Malt1 (NM 172833) Mouse Recombinant Protein Product Data

Total Page：16

File Type：pdf, Size：1020Kb

Malt1 (NM 172833) Mouse Recombinant Protein Product Data

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 TP524110 Malt1 (NM_172833) Mouse Recombinant Protein Product data: Product Type: Recombinant Proteins Description: Purified recombinant protein of Mouse mucosa associated lymphoid tissue lymphoma translocation gene 1 (Malt1), full length, with C-terminal MYC/DDK tag, expressed in HEK293T cells, 20ug Species: Mouse Expression Host: HEK293T Tag: C-Myc/DDK Predicted MW: 92.5 kDa Concentration: >50 ug/mL as determined by microplate BCA method Purity: > 80% as determined by SDS-PAGE and Coomassie blue staining Buffer: 25 mM Tris.HCl, pH 7.3, 100 mM glycine, 10% glycerol. Storage: Store at -80°C. Avoid repeated freeze-thaw cycles. Stable for at least 3 months from receipt of products under proper storage and handling conditions. Stability: Stable for 12 months from the date of receipt of the product under proper storage and handling conditions. Avoid repeated freeze-thaw cycles. RefSeq: NP_766421 Locus ID: 240354 UniProt ID: Q2TBA3 RefSeq Size: 5008 Cytogenetics: 18 E1 RefSeq ORF: 2463 Synonyms: A630046N12; D430033E09Rik; Pcasp1 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 Malt1 (NM_172833) Mouse Recombinant Protein – TP524110 Summary: Enhances BCL10-induced activation of NF-kappa-B. Involved in nuclear export of BCL10. Binds to TRAF6, inducing TRAF6 oligomerization and activation of its ligase activity. Has ubiquitin ligase activity (By similarity). MALT1-dependent BCL10 cleavage plays an important role in T-cell antigen receptor-induced integrin adhesion (By similarity). Involved in the induction of T helper 17 cells (Th17) differentiation. Cleaves RC3H1 and ZC3H12A in response to T-cell receptor (TCR) stimulation which releases their cooperatively repressed targets to promote Th17 cell differentiation (PubMed:25282160).[UniProtKB/Swiss-Prot Function] Product images: Coomassie blue staining of purified Malt1 protein (Cat# TP524110). The protein was produced from HEK293T cells transfected with Malt1 cDNA clone (Cat# [MR224110]) using MegaTran 2.0 (Cat# [TT210002]). This product is to be used for laboratory only. Not for diagnostic or therapeutic use. ©2021 OriGene Technologies, Inc., 9620 Medical Center Drive, Ste 200, Rockville, MD 20850, US 2 / 2.

Copy Link

Recommended publications

Role of CCCH-Type Zinc Finger Proteins in Human Adenovirus Infections
viruses Review Role of CCCH-Type Zinc Finger Proteins in Human Adenovirus Infections Zamaneh Hajikhezri 1, Mahmoud Darweesh 1,2, Göran Akusjärvi 1 and Tanel Punga 1,* 1 Department of Medical Biochemistry and Microbiology, Uppsala University, 75123 Uppsala, Sweden; [email protected] (Z.H.); [email protected] (M.D.); [email protected] (G.A.) 2 Department of Microbiology and Immunology, Al-Azhr University, Assiut 11651, Egypt * Correspondence: [email protected]; Tel.: +46-733-203-095 Received: 28 October 2020; Accepted: 16 November 2020; Published: 18 November 2020 Abstract: The zinc finger proteins make up a significant part of the proteome and perform a huge variety of functions in the cell. The CCCH-type zinc finger proteins have gained attention due to their unusual ability to interact with RNA and thereby control different steps of RNA metabolism. Since virus infections interfere with RNA metabolism, dynamic changes in the CCCH-type zinc finger proteins and virus replication are expected to happen. In the present review, we will discuss how three CCCH-type zinc finger proteins, ZC3H11A, MKRN1, and U2AF1, interfere with human adenovirus replication. We will summarize the functions of these three cellular proteins and focus on their potential pro- or anti-viral activities during a lytic human adenovirus infection. Keywords: human adenovirus; zinc finger protein; CCCH-type; ZC3H11A; MKRN1; U2AF1 1. Zinc Finger Proteins Zinc finger proteins are a big family of proteins with characteristic zinc finger (ZnF) domains present in the protein sequence. The ZnF domains consists of various ZnF motifs, which are short 30–100 amino acid sequences, coordinating zinc ions (Zn2+).
