SSX2IP Antibody Cat

Total Page：16

File Type：pdf, Size：1020Kb

SSX2IP Antibody Cat. No.: 46-435 SSX2IP Antibody Specifications HOST SPECIES: Goat SPECIES REACTIVITY: Human HOMOLOGY: Expected Species Reactivity based on sequence homology: Dog IMMUNOGEN: The immunogen for this antibody is: C-SYTNSHVEKDDLP TESTED APPLICATIONS: ELISA, ICC, IF Peptide ELISA: antibody detection limit dilution 1:16000.Western Blot:We find no specific signal but low background (at antibody concentration up to 1ug/ml) in lysates of cell line APPLICATIONS: K562.Immunocytochemsitry/Immunofluorescence: This product has been successfully used in ICC/IF on K562 cell line. Properties Purified from goat serum by ammonium sulphate precipitation followed by antigen PURIFICATION: affinity chromatography using the immunizing peptide. CLONALITY: Polyclonal CONJUGATE: Unconjugated PHYSICAL STATE: Liquid September 30, 2021 1 https://www.prosci-inc.com/ssx2ip-antibody-46-435.html Supplied at 0.5 mg/ml in Tris saline, 0.02% sodium azide, pH7.3 with 0.5% bovine serum BUFFER: albumin. Aliquot and store at -20°C. Minimize freezing and thawing. CONCENTRATION: 500 ug/mL STORAGE CONDITIONS: Aliquot and store at -20˚C. Minimize freezing and thawing. Additional Info OFFICIAL SYMBOL: SSX2IP SSX2IP, ADIP, KIAA0923, synovial sarcoma, X breakpoint 2 interacting protein, afadin- and ALTERNATE NAMES: alpha-actinin-binding protein, FLJ10848, MGC75026 ACCESSION NO.: NP_054740.2 PROTEIN GI NO.: 41281571 GENE ID: 117178 Background and References 1) de Bruijn DR, dos Santos NR, Kater-Baats E, Thijssen J, van den Berk L, Stap J, Balemans M, Schepens M, Merkx G, van Kessel AG. The cancer-related protein SSX2 interacts with REFERENCES: the human homologue of a Ras-like GTPase interactor, RAB3IP, and a novel nuclear protein, SSX2IP. Genes Chromosomes Cancer. 2002 Jul;34(3):285-98. ANTIBODIES FOR RESEARCH USE ONLY. For additional information, visit ProSci's Terms & Conditions Page. September 30, 2021 2 https://www.prosci-inc.com/ssx2ip-antibody-46-435.html.

Copy Link

Recommended publications

Gene Section Short Communication
Atlas of Genetics and Cytogenetics in Oncology and Haematology OPEN ACCESS JOURNAL INIST -CNRS Gene Section Short Communication SSX2IP (synovial sarcoma, X breakpoint 2 interacting protein) Ghazala Khan, Barbara Guinn University of Bedfordshire, Division of Science, Park Square, Luton, Bedfordshire, UK (GK), University of Bedfordshire, Division of Science, Park Square, Luton, Bedfordshire, UK; Cancer Sciences Unit, University of Southampton, Southampton, UK; Department of Haematological Medicine, Kings College, London, UK (BG) Published in Atlas Database: March 2012 Online updated version : http://AtlasGeneticsOncology.org/Genes/SSX2IPID42407ch1p22.html DOI: 10.4267/2042/47489 This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 2.0 France Licence. © 2012 Atlas of Genetics and Cytogenetics in Oncology and Haematology exons however the first one is not translated (de Bruijn Identity et al., 2002). Other names: ADIP Transcription HGNC (Hugo): SSX2IP The gene contains 33 introns. 18 different mRNAs are Location: 1p22.3 produced; 17 spliced and 1 un-spliced form (Thierry- Note Mieg and Thierry-Mieg, 2006). SSX2IP gene encodes the protein SSX2IP which Pseudogene interacts with the cancer-testis antigen SSX2. It is A pseudogene of this gene is found on chromosome 3 thought that SSX2IP regulates the function of SSX2 in (provided by RefSeq, Oct 2009 from Entrez Gene). the testes and malignant cells. The rodent equivalent is known as afadin DIL domain-interacting protein (ADIP) and the chicken orthologue is called clock- Protein controlled gene (LCG) (Breslin et al., 2007). Note SSX2IP was discovered due to its interaction with DNA/RNA SSX2 in a yeast two-hybrid system and believed to regulate the function of SSX2 in the testes and Note malignant cells (de Bruijn et al., 2002).
