SSX6 Antibody Cat

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SSX6 Antibody Cat. No.: 25-337 SSX6 Antibody Specifications HOST SPECIES: Rabbit SPECIES REACTIVITY: Human Antibody produced in rabbits immunized with a synthetic peptide corresponding a region IMMUNOGEN: of human SSX6. TESTED APPLICATIONS: ELISA, WB SSX6 antibody can be used for detection of SSX6 by ELISA at 1:1562500. SSX6 antibody can APPLICATIONS: be used for detection of SSX6 by western blot at 1 μg/mL, and HRP conjugated secondary antibody should be diluted 1:50,000 - 100,000. POSITIVE CONTROL: 1) Cat. No. 1211 - HepG2 Cell Lysate PREDICTED MOLECULAR 22 kDa WEIGHT: Properties PURIFICATION: Antibody is purified by peptide affinity chromatography method. CLONALITY: Polyclonal CONJUGATE: Unconjugated PHYSICAL STATE: Liquid October 2, 2021 1 https://www.prosci-inc.com/ssx6-antibody-25-337.html Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% BUFFER: sucrose. CONCENTRATION: batch dependent For short periods of storage (days) store at 4˚C. For longer periods of storage, store SSX6 STORAGE CONDITIONS: antibody at -20˚C. As with any antibody avoid repeat freeze-thaw cycles. Additional Info OFFICIAL SYMBOL: SSX6 ALTERNATE NAMES: SSX6, dJ54B20.1, SSXP2, psiSSX2 ACCESSION NO.: NP_775493 PROTEIN GI NO.: 27659730 GENE ID: 280657 USER NOTE: Optimal dilutions for each application to be determined by the researcher. Background and References SSX6 belongs to the family of highly homologous synovial sarcoma X (SSX) breakpoint proteins. These proteins may function as transcriptional repressors. They are also capable of eliciting spontaneously humoral and cellular immune responses in cancer patients, and are potentially useful targets in cancer vaccine-based immunotherapy.The product of this gene belongs to the family of highly homologous synovial sarcoma X (SSX) breakpoint BACKGROUND: proteins. These proteins may function as transcriptional repressors. They are also capable of eliciting spontaneously humoral and cellular immune responses in cancer patients, and are potentially useful targets in cancer vaccine-based immunotherapy. SSX1, SSX2 and SSX4 genes have been involved in the t (X;18) translocation characteristically found in all synovial sarcomas. This gene appears not to be involved in this type of chromosome translocation. REFERENCES: 1) de (2007) Genes Chromosomes Cancer 46 (2), 107-117. ANTIBODIES FOR RESEARCH USE ONLY. For additional information, visit ProSci's Terms & Conditions Page. October 2, 2021 2 https://www.prosci-inc.com/ssx6-antibody-25-337.html.

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SS18 (SYT) (18Q11) Gene Rearrangement by FISH Indications for Ordering Genetics
SS18 (SYT) (18q11) Gene Rearrangement by FISH Indications for Ordering Genetics Diagnosis of synovial sarcoma in conjunction with histologic Translocations – SS18-SSX1, SS18-SSX2 and clinical information Structure/function Test Description • SS18 is located on chromosome 18 • SSX1 and SSX2 are located on the X-chromosome Fluorescence in situ hybridization • Each gene in the translocation codes for proteins that have opposite transcriptional functions Tests to Consider o SS18 – activator of oncogenes Primary test o SSX1, SSX2 – tumor suppression SS18 (SYT) (18q11) Gene Rearrangement by FISH 3001303 Test Interpretation • Molecular diagnosis of synovial sarcoma Results Related test • Positive – SS18 rearrangement is detected Chromosome FISH, Interphase 2002298 o SSX translocation partner is not identified with this • Specific probe for SS18 (SYT) rearrangement must be testing methodology requested o Synovial sarcoma likely • Fresh tissue specimens only • Negative – no SS18 rearrangement detected Disease Overview o Does not entirely exclude the presence of an SS18 rearrangement as some translocations are cryptic and Incidence – rare not evaluable by this testing methodology • Synovial sarcomas account for 8-10% of all soft tissue o Does not entirely exclude diagnosis of synovial sarcoma sarcomas Limitations Diagnostic/prognostic issues • Testing using tissue fixed in alcohol-based or non-formalin • Synovial sarcomas may resemble other neoplasms, fixatives has not been validated using this method particularly those displaying an epithelioid, spindle cell, or • SS18 fusion partners are not detected with this test combined morphology • t(X;18)(p11.2;q11.2) translocation serves as a specific marker for synovial sarcoma o SS18 (SYT) gene fuses with SSX gene . Fusion with SSX1 in ~65% of synovial sarcomas .