[Show full text]
Binding Specificities of Human RNA Binding Proteins Towards Structured
bioRxiv preprint doi: https://doi.org/10.1101/317909; this version posted March 1, 2019. 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. 1 Binding specificities of human RNA binding proteins towards structured and linear 2 RNA sequences 3 4 Arttu Jolma1,#, Jilin Zhang1,#, Estefania Mondragón4,#, Teemu Kivioja2, Yimeng Yin1, 5 Fangjie Zhu1, Quaid Morris5,6,7,8, Timothy R. Hughes5,6, Louis James Maher III4 and Jussi 6 Taipale1,2,3,* 7 8 9 AUTHOR AFFILIATIONS 10 11 1Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Solna, Sweden 12 2Genome-Scale Biology Program, University of Helsinki, Helsinki, Finland 13 3Department of Biochemistry, University of Cambridge, Cambridge, United Kingdom 14 4Department of Biochemistry and Molecular Biology and Mayo Clinic Graduate School of 15 Biomedical Sciences, Mayo Clinic College of Medicine and Science, Rochester, USA 16 5Department of Molecular Genetics, University of Toronto, Toronto, Canada 17 6Donnelly Centre, University of Toronto, Toronto, Canada 18 7Edward S Rogers Sr Department of Electrical and Computer Engineering, University of 19 Toronto, Toronto, Canada 20 8Department of Computer Science, University of Toronto, Toronto, Canada 21 #Authors contributed equally 22 *Correspondence: [email protected] 23 24 25 SUMMARY 26 27 Sequence specific RNA-binding proteins (RBPs) control many important 28 processes affecting gene expression. They regulate RNA metabolism at multiple 29 levels, by affecting splicing of nascent transcripts, RNA folding, base modification, 30 transport, localization, translation and stability. Despite their central role in most 31 aspects of RNA metabolism and function, most RBP binding specificities remain 32 unknown or incompletely defined.
[Show full text]
Analysis of the Indacaterol-Regulated Transcriptome in Human Airway
Supplemental material to this article can be found at: http://jpet.aspetjournals.org/content/suppl/2018/04/13/jpet.118.249292.DC1 1521-0103/366/1/220–236$35.00 https://doi.org/10.1124/jpet.118.249292 THE JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS J Pharmacol Exp Ther 366:220–236, July 2018 Copyright ª 2018 by The American Society for Pharmacology and Experimental Therapeutics Analysis of the Indacaterol-Regulated Transcriptome in Human Airway Epithelial Cells Implicates Gene Expression Changes in the s Adverse and Therapeutic Effects of b2-Adrenoceptor Agonists Dong Yan, Omar Hamed, Taruna Joshi,1 Mahmoud M. Mostafa, Kyla C. Jamieson, Radhika Joshi, Robert Newton, and Mark A. Giembycz Departments of Physiology and Pharmacology (D.Y., O.H., T.J., K.C.J., R.J., M.A.G.) and Cell Biology and Anatomy (M.M.M., R.N.), Snyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada Received March 22, 2018; accepted April 11, 2018 Downloaded from ABSTRACT The contribution of gene expression changes to the adverse and activity, and positive regulation of neutrophil chemotaxis. The therapeutic effects of b2-adrenoceptor agonists in asthma was general enriched GO term extracellular space was also associ- investigated using human airway epithelial cells as a therapeu- ated with indacaterol-induced genes, and many of those, in- tically relevant target. Operational model-fitting established that cluding CRISPLD2, DMBT1, GAS1, and SOCS3, have putative jpet.aspetjournals.org the long-acting b2-adrenoceptor agonists (LABA) indacaterol, anti-inflammatory, antibacterial, and/or antiviral activity. Numer- salmeterol, formoterol, and picumeterol were full agonists on ous indacaterol-regulated genes were also induced or repressed BEAS-2B cells transfected with a cAMP-response element in BEAS-2B cells and human primary bronchial epithelial cells by reporter but differed in efficacy (indacaterol $ formoterol .
