Melan-A Antibody [MLANA/788] Cat

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Melan-A Antibody [MLANA/788] Cat. No.: 33-360 Melan-A Antibody [MLANA/788] Formalin-fixed, paraffin-embedded human melanoma stained with Melan-A antibody (MLANA/788). Specifications HOST SPECIES: Mouse SPECIES REACTIVITY: Dog, Human, Mouse, Rat Recombinant human MLANA protein was used as the immunogen for the Melan-A IMMUNOGEN: antibody. TESTED APPLICATIONS: Flow, IF, IHC-P, WB September 26, 2021 1 https://www.prosci-inc.com/melan-a-antibody-mlana-788-33-360.html Flow Cytometry: 0.5-1 ug/million cells in 0.1ml Immunofluorescence: 0.5-1 ug/ml Immunohistochemistry (FFPE): 0.5-1 ug/ml for 30 min at RT (1) Western blot: 0.5-1 ug/ml APPLICATIONS: Prediluted format : incubate for 30 min at RT (2) Optimal dilution of the Melan-A antibody should be determined by the researcher. 1. Staining of formalin-fixed tissues is enhanced by boiling tissue sections in 10mM Citrate buffer, pH 6.0, for 10-20 min followed by cooling at RT for 20 minutes 2. The prediluted format is supplied in a dropper bottle and is optimized for use in IHC. After epitope retrieval step (if required), drip mAb solution onto the tissue section and incubate at RT for 30 min. Properties PURIFICATION: Protein G affinity chromatography CLONALITY: Monoclonal ISOTYPE: IgG1 CONJUGATE: Unconjugated PHYSICAL STATE: Liquid BUFFER: PBS with 0.1 mg/ml BSA and 0.05% sodium azide CONCENTRATION: 0.2 mg/mL STORAGE CONDITIONS: Aliquot and Store at 2-8˚C. Avoid freez-thaw cycles. Additional Info OFFICIAL SYMBOL: MLANA ALTERNATE NAMES: MLANA, Antigen LB39-AA, Antigen SK29-AA, Melan-A, Protein Melan-A, MART-1, MART1 GENE ID: 2315 USER NOTE: Optimal dilutions for each application to be determined by the researcher Background and References This antibody recognizes a protein doublet of 20-22kDa, identified as MART-1 (Melanoma Antigen Recognized by T cells 1) or Melan-A. MART-1 is a newly identified melanocyte differentiation antigen recognized by autologous cytotoxic T lymphocytes. Seven other melanoma associated antigens recognized by autologous BACKGROUND: cytotoxic T cells include MAGE-1, MAGE-3, tyrosinase, gp100, gp75, BAGE-1, and GAGE-1. Subcellular fractionation shows that MART-1 is present in melanosomes and endoplasmic reticulum. This mAb labels melanomas and other tumors showing melanocytic differentiation. It is also a useful positive-marker for angiomyolipomas. It does not stain tumor cells of epithelial, lymphoid, glial, or mesenchymal origin. September 26, 2021 2 https://www.prosci-inc.com/melan-a-antibody-mlana-788-33-360.html ANTIBODIES FOR RESEARCH USE ONLY. For additional information, visit ProSci's Terms & Conditions Page. September 26, 2021 3 https://www.prosci-inc.com/melan-a-antibody-mlana-788-33-360.html.

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Enhancer-Targeted Genome Editing Selectively Blocks Innate Resistance to Oncokinase Inhibition
Downloaded from genome.cshlp.org on September 26, 2021 - Published by Cold Spring Harbor Laboratory Press Webster et al. Enhancer-targeted genome editing selectively blocks innate resistance to oncokinase inhibition Dan E. Webster1, Brook Barajas1*, Rose T. Bussat1*, Karen J. Yan1, Poornima H. Neela1, Ross J. Flockhart1, Joanna Kovalski1, Ashley Zehnder1, and Paul A. Khavari1, ¶ 1The Program in Epithelial Biology, Stanford University School of Medicine, Stanford, CA 94305 USA *These authors made equal and independent contributions. ¶ Correspondence to: P.A.K. at [email protected] Running title: Enhancer disruption blocks oncokinase resistance Keywords: Cancer Epigenomics, Enhancer, TALE nuclease, Chromosome conformation, BRAF, MITF Downloaded from genome.cshlp.org on September 26, 2021 - Published by Cold Spring Harbor Laboratory Press ABSTRACT Thousands of putative enhancers are characterized in the human genome, yet few have been shown to have a functional role in cancer progression. Inhibiting oncokinases, such as EGFR, ALK, ERBB2, and BRAF, is a mainstay of current cancer therapy but is hindered by innate drug resistance mediated by upregulation of the HGF receptor, MET. The mechanisms mediating such genomic responses to targeted therapy are unknown. Here, we identify lineage- specific enhancers at the MET locus for multiple common tumor types, including a melanoma lineage-specific enhancer 63kb downstream of the MET TSS. This enhancer displays inducible chromatin looping with the MET promoter to upregulate MET expression upon BRAF inhibition. Epigenomic analysis demonstrated that the melanocyte-specific transcription factor, MITF, mediates this enhancer function. Targeted genomic deletion (<7bp) of the MITF motif within the MET enhancer suppressed inducible chromatin looping and innate drug resistance, while maintaining MITF-dependent, inhibitor-induced melanoma cell differentiation.
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Supplementary Materials
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Crystal Structure of the Gamma-2 Herpesvirus LANA DNA Binding Domain Identifies Charged Surface Residues Which Impact Viral Latency The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Correia, B., S. A. Cerqueira, C. Beauchemin, M. Pires de Miranda, S. Li, R. Ponnusamy, L. Rodrigues, et al. 2013. “Crystal Structure of the Gamma-2 Herpesvirus LANA DNA Binding Domain Identifies Charged Surface Residues Which Impact Viral Latency.” PLoS Pathogens 9 (10): e1003673. doi:10.1371/journal.ppat.1003673. http://dx.doi.org/10.1371/journal.ppat.1003673. Published Version doi:10.1371/journal.ppat.1003673 Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:11878899 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA Crystal Structure of the Gamma-2 Herpesvirus LANA DNA Binding Domain Identifies Charged Surface Residues Which Impact Viral Latency Bruno Correia1., Sofia A. Cerqueira2., Chantal Beauchemin3, Marta Pires de Miranda2, Shijun Li3, Rajesh Ponnusamy1,Le´nia Rodrigues2, Thomas R. Schneider4, Maria A. Carrondo1*, Kenneth M. Kaye3*, J. Pedro Simas2*, Colin E. McVey1* 1 Instituto de Tecnologia Quı´mica e Biolo´gica, Universidade Nova de Lisboa, Oeiras, Portugal, 2 Instituto de Microbiologia e Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal, 3 Departments of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, United States of America, 4 EMBL c/o DESY, Hamburg, Germany Abstract Latency-associated nuclear antigen (LANA) mediates c2-herpesvirus genome persistence and regulates transcription.
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By MITF in Melanocytes and Melanoma
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