[Show full text]
Open Dogan Phdthesis Final.Pdf
The Pennsylvania State University The Graduate School Eberly College of Science ELUCIDATING BIOLOGICAL FUNCTION OF GENOMIC DNA WITH ROBUST SIGNALS OF BIOCHEMICAL ACTIVITY: INTEGRATIVE GENOME-WIDE STUDIES OF ENHANCERS A Dissertation in Biochemistry, Microbiology and Molecular Biology by Nergiz Dogan © 2014 Nergiz Dogan Submitted in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy August 2014 ii The dissertation of Nergiz Dogan was reviewed and approved* by the following: Ross C. Hardison T. Ming Chu Professor of Biochemistry and Molecular Biology Dissertation Advisor Chair of Committee David S. Gilmour Professor of Molecular and Cell Biology Anton Nekrutenko Professor of Biochemistry and Molecular Biology Robert F. Paulson Professor of Veterinary and Biomedical Sciences Philip Reno Assistant Professor of Antropology Scott B. Selleck Professor and Head of the Department of Biochemistry and Molecular Biology *Signatures are on file in the Graduate School iii ABSTRACT Genome-wide measurements of epigenetic features such as histone modifications, occupancy by transcription factors and coactivators provide the opportunity to understand more globally how genes are regulated. While much effort is being put into integrating the marks from various combinations of features, the contribution of each feature to accuracy of enhancer prediction is not known. We began with predictions of 4,915 candidate erythroid enhancers based on genomic occupancy by TAL1, a key hematopoietic transcription factor that is strongly associated with gene induction in erythroid cells. Seventy of these DNA segments occupied by TAL1 (TAL1 OSs) were tested by transient transfections of cultured hematopoietic cells, and 56% of these were active as enhancers. Sixty-six TAL1 OSs were evaluated in transgenic mouse embryos, and 65% of these were active enhancers in various tissues.
[Show full text]
A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated.
[Show full text]
The Genetic Basis of Dupuytren's Disease Gloria Sue Yale School of Medicine, [email protected]
Yale University EliScholar – A Digital Platform for Scholarly Publishing at Yale Yale Medicine Thesis Digital Library School of Medicine January 2014 The Genetic Basis Of Dupuytren's Disease Gloria Sue Yale School of Medicine, [email protected] Follow this and additional works at: http://elischolar.library.yale.edu/ymtdl Recommended Citation Sue, Gloria, "The Genetic Basis Of Dupuytren's Disease" (2014). Yale Medicine Thesis Digital Library. 1926. http://elischolar.library.yale.edu/ymtdl/1926 This Open Access Thesis is brought to you for free and open access by the School of Medicine at EliScholar – A Digital Platform for Scholarly Publishing at Yale. It has been accepted for inclusion in Yale Medicine Thesis Digital Library by an authorized administrator of EliScholar – A Digital Platform for Scholarly Publishing at Yale. For more information, please contact [email protected]. The Genetic Basis of Dupuytren’s Disease A Thesis Submitted to the Yale University School of Medicine In Partial Fulfillment of the Requirements for the Degree of Doctor of Medicine by Gloria R. Sue 2014 THE GENETIC BASIS OF DUPUYTREN’S DISEASE. Gloria R. Sue, Deepak Narayan. Section of Plastic and Reconstructive Surgery, Department of Surgery, Yale University School of Medicine, New Haven, CT. Dupuytren’s disease is a common heritable connective tissue disorder of poorly understood etiology. It is thought that oxidative stress pathways may play a critical role in the development of Dupuytren’s disease, given the various disease associations that have been observed. We sought to sequence the mitochondrial and nuclear genomes of patients affected with Dupuytren’s disease using next-generation sequencing technology to potentially identify genes of potential pathogenetic interest.