[Show full text]
The Roles of Malt1 in Nf-Κb Activation and Solid Tumor Progression
The Texas Medical Center Library DigitalCommons@TMC The University of Texas MD Anderson Cancer Center UTHealth Graduate School of The University of Texas MD Anderson Cancer Biomedical Sciences Dissertations and Theses Center UTHealth Graduate School of (Open Access) Biomedical Sciences 5-2016 THE ROLES OF MALT1 IN NF-κB ACTIVATION AND SOLID TUMOR PROGRESSION Deng Pan Follow this and additional works at: https://digitalcommons.library.tmc.edu/utgsbs_dissertations Part of the Animal Diseases Commons, Animals Commons, Biochemistry Commons, Cancer Biology Commons, Cell Biology Commons, Disease Modeling Commons, Molecular Biology Commons, Molecular Genetics Commons, and the Oncology Commons Recommended Citation Pan, Deng, "THE ROLES OF MALT1 IN NF-κB ACTIVATION AND SOLID TUMOR PROGRESSION" (2016). The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences Dissertations and Theses (Open Access). 651. https://digitalcommons.library.tmc.edu/utgsbs_dissertations/651 This Dissertation (PhD) is brought to you for free and open access by the The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences at DigitalCommons@TMC. It has been accepted for inclusion in The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences Dissertations and Theses (Open Access) by an authorized administrator of DigitalCommons@TMC. For more information, please contact [email protected]. THE ROLES OF MALT1 IN NF-κB ACTIVATION AND SOLID TUMOR PROGRESSION by Deng Pan, B.S. APPROVED: ______________________________ Xin Lin, Ph.D. , Advisory Professor ______________________________ Paul Chiao, Ph.D. ______________________________ Dos Sarbassov, Ph.D. ______________________________ M. James You, M.D., Ph.D. ______________________________ Chengming Zhu, Ph.D.
[Show full text]
RC3H1 Antibody (C-Term) Affinity Purified Rabbit Polyclonal Antibody (Pab) Catalog # Ap14162b
10320 Camino Santa Fe, Suite G San Diego, CA 92121 Tel: 858.875.1900 Fax: 858.622.0609 RC3H1 Antibody (C-term) Affinity Purified Rabbit Polyclonal Antibody (Pab) Catalog # AP14162b Specification RC3H1 Antibody (C-term) - Product Information Application WB, IHC-P,E Primary Accession Q5TC82 Other Accession Q6NUC6, Q4VGL6, NP_742068.1 Reactivity Human Predicted Mouse, Xenopus Host Rabbit Clonality Polyclonal Isotype Rabbit Ig Calculated MW 125736 Antigen Region 1015-1043 RC3H1 Antibody (C-term) - Additional Information RC3H1 Antibody (C-term) (Cat. #AP14162b) western blot analysis in NCI-H460 cell line Gene ID 149041 lysates (35ug/lane).This demonstrates the RC3H1 antibody detected the RC3H1 protein Other Names (arrow). Roquin-1, Roquin, RING finger and C3H zinc finger protein 1, RING finger and CCCH-type zinc finger domain-containing protein 1, RING finger protein 198, RC3H1, KIAA2025, RNF198 Target/Specificity This RC3H1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 1015-1043 amino acids from the C-terminal region of human RC3H1. Dilution WB~~1:1000 IHC-P~~1:10~50 Format Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This RC3H1 Antibody (C-term) antibody is purified through a protein A (AP14162b)immunohistochemistry analysis in column, followed by peptide affinity formalin fixed and paraffin embedded human purification. kidney tissue followed by peroxidase conjugation of the secondary antibody and Storage DAB staining.This data demonstrates the use Maintain refrigerated at 2-8°C for up to 2 of RC3H1 Antibody (C-term) for weeks. For long term storage store at -20°C immunohistochemistry.
