant protein with lymphocytes. This encoded protein is known to GST-tag at N-terminal. associate with phytanoyl-CoA alpha-hydroxylase. It can also associate with two heat shock proteins (hsp90 and Sequence: hsp70) and thus may play a role in the intracellular EYESSFSNEEAQKAQALRLASHLNLAMCHLKLQAFSA trafficking of hetero-oligomeric forms of the steroid AIESCNKALELDSNNEKGLFRRGEAHLAVNDFELARAD hormone receptors. This protein correlates strongly with FQKVLQLYPNNKAAKTQLAVCQQRIRRQLAREKKL adeno-associated virus type 2 vectors (AAV) resulting in a significant increase in AAV-mediated transgene Host: Wheat Germ (in vitro) expression in human cell lines. Thus this encoded protein is thought to have important implications for the Theoretical MW (kDa): 37.84 optimal use of AAV vectors in human gene therapy. -
Genetics and Molecular Biology, 44, 1, E20190410 (2021) Copyright © Sociedade Brasileira De Genética
Genetics and Molecular Biology, 44, 1, e20190410 (2021) Copyright © Sociedade Brasileira de Genética. DOI: https://doi.org/10.1590/1678-4685-GMB-2019-0410 Research Article Human and Medical Genetics Integrated analysis of label-free quantitative proteomics and bioinformatics reveal insights into signaling pathways in male breast cancer Talita Helen Bombardelli Gomig1*, Amanda Moletta Gontarski1*, Iglenir João Cavalli1, Ricardo Lehtonen Rodrigues de Souza1 , Aline Castro Rodrigues Lucena2, Michel Batista2,3, Kelly Cavalcanti Machado3, Fabricio Klerynton Marchini2,3, Fabio Albuquerque Marchi4, Rubens Silveira Lima5, Cícero de Andrade Urban5, Rafael Diogo Marchi6, Luciane Regina Cavalli6,7and Enilze Maria de Souza Fonseca Ribeiro1 1Universidade Federal do Paraná, Departamento de Genética, Programa de Pós-graduação em Genética, Curitiba, PR, Brazil. 2Instituto Carlos Chagas, Laboratório de Genômica Funcional, Curitiba, PR, Brazil. 3Fundação Oswaldo Cruz (Fiocruz), Plataforma de Espectrometria de Massas, Curitiba, PR, Brazil. 4Hospital A.C. Camargo Cancer Center, Centro de Pesquisa Internacional, São Paulo, SP, Brazil. 5Hospital Nossa Senhora das Graças, Centro de Doenças da Mama, Curitiba, PR, Brazil. 6Instituto de Pesquisa Pelé Pequeno Príncipe, Curitiba, PR, Brazil. 7Georgetown University, Lombardi Comprehensive Cancer Center, Washington, USA. * These authors contributed equally to this study. Abstract Male breast cancer (MBC) is a rare malignancy that accounts for about 1.8% of all breast cancer cases. In contrast to the high number of