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SYT-SSX1 and SYT-SSX2 Interfere with Repression of E-Cadherin by Snail and Slug
Research Article SYT-SSX1 and SYT-SSX2 Interfere with Repression of E-Cadherin by Snail and Slug: A Potential Mechanism for Aberrant Mesenchymal to Epithelial Transition in Human Synovial Sarcoma Tsuyoshi Saito, Makoto Nagai, and Marc Ladanyi Department of Pathology, Memorial Sloan-Kettering Cancer Center, New York, New York Abstract open spaces [i.e., glandular epithelial differentiation (GED)] in a Synovial sarcoma is a primitive mesenchymal neoplasm background of spindle cells (Supplementary Fig. S1). Both the characterized in almost all cases by a t(X;18) fusing the SYT spindle and epithelial elements of synovial sarcoma contain transcriptional coactivator gene with either SSX1 or SSX2, the t(X;18) and are thus clonally related (2, 3). The GED in synovial with the resulting fusion gene encoding an aberrant tran- sarcoma has the hallmarks of a genuine mesenchymal to epithelial scriptional regulator.A subset of synovial sarcoma, predom- transition (MET) akin to those seen in embryonic development inantly cases with the SYT-SSX1 fusion, shows foci of (e.g., in developing kidney). Thus, the epithelial cells in synovial h morphologic epithelial differentiation in the form of nests of sarcoma express E-cadherin, keratins, a-catenin, -catenin, and glandular epithelium.The striking spontaneous mesenchymal g-catenin, whereas the spindle cells express vimentin and, focally, to epithelial differentiation in this cancer is reminiscent of a N-cadherin (4, 5). Epithelial differentiation in synovial sarcoma is developmental switch, but the only
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A Novel Type of SYT/SSX Fusion
A Novel Type of SYT/SSX Fusion: Methodological and Biological Implications Maria Törnkvist, M.Sc., Bertha Brodin, Ph.D., Armando Bartolazzi, M.D., Ph.D., Olle Larsson, M.D., Ph.D. Department of Cellular and Molecular Tumor Pathology, Cancer Centrum Karolinska, Karolinska Hospital (MT, BB, AB, OL), Stockholm, Sweden; and Department of Pathology, Regina Elena Cancer Institute (AB), Rome, Italy the presence of SYT/SSX transcripts in two cases Synovial sarcoma (SS) is a rare soft-tissue tumor using the proposed RT-PCR approach. Applications that affects children and young adults. It is charac- of optimized RT-PCR can contribute to reduce false- terized by the chromosomal translocation t(X; negative SYT/SSX SS cases reported in literature. 18)(p11.2;q11.2), which results in the fusion of the SYT gene on chromosome 18 with a SSX gene on KEY WORDS: RT-PCR, Synovial sarcoma, SYT/SSX chromosome X. In the majority of cases, SYT is fusion gene, SYT/SSX variants. fused to exon 5 of SSX1 (64%), SSX2 (36%), or, Mod Pathol 2002;15(6):679–685 rarely, SSX4. A novel fusion transcript variant deriv- ing from the fusion of SYT to exon 6 of SSX4 gene Synovial sarcomas (SS) account for 7 to 10% of all (SYT/SSX4v) was found coexpressed in one of the human soft-tissue sarcomas and are mainly located previously reported SYT/SSX4 cases. In the present in the extremities in the vicinity of large joints (1). investigation, we describe a new SS case that was Depending on histomorphological appearance, SSs previously shown to be negative for SYT/SSX1 and are usually subdivided into two major forms, bipha- SYT/SSX2 expression by conventional reverse tran- sic and monophasic.