[Show full text]
Role and Regulation of the P53-Homolog P73 in the Transformation of Normal Human Fibroblasts
Role and regulation of the p53-homolog p73 in the transformation of normal human fibroblasts Dissertation zur Erlangung des naturwissenschaftlichen Doktorgrades der Bayerischen Julius-Maximilians-Universität Würzburg vorgelegt von Lars Hofmann aus Aschaffenburg Würzburg 2007 Eingereicht am Mitglieder der Promotionskommission: Vorsitzender: Prof. Dr. Dr. Martin J. Müller Gutachter: Prof. Dr. Michael P. Schön Gutachter : Prof. Dr. Georg Krohne Tag des Promotionskolloquiums: Doktorurkunde ausgehändigt am Erklärung Hiermit erkläre ich, dass ich die vorliegende Arbeit selbständig angefertigt und keine anderen als die angegebenen Hilfsmittel und Quellen verwendet habe. Diese Arbeit wurde weder in gleicher noch in ähnlicher Form in einem anderen Prüfungsverfahren vorgelegt. Ich habe früher, außer den mit dem Zulassungsgesuch urkundlichen Graden, keine weiteren akademischen Grade erworben und zu erwerben gesucht. Würzburg, Lars Hofmann Content SUMMARY ................................................................................................................ IV ZUSAMMENFASSUNG ............................................................................................. V 1. INTRODUCTION ................................................................................................. 1 1.1. Molecular basics of cancer .......................................................................................... 1 1.2. Early research on tumorigenesis ................................................................................. 3 1.3. Developing
[Show full text]
SSX2 Is Differentially Expressed in Models of MERS Coronavirus-PDF 042820
1 SSX2 is differentially expressed in models of MERS coronavirus infection. 2 Shahan Mamoor, MS1 1Thomas Jefferson School of Law 3 San Diego, CA 92101 4 [email protected] 5 The coronavirus COVID19 pandemic is an emerging biosafety threat to the nation and the 6 world (1). There are no treatments approved for coronavirus infection in humans (2) and there is a lack of information available regarding the basic transcriptional behavior of human cells 7 and mammalian tissues following coronavirus infection. We mined multiple independent public 8 (3) or published datasets (4-8) containing transcriptome data from infection models of human coronavirus 229E, the severe acute respiratory syndrome (SARS) coronavirus and Middle East 9 respiratory syndrome (MERS) coronavirus to discover genes whose differential expression was conserved across the coronavirus family. We identified SSX2 (9) as a differentially expressed 10 gene following infection of human cells specifically with two types of MERS coronaviruses. and not after infection of human cells with human coronavirus 229E, or and in the lungs of mice 11 and ferrets infected with SARS coronavirus. An SSX2 interacting protein, SSX2IP, was among the genes most differentially expressed in the ferret blood after infection with SARS 12 coronavirus. The expression of SSX2 is modulated to a degree unlike most any other gene 13 following infection with MERS coronaviruses. 14 15 16 17 18 19 20 21 22 23 24 25 26 27 Keywords: SSX2, coronavirus, MERS coronavirus, SARS coronavirus, human coronavirus 28 229E, SARS-CoV-2, COVID19, systems biology of viral infection. 1 1 Viruses are classified according to a system known as the “Baltimore” classification of 2 viruses (10) wherein the characteristics of the viral genome - whether it is positive-sense or 3 negative-sense, whether it is single-stranded or double-stranded, whether it is composed or 4 RNA or DNA - are used to group viruses into families.