[Show full text]
Regnase-1, a Rapid Response Ribonuclease Regulating Inflammation and Stress Responses
Cellular & Molecular Immunology (2017) 14, 412–422 & 2017 CSI and USTC All rights reserved 2042-0226/17 $32.00 www.nature.com/cmi REVIEW Regnase-1, a rapid response ribonuclease regulating inflammation and stress responses Renfang Mao1, Riyun Yang1, Xia Chen1, Edward W Harhaj2, Xiaoying Wang3 and Yihui Fan1,3 RNA-binding proteins (RBPs) are central players in post-transcriptional regulation and immune homeostasis. The ribonuclease and RBP Regnase-1 exerts critical roles in both immune cells and non-immune cells. Its expression is rapidly induced under diverse conditions including microbial infections, treatment with inflammatory cytokines and chemical or mechanical stimulation. Regnase-1 activation is transient and is subject to negative feedback mechanisms including proteasome-mediated degradation or mucosa-associated lymphoid tissue 1 (MALT1) mediated cleavage. The major function of Regnase-1 is promoting mRNA decay via its ribonuclease activity by specifically targeting a subset of genes in different cell types. In monocytes, Regnase-1 downregulates IL-6 and IL-12B mRNAs, thus mitigating inflammation, whereas in T cells, it restricts T-cell activation by targeting c-Rel, Ox40 and Il-2 transcripts. In cancer cells, Regnase-1 promotes apoptosis by inhibiting anti-apoptotic genes including Bcl2L1, Bcl2A1, RelB and Bcl3. Together with up-frameshift protein-1 (UPF1), Regnase-1 specifically cleaves mRNAs that are active during translation by recognizing a stem-loop (SL) structure within the 3′UTRs of these genes in endoplasmic reticulum-bound ribosomes. Through this mechanism, Regnase-1 rapidly shapes mRNA profiles and associated protein expression, restricts inflammation and maintains immune homeostasis. Dysregulation of Regnase-1 has been described in a multitude of pathological states including autoimmune diseases, cancer and cardiovascular diseases.
[Show full text]
RC3H1 Antibody Catalog # ASC11623
10320 Camino Santa Fe, Suite G San Diego, CA 92121 Tel: 858.875.1900 Fax: 858.622.0609 RC3H1 Antibody Catalog # ASC11623 Specification RC3H1 Antibody - Product Information Application WB, IHC, IF Primary Accession Q5TC82 Other Accession NP_742068, 73695473 Reactivity Human, Mouse, Rat Host Rabbit Clonality Polyclonal Isotype IgG Calculated MW 125 kDa KDa Application Notes RC3H1 antibody can be used for detection of RC3H1 by Western blot at 1 - 2 µg/mL. Western blot analysis of RC3H1 in HeLa cell lysate with RC3H1 antibody at 1 µg/mL RC3H1 Antibody - Additional Information Gene ID 149041 Target/Specificity RC3H1; At least three isoforms of RC3H1 are known to exist; this antibody will detect all three isoforms. Reconstitution & Storage RC3H1 antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. Precautions RC3H1 Antibody is for research use only Immunohistochemistry of RC3H1 in human and not for use in diagnostic or therapeutic procedures. small intestine tissue with RC3H1 antibody at 5 µg/ml. RC3H1 Antibody - Protein Information Name RC3H1 (HGNC:29434) Synonyms KIAA2025, RNF198 Function Post-transcriptional repressor of mRNAs containing a conserved stem loop motif, Page 1/3 10320 Camino Santa Fe, Suite G San Diego, CA 92121 Tel: 858.875.1900 Fax: 858.622.0609 called constitutive decay element (CDE), which is often located in the 3'-UTR, as in HMGXB3, ICOS, IER3, NFKBID, NFKBIZ, PPP1R10, TNF, TNFRSF4 and in many more mRNAs (PubMed:<a href="http://www.unipr ot.org/citations/25026078" target="_blank">25026078</a>). Cleaves translationally inactive mRNAs harboring a stem-loop (SL), often located in their 3'-UTRs, during the early phase of inflammation in a helicase UPF1-independent manner (By similarity).