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A Novel FISH Assay for SS18–SSX Fusion Type in Synovial Sarcoma
Laboratory Investigation (2004) 84, 1185–1192 & 2004 USCAP, Inc All rights reserved 0023-6837/04 $30.00 www.laboratoryinvestigation.org A novel FISH assay for SS18–SSX fusion type in synovial sarcoma Cecilia Surace1,2, Ioannis Panagopoulos1, Eva Pa˚lsson1, Mariano Rocchi2, Nils Mandahl1 and Fredrik Mertens1 1Department of Clinical Genetics, Lund University Hospital, Lund, Sweden and 2DAPEG, Section of Genetics, University of Bari, Bari, Italy Synovial sarcoma is a morphologically, clinically and genetically distinct entity that accounts for 5–10% of all soft tissue sarcomas. The t(X;18)(p11.2;q11.2) is the cytogenetic hallmark of synovial sarcoma and is present in more than 90% of the cases. It produces three types of fusion gene formed in part by SS18 from chromosome 18 and by SSX1, SSX2 or, rarely, SSX4 from the X chromosome. The SS18–SSX fusions do not seem to occur in other tumor types, and it has been shown that in synovial sarcoma a clear correlation exists between the type of fusion gene and histologic subtype and, more importantly, clinical outcome. Previous analyses regarding the type of fusion genes have been based on PCR amplification of the fusion transcript, requiring access to good- quality RNA. In order to obtain an alternative tool to diagnose and follow this malignancy, we developed a fluorescence in situ hybridization (FISH) assay that could distinguish between the two most common fusion genes, that is, SS18–SSX1 and SS18–SSX2. The specificity of the selected bacterial artificial chromosome clones used in the detection of these fusion genes, as well as the sensitivity of the analysis in metaphase and interphase cells, was examined in a series of 28 synovial sarcoma samples with known fusion gene status.
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Gene Section Review
Atlas of Genetics and Cytogenetics in Oncology and Haematology OPEN ACCESS JOURNAL AT INIST-CNRS Gene Section Review SSX2 (Synovial Sarcoma, X breakpoint 2) Josiane Eid, Christina Garcia, Andrea Frump Department of Cancer Biology, Vanderbilt University Medical Center, Nashville, TN 37232, USA (JE, CG, AF) Published in Atlas Database: April 2008 Online updated version: http://AtlasGeneticsOncology.org/Genes/SSX2ID42406chXp11.html DOI: 10.4267/2042/44431 This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 2.0 France Licence. © 2009 Atlas of Genetics and Cytogenetics in Oncology and Haematology detected in liver, testis, skin melanoma, endometrium, Identity choriocarcinoma, placenta, spleen of Hodgkins Other names: CT5.2; HD21; HOM-MEL-40; lymphoma. MGC119055; MGC15364; MGC3884; RP11-552J9.2; SSX; SSX2A; SSX2B Protein HGNC (Hugo): SSX2 Location: Xp11.22 Description So far, two SSX2 protein isoforms (a and b) are known DNA/RNA to exist. Their mRNAs correspond to SV1 (1466 bases) and SV3 (1322 bases) splice variants, respectively. The Description start codon for both isoforms is located in Exon 2. The SSX2 gene locus encompasses 9 exons and 10,304 SSX2 isoform a is 233 amino acids (26.5 kD) and bp (Xp11; 52,752,974-52,742,671). SSX2 isoform b 188 amino acids (21.6 kD). Of both isoforms, SSX2 isoform b is the most commonly seen Transcription and so far the best studied. The SSX2 gene is transcribed on the minus strand. 7 SSX2 mRNA splice variants (SV1-SV7) have been SSX2 Locus and mRNA Splice Variants. Note: Exons are drawn to scale. Atlas Genet Cytogenet Oncol Haematol.