[Show full text]
Genomic and Expression Profiling of Human Spermatocytic Seminomas: Primary Spermatocyte As Tumorigenic Precursor and DMRT1 As Candidate Chromosome 9 Gene
Research Article Genomic and Expression Profiling of Human Spermatocytic Seminomas: Primary Spermatocyte as Tumorigenic Precursor and DMRT1 as Candidate Chromosome 9 Gene Leendert H.J. Looijenga,1 Remko Hersmus,1 Ad J.M. Gillis,1 Rolph Pfundt,4 Hans J. Stoop,1 Ruud J.H.L.M. van Gurp,1 Joris Veltman,1 H. Berna Beverloo,2 Ellen van Drunen,2 Ad Geurts van Kessel,4 Renee Reijo Pera,5 Dominik T. Schneider,6 Brenda Summersgill,7 Janet Shipley,7 Alan McIntyre,7 Peter van der Spek,3 Eric Schoenmakers,4 and J. Wolter Oosterhuis1 1Department of Pathology, Josephine Nefkens Institute; Departments of 2Clinical Genetics and 3Bioinformatics, Erasmus Medical Center/ University Medical Center, Rotterdam, the Netherlands; 4Department of Human Genetics, Radboud University Medical Center, Nijmegen, the Netherlands; 5Howard Hughes Medical Institute, Whitehead Institute and Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts; 6Clinic of Paediatric Oncology, Haematology and Immunology, Heinrich-Heine University, Du¨sseldorf, Germany; 7Molecular Cytogenetics, Section of Molecular Carcinogenesis, The Institute of Cancer Research, Sutton, Surrey, United Kingdom Abstract histochemistry, DMRT1 (a male-specific transcriptional regulator) was identified as a likely candidate gene for Spermatocytic seminomas are solid tumors found solely in the involvement in the development of spermatocytic seminomas. testis of predominantly elderly individuals. We investigated these tumors using a genome-wide analysis for structural and (Cancer Res 2006; 66(1): 290-302) numerical chromosomal changes through conventional kar- yotyping, spectral karyotyping, and array comparative Introduction genomic hybridization using a 32 K genomic tiling-path Spermatocytic seminomas are benign testicular tumors that resolution BAC platform (confirmed by in situ hybridization).
[Show full text]
Supplementary Information Supplementary Note
Supplementary Information Supplementary Note Bulk RNA Sequencing and Data Processing: Total RNAs from the dorsolateral prefrontal cortex (Brodmann area 8/9) of 208 brains from the FHS/BUADC study were extracted using the Promega Maxwell RSC simplyRNA Tissue Kit (Cat No# AS1340) according to the manufacturer’s protocol. The integrity and quality of RNA (RNA integrity number, RIN) was determined using the Agilent 2100 Bioanalyzer with RNA 600 Nano Chips (Cat No# 5067-1511). After excluding brain samples with RIN < 5, brain samples were randomized into seven library batches based on diagnosis, APOE genotype, sex, and RIN. Since there were only seven samples from AD cases with APOE genotypes 2/2 or 2/3, these specimens were included in batches 1 to 3 only. The BU Microarray & Sequencing Resource Core performed RNA sequencing (RNA-seq) library preparation. The libraries were prepared from total RNA enriched for mRNA using NEBNext Poly(A) mRNA Magnetic Isolation Module and NEBNext Ultra II Directional RNA Library Preparation Kit for Illumina (New England Biolabs, USA) and sequenced on an Illumina NextSeq 500 instrument (Illumina, USA). A total of 193 of the 208 samples remained for mapping after pre-processing. The average coverage of the remaining samples was 50 million reads for the entire sample. RNA-seq data from 193 FHS/BUADC brains were processed by our automated pipeline. We conducted quality control of the RNA-seq data for sequencing quality, over-abundance of adaptors, and over-represented sequence using the FastQC. Low-quality reads (5% of the total) were filtered out using the Trimmomatic option, which is a fast, multithreaded command line tool to trim and crop Illumina (FASTQ) data and remove adapters 1.