[Show full text]
An Auto-Regulatory Module Controls Fat Metabolism in Caenorhabditis
An auto-regulatory module controls fat metabolism in Caenorhabditis elegans Inauguraldissertation zur Erlangung der Würde einer Doktorin der Philosophie vorgelegt der Philosophisch-Naturwisschenschaftlichen Fakultät der Universität Basel von Cornelia Habacher aus Österreich Basel, 2018 Originaldokument gespeichert auf dem Dokumentenserver der Universität Basel edoc.unibas.ch Genemigt von der Philosophisch-Naturwissenschaftlichen Fakultät auf Antrag von: Prof. Dr. Michael Hall Dr. Rafal Ciosk Dr. Hugo Aguilaniu Basel, den 23. Mai 2017 Prof. Dr. Martin Spiess (Dekan der Philosophisch-Naturwissenschaftlichen Fakultät der Universität Basel) 2 TABLE OF CONTENTS SUMMARY .........................................................................................................................................4 1. INTRODUCTION ..............................................................................................................................5 1.1 Fat metabolism in Caenorhabditis elegans ......................................................................................... 5 1.1.1 Absorption of nutrients ................................................................................................................ 6 1.1.2 Lipid composition and fat accumulation ...................................................................................... 8 1.1.3 Lipid degradation ......................................................................................................................... 9 1.1.4 Signaling pathways regulating lipid
[Show full text]
C/EBPÎ²-LIP Induces Cancer-Type Metabolic Reprogramming by Regulating the Let-7/LIN28B Circuit in Mice
University of Groningen C/EBP beta-LIP induces cancer-type metabolic reprogramming by regulating the let-7/LIN28B circuit in mice Ackermann, Tobias; Hartleben, Gotz; Mueller, Christine; Mastrobuoni, Guido; Groth, Marco; Sterken, Britt A.; Zaini, Mohamad A.; Youssefi, Sameh A.; Zuidhof, Hidde R.; Krauss, Sara R. Published in: Communications biology DOI: 10.1038/s42003-019-0461-z IMPORTANT NOTE: You are advised to consult the publisher's version (publisher's PDF) if you wish to cite from it. Please check the document version below. Document Version Publisher's PDF, also known as Version of record Publication date: 2019 Link to publication in University of Groningen/UMCG research database Citation for published version (APA): Ackermann, T., Hartleben, G., Mueller, C., Mastrobuoni, G., Groth, M., Sterken, B. A., ... Calkhoven, C. F. (2019). C/EBP beta-LIP induces cancer-type metabolic reprogramming by regulating the let-7/LIN28B circuit in mice. Communications biology, 2, [208]. https://doi.org/10.1038/s42003-019-0461-z Copyright Other than for strictly personal use, it is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), unless the work is under an open content license (like Creative Commons). Take-down policy If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim. Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons the number of authors shown on this cover page is limited to 10 maximum.
[Show full text]
Potential Molecular Mechanisms of Chaihu-Shugan-San in Treatment of Breast Cancer Based on Network Pharmacology
Hindawi Evidence-Based Complementary and Alternative Medicine Volume 2020, Article ID 3670309, 9 pages https://doi.org/10.1155/2020/3670309 Research Article Potential Molecular Mechanisms of Chaihu-Shugan-San in Treatment of Breast Cancer Based on Network Pharmacology Kunmin Xiao,1,2 Kexin Li,1 Sidan Long,1 Chenfan Kong,1 and Shijie Zhu 1,2 1Graduate School, Beijing University of Chinese Medicine, Beijing 100029, China 2Department of Oncology, Wangjing Hospital, China Academy of Chinese Medical Sciences, Beijing 100102, China Correspondence should be addressed to Shijie Zhu; [email protected] Received 16 May 2020; Accepted 5 August 2020; Published 25 September 2020 Guest Editor: Azis Saifudin Copyright © 2020 Kunmin Xiao et al. /is is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Breast cancer is one of the most common cancers endangering women’s health all over the world. Traditional Chinese medicine is increasingly recognized as a possible complementary and alternative therapy for breast cancer. Chaihu-Shugan-San is a traditional Chinese medicine prescription, which is extensively used in clinical practice. Its therapeutic eﬀect on breast cancer has attracted extensive attention, but its mechanism of action is still unclear. In this study, we explored the molecular mechanism of Chaihu- Shugan-San in the treatment of breast cancer by network pharmacology. /e results showed that 157 active ingredients and 8074 potential drug targets were obtained in the TCMSP database according to the screening conditions. 2384 disease targets were collected in the TTD, OMIM, DrugBank, GeneCards disease database.