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Aneuploidy: Using Genetic Instability to Preserve a Haploid Genome?
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Li Et Al. 1 Genetic Interactions Between Mediator and the Late G1
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SSX4 Antibody Cat
SSX4 Antibody Cat. No.: 56-923 SSX4 Antibody Specifications HOST SPECIES: Rabbit SPECIES REACTIVITY: Human This SSX4 antibody is generated from rabbits immunized with a KLH conjugated synthetic IMMUNOGEN: peptide between 63-91 amino acids from the Central region of human SSX4. TESTED APPLICATIONS: WB APPLICATIONS: For WB starting dilution is: 1:1000 PREDICTED MOLECULAR 22 kDa WEIGHT: Properties This antibody is purified through a protein A column, followed by peptide affinity PURIFICATION: purification. CLONALITY: Polyclonal ISOTYPE: Rabbit Ig CONJUGATE: Unconjugated PHYSICAL STATE: Liquid September 25, 2021 1 https://www.prosci-inc.com/ssx4-antibody-56-923.html BUFFER: Supplied in PBS with 0.09% (W/V) sodium azide. CONCENTRATION: batch dependent Store at 4˚C for three months and -20˚C, stable for up to one year. As with all antibodies STORAGE CONDITIONS: care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures. Additional Info OFFICIAL SYMBOL: SSX4 ALTERNATE NAMES: Protein SSX4, Cancer/testis antigen 54, CT54, SSX4, SSX4A ACCESSION NO.: O60224 GENE ID: 548313, 6759 USER NOTE: Optimal dilutions for each application to be determined by the researcher. Background and References The product of this gene belongs to the family of highly homologous synovial sarcoma X (SSX) breakpoint proteins. These proteins may function as transcriptional repressors. They are also capable of eliciting spontaneously humoral and cellular immune responses in cancer patients, and are potentially useful targets in cancer vaccine-based immunotherapy. SSX1, SSX2 and SSX4 genes have been involved in the t(X;18) BACKGROUND: translocation characteristically found in all synovial sarcomas.
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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.
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Product Sheet CA1235
SSX2 Antibody Applications: WB, IHC Detected MW: 25 kDa Cat. No. CA1235 Species & Reactivity: Human, Mouse, Rat Isotype: Rabbit IgG BACKGROUND SSX2 belongs to the family of highly homologous based immunotherapy.4 Two transcript variants synovial sarcoma X (SSX) breakpoint proteins. encoding distinct isoforms have been identified for The SSX gene family is composed of at least 9 SSX2 gene. SSX2 is thought to function in functional and highly homologous members and development and germ line cells as a repressive shown to be located on chromosome X. The gene regulator. Its control of gene expression is normal testis expresses SSX1, 2, 3, 4, 5, and 7, believed to be epigenetic in nature and to involve but not 6, 8, or 9. In tumors, SSX1, 2, and 4 are chromatin modification and remodeling. It is most expressed at varying frequencies, whereas SSX3, likely mediated by the association of SSX2 with the 5, and 6 are rarely expressed. In addition, no Polycomb gene silencing complex at the SSXRD expression of SSX8, or 9 has been observed. SSX1 domain. Polycomb silencing involves chromatin to SSX5 are also normally expressed in thyroid.1 compaction, DNA methylation, repressive histone The SSX family shares nucleotide homology modifications and inaccessibility of promoter ranging from 88% to 95%, and amino acid regions to transcription machineries. Other SSX2- homology ranging from 77% to 91%. The NH2- interacting partners include the LIM homeobox terminal moieties of the SSX proteins exhibit protein LHX4, a Ras-like GTPase Interactor, homology to the Krüppel-associated box (KRAB) RAB3IP thought to be involved in vesicular domain, a domain that is known to be involved in transport, and SSX2IP, a putative cell transcriptional repression.