[Show full text]
The Impact of Chromosomal Translocation Locus and Fusion Oncogene Coding Sequence in Synovial Sarcomagenesis
HHS Public Access Author manuscript Author ManuscriptAuthor Manuscript Author Oncogene Manuscript Author . Author manuscript; Manuscript Author available in PMC 2016 September 23. Published in final edited form as: Oncogene. 2016 September 22; 35(38): 5021–5032. doi:10.1038/onc.2016.38. The impact of chromosomal translocation locus and fusion oncogene coding sequence in synovial sarcomagenesis Kevin B. Jones1,2,3,*, Jared J. Barrott1,2,3, Mingchao Xie4, Malay Haldar5, Huifeng Jin1,2,3, Ju-Fen Zhu1,2,3, Michael J. Monument1,3, Tim L. Mosbruger3,6, Ellen M. Langer5, R. Lor Randall1,3, Richard K. Wilson4,7,8,9, Bradley R. Cairns2,3,10, Li Ding4,7,8,9, and Mario R. Capecchi5 1Department of Orthopaedics, University of Utah, Salt Lake City, Utah 84112, USA 2Department of Oncological Sciences, University of Utah, Salt Lake City, Utah 84112, USA 3Huntsman Cancer Institute, University of Utah, Salt Lake City, Utah 84112, USA 4Department of Medicine, Washington University, St. Louis, Missouri 63108, USA 5Department of Human Genetics, University of Utah, Salt Lake City, Utah, USA 6Deparment of Bioinformatics, University of Utah, Salt Lake City, Utah, 84112, USA 7McDonnell Genome Institute, Washington University, St. Louis, Missouri 63108, USA 8Department of Genetics, Washington University, St. Louis, Missouri 63108, USA 9Siteman Cancer Center, Washington University, St. Louis, Missouri 63108, USA 10Howard Hughes Medical Institute, University of Utah, Salt Lake City, UT 84112, USA Abstract Synovial sarcomas are aggressive soft-tissue malignancies that express chromosomal translocation-generated fusion genes, SS18-SSX1 or SS18-SSX2 in most cases. Here, we report a mouse sarcoma model expressing SS18-SSX1, complementing our prior model expressing SS18- SSX2.
[Show full text]
SSX2IP Mouse Monoclonal Antibody [Clone ID: OTI1B6] – TA807385S | Origene
OriGene Technologies, Inc. 9620 Medical Center Drive, Ste 200 Rockville, MD 20850, US Phone: +1-888-267-4436 [email protected] EU: [email protected] CN: [email protected] Product datasheet for TA807385S SSX2IP Mouse Monoclonal Antibody [Clone ID: OTI1B6] Product data: Product Type: Primary Antibodies Clone Name: OTI1B6 Applications: WB Recommended Dilution: WB 1:2000 Reactivity: Human, Mouse, Rat Host: Mouse Isotype: IgG1 Clonality: Monoclonal Immunogen: Human recombinant protein fragment corresponding to amino acids 1-272 of human SSX2IP(NP_054740) produced in E.coli. Formulation: PBS (PH 7.3) containing 1% BSA, 50% glycerol and 0.02% sodium azide. Concentration: 1 mg/ml Purification: Purified from mouse ascites fluids or tissue culture supernatant by affinity chromatography (protein A/G) Conjugation: Unconjugated Storage: Store at -20°C as received. Stability: Stable for 12 months from date of receipt. Predicted Protein Size: 71.1 kDa Gene Name: SSX family member 2 interacting protein Database Link: NP_054740 Entrez Gene 308023 RatEntrez Gene 117178 Human Q9Y2D8 Background: This gene encodes a protein that binds the cancer-testis antigen Synovial Sarcoma X breakpoint 2 protein. The encoded protein may regulate the activity of Synovial Sarcoma X breakpoint 2 protein in malignant cells. Alternate splicing results in multiple transcript variants. A pseudogene of this gene is found on chromosome 3. [provided by RefSeq, Oct 2009] This product is to be used for laboratory only. Not for diagnostic or therapeutic use. View online » ©2021 OriGene Technologies, Inc., 9620 Medical Center Drive, Ste 200, Rockville, MD 20850, US 1 / 2 SSX2IP Mouse Monoclonal Antibody [Clone ID: OTI1B6] – TA807385S Synonyms: ADIP; hMsd1 Protein Pathways: Adherens junction Product images: HEK293T cells were transfected with the pCMV6- ENTRY control (Left lane) or pCMV6-ENTRY SSX2IP ([RC207526], Right lane) cDNA for 48 hrs and lysed.