[Show full text]
Mouse Rc3h1 Conditional Knockout Project (CRISPR/Cas9)
https://www.alphaknockout.com Mouse Rc3h1 Conditional Knockout Project (CRISPR/Cas9) Objective: To create a Rc3h1 conditional knockout mouse model (C57BL/6N) by CRISPR/Cas-mediated genome engineering. Strategy summary: The Rc3h1 gene (NCBI Reference Sequence: NM_001024952 ; Ensembl: ENSMUSG00000040423 ) is located on mouse chromosome 1. 20 exons are identified, with the ATG start codon in exon 2 and the TAG stop codon in exon 20 (Transcript: ENSMUST00000161609). Exon 3 will be selected as conditional knockout region (cKO region). Deletion of this region should result in the loss of function of the mouse Rc3h1 gene. To engineer the targeting vector, homologous arms and cKO region will be generated by PCR using BAC clone RP23-162J18 as template. Cas9, gRNA and targeting vector will be co-injected into fertilized eggs for cKO mouse production. The pups will be genotyped by PCR followed by sequencing analysis. Note: A single recessive mutation on this gene resulted in severe autoimmune disease with phenotype resembling human systemic lupus erythematosus. Exon 3 starts from about 6.84% of the coding region. The knockout of Exon 3 will result in frameshift of the gene. The size of intron 2 for 5'-loxP site insertion: 7767 bp, and the size of intron 3 for 3'-loxP site insertion: 1762 bp. The size of effective cKO region: ~621 bp. The cKO region does not have any other known gene. Page 1 of 7 https://www.alphaknockout.com Overview of the Targeting Strategy Wildtype allele gRNA region 5' gRNA region 3' 1 3 4 20 Targeting vector Targeted allele Constitutive KO allele (After Cre recombination) Legends Exon of mouse Rc3h1 Homology arm cKO region loxP site Page 2 of 7 https://www.alphaknockout.com Overview of the Dot Plot Window size: 10 bp Forward Reverse Complement Note: The sequence of homologous arms and cKO region is aligned with itself to determine if there are tandem repeats.
[Show full text]
Genomic Analysis and Engineering of Chinese Hamster Ovary Cells for Improved Therapeutic Protein Production
Genomic analysis and engineering of Chinese Hamster Ovary cells for improved therapeutic protein production A DISSERTATION SUBMITTED TO THE FACULTY OF THE UNIVERSITY OF MINNESOTA BY Sofie Alice O’Brien IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF DOCTOR OF PHILOSOPHY Advisor: Professor Wei-Shou Hu May 2020 Ó Sofie Alice O’Brien 2020 Acknowledgements First, I would like to express gratitude to my advisor, Professor Wei-Shou Hu, for his help and guidance throughout the years. I have learned so much from him and grown both as a scientist and as a person over my time in graduate school. I will always be thankful for the time and effort he put into my training, and I will carry his lessons with me for the rest of my career. Much of my work was the result of collaborations with many other talented scientists. I would like to thank Dr. Gary Dunny, Dr. Aaron Barnes, Dr. Rebecca Erickson, and the rest of the Dunny lab for their support at the beginning of my PhD. I thank Dr. Michael Smanski and Dr. Nik Somia for their help with vector design and the transgene swapping project. I am also grateful to Dr. Juhi OJha and Dr. Paul Wu for our collaboration on the development of an algorithm for integration site analysis. Thank you to Dr. Casim Sarkar, Dr. Samira Azarin, and Dr. Scott McIvor for serving on my thesis committee, and providing valuable feedback on my work. I am especially thankful for the wonderful members of the Hu lab who have supported me during graduate school.
[Show full text]