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Identification of SYT-SSX Transcripts from Synovial Sarcomas Using RT-Multiplex PCR and Capillary Electrophoresis
Modern Pathology (2006) 19, 641–647 & 2006 USCAP, Inc All rights reserved 0893-3952/06 $30.00 www.modernpathology.org Identification of SYT-SSX transcripts from synovial sarcomas using RT-multiplex PCR and capillary electrophoresis John A Thorson, Helmut C Weigelin, Robert E Ruiz, Jennifer K Howard and David R Lucas Department of Pathology, University of Michigan, Ann Arbor, MI, USA Synovial sarcomas are highly malignant tumors of soft tissue which are characterized by the t(X;18) resulting in SYT-SSX fusion transcript production. Diagnosis of these tumors based on histology can be challenging, particularly when minimal biopsy specimens are presented to the pathologist. Demonstration by molecular methods of SYT-SSX transcripts is a useful adjunct for diagnosis in these situations. We have developed an assay, which combines one-step RT-multiplex PCR with capillary electrophoresis to detect and genotype the SYT-SSX transcripts from synovial sarcomas. Small amplicons from chimeric transcripts as well as GAPD transcripts are differentially labeled with fluorophores, allowing detection and size discrimination by capillary electrophoresis. In a study of 32 formalin-fixed soft tissue tumor specimens, the assay detected chimeric transcripts from 17/22 (77%) synovial sarcomas. All five assay negative specimens yielded no intact RNA as evidenced by lack of a GAPD amplicon. Chimeric transcripts were not detected in 9/9 malignant peripheral nerve sheath tumors or 1/1 epithelioid sarcoma. Representative amplicons were sequenced and confirmed the genotype results obtained by capillary electrophoresis. One-step RT-multiplex PCR combined with capillary electrophoresis is a rapid and accurate method for the detection and genotypic classification of SYT-SSX transcripts from fixed tissue specimens.
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Multi-Omics Discovery of Exome-Derived Neoantigens in Hepatocellular Carcinoma Markus W
Löffler et al. Genome Medicine (2019) 11:28 https://doi.org/10.1186/s13073-019-0636-8 RESEARCH Open Access Multi-omics discovery of exome-derived neoantigens in hepatocellular carcinoma Markus W. Löffler1,2,3,4*† , Christopher Mohr5,6†, Leon Bichmann2,7,8, Lena Katharina Freudenmann2,3, Mathias Walzer2,7,8,9, Christopher M. Schroeder10, Nico Trautwein2, Franz J. Hilke10, Raphael S. Zinser2, Lena Mühlenbruch2, Daniel J. Kowalewski2,11, Heiko Schuster2,11, Marc Sturm10, Jakob Matthes10, Olaf Riess10,12, Stefan Czemmel6, Sven Nahnsen6, Ingmar Königsrainer1, Karolin Thiel1, Silvio Nadalin1, Stefan Beckert1,13, Hans Bösmüller14, Falko Fend14, Ana Velic15, Boris Maček15, Sebastian P. Haen2,3,16, Luigi Buonaguro17, Oliver Kohlbacher3,5,6,7,8,12,18, Stefan Stevanović2,3, Alfred Königsrainer1,3, HEPAVAC Consortium and Hans-Georg Rammensee2,3 Abstract Background: Although mutated HLA ligands are considered ideal cancer-specific immunotherapy targets, evidence for their presentation is lacking in hepatocellular carcinomas (HCCs). Employing a unique multi-omics approach comprising a neoepitope identification pipeline, we assessed exome-derived mutations naturally presented as HLA class I ligands in HCCs. Methods: In-depth multi-omics analyses included whole exome and transcriptome sequencing to define individual patient-specific search spaces of neoepitope candidates. Evidence for the natural presentation of mutated HLA ligands was investigated through an in silico pipeline integrating proteome and HLA ligandome profiling data. Results: The approach was successfully validated in a state-of-the-art dataset from malignant melanoma, and despite multi-omics evidence for somatic mutations, mutated naturally presented HLA ligands remained elusive in HCCs. An analysis of extensive cancer datasets confirmed fundamental differences of tumor mutational burden in HCC and malignant melanoma, challenging the notion that exome-derived mutations contribute relevantly to the expectable neoepitope pool in malignancies with only few mutations.
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