[Show full text]
SSX2IP Promotes Metastasis and Chemotherapeutic Resistance of Hepatocellular Carcinoma Pu Li1,2†, Ying Lin1†, Yu Zhang3, Zhenggang Zhu2* and Keke Huo1*
Li et al. Journal of Translational Medicine 2013, 11:52 http://www.translational-medicine.com/content/11/1/52 RESEARCH Open Access SSX2IP promotes metastasis and chemotherapeutic resistance of hepatocellular carcinoma Pu Li1,2†, Ying Lin1†, Yu Zhang3, Zhenggang Zhu2* and Keke Huo1* Abstract Background: Synovial sarcoma, X breakpoint 2 interacting protein (SSX2IP), which has been identified as an acute myeloid leukemia associated antigen, is a potential target for leukemia immunotherapy. In rodents, its homologous gene, ADIP, plays an important role in the regulation of cell adhesion and migration, underlying its potential role in promoting metastasis of other cancers. Methods: To investigate the correlation between the expression level of SSX2IP and the clinicopathologic factors of hepatocellular carcinoma (HCC), 53 cases were studied by qPCR and statisted. To directly testing SSX2IP’s contribution to HCC in animal models, 45 nude mice were enrolled in peritoneal spreading and liver metastasis models. For the migration and invasion assays, cell culture experiments were performed using QCMTM 24-Well Colorimetric Migration Assay Kit and Cell Invasion Assay Kit (Millipore). Moreover we examined the influence of SSX2IP overexpression on the chemosensitivity of hepatocellular carcinoma cells to two most common chemotherapy drugs (5-Fu and CDDP) using Cell counting kit-8 (CCK-8). The chemotherapeutic drugs sensitivity was evaluated by IC50 parameter. Results: Statistical analysis of clinical cases revealed that the SSX2IP high expression group had inclinations towards larger tumor size, more tumor thrombus and shorter survival period, implying a strong correlation between the expression level of SSX2IP and HCC tumorigenesis. Consistently in abdominal cavity metastasis and liver metastasis models of immune-deficient mice, SSX2IP was able to promote the metastasis of hepatoma cells.
[Show full text]
Supporting Information
Supporting Information Friedman et al. 10.1073/pnas.0812446106 SI Results and Discussion intronic miR genes in these protein-coding genes. Because in General Phenotype of Dicer-PCKO Mice. Dicer-PCKO mice had many many cases the exact borders of the protein-coding genes are defects in additional to inner ear defects. Many of them died unknown, we searched for miR genes up to 10 kb from the around birth, and although they were born at a similar size to hosting-gene ends. Out of the 488 mouse miR genes included in their littermate heterozygote siblings, after a few weeks the miRBase release 12.0, 192 mouse miR genes were found as surviving mutants were smaller than their heterozygote siblings located inside (distance 0) or in the vicinity of the protein-coding (see Fig. 1A) and exhibited typical defects, which enabled their genes that are expressed in the P2 cochlear and vestibular SE identification even before genotyping, including typical alopecia (Table S2). Some coding genes include huge clusters of miRNAs (in particular on the nape of the neck), partially closed eyelids (e.g., Sfmbt2). Other genes listed in Table S2 as coding genes are [supporting information (SI) Fig. S1 A and C], eye defects, and actually predicted, as their transcript was detected in cells, but weakness of the rear legs that were twisted backwards (data not the predicted encoded protein has not been identified yet, and shown). However, while all of the mutant mice tested exhibited some of them may be noncoding RNAs. Only a single protein- similar deafness and stereocilia malformation in inner ear HCs, coding gene that is differentially expressed in the cochlear and other defects were variable in their severity.
[Show full text]