June 2019 to May 2020 Contents U.S.A., Canada and Mexico

Total Page:16

File Type:pdf, Size:1020Kb

June 2019 to May 2020 Contents U.S.A., Canada and Mexico JAX® Mice, Clinical & Research Services PRICE LIST USA, CANADA AND MEXIC0 June 2019 to May 2020 Contents U.S.A., Canada and Mexico 3 Service and Support 4 Order Information 4 Order Placement 4 Payment/Invoices 5 Order Cancellation, Changes, and Credit Policies 5 Availability 9 Dedicated Ground Transport 10 JAX® Cells, Tissues, and Products 10 Cyrorecovery Pricing 11 Readily Available and Available Now Strains 62 Repository Live 373 General Terms and Conditions Copyright © The Jackson Laboratory 2019-2020. All rights reserved. JAX® is a registered trademark of The Jackson Laboratory. *NSG™ NSG is a trademark of The Jackson Laboratory. The Jackson Laboratory is fully accredited by the Association for Assessment and Accreditation for Laboratory Animal Care International (AAALAC International). 2 1-800-422-6423 or 1-207-288-5845 • jax.org/jax-mice-and-services Service and Support U.S.A., Canada and Mexico Our knowledgeable Customer Service and Technical Support teams provide comprehensive solutions and support to advance your research. Our Regional Representatives are also available for onsite discussions at your institution. Contact Information Customer Service To place an order or inquire about prices or availability: Customer Service Hours 24hrs from 8pm Eastern Time Sunday to 8pm Eastern Time Friday Tel: 1-800-422-6423 (from U.S.A., Canada & Puerto Rico only) +1-207-288-5845 (international locations) Fax: 207-288-6150 Secure Fax: 207-288-6980 Email: [email protected] Online: jax.org/customer-service Technical Support To obtain technical information or discuss research applications for JAX® Mice Strains: Technical Support Hours: 8am Eastern Time to 8pm Eastern Time M-F Tel: 1-800-422-6423 (from U.S.A., Canada & Puerto Rico only) +1-207-288-5845 (international locations) Fax: 207-288-6629 Email: [email protected] Online: jax.org/technical-support JAX® Services Tel: 1-207-288-6294 Email: [email protected] 3 1-800-422-6423 or 1-207-288-5845 • jax.org/jax-mice-and-services Ordering Information U.S.A., Canada and Mexico JAX® Mice International Distributors Order Placement Researchers around the world may continue to order JAX® Mice strains directly from The Jackson Laboratory or through our autho- To place order, or inquire about prices or availability: rized distributors. To view a list of distributors, visit our website at Tel: 1-800-422-6423 jax.org/international-distributors. (from U.S.A., Canada & Puerto Rico only) Charles River Supplies JAX® Mice Strains +1-207-288-5845 (international locations) Fax: 207-288-6150 to Many European and Asian Countries Secure Fax: 207-288-6980 The Jackson Laboratory and Charles River have a cooperative Email: [email protected] agreement to provide JAX® Mice strains and research services using Online: jax.org/mouse-order JAX® Mice to biomedical researchers in many European and Asian Mail: The Jackson Laboratory countries. Through this agreement, Charles River serves as our exclusive commercial breeder of many popular JAX® Mice strains in Customer Service Europe and Japan, and also as our exclusive commercial distributor 610 Main Street of imported JAX® Mice strains. Bar Harbor, ME 04609-1526 U.S.A: To expedite order processing, please provide the fol- Only JAX® Mice strains bred by Charles River are lowing information with your order: equivalent in genetic quality to those bred by The • Account number. Jackson Laboratory. • Institution name. • Billing address. Expediting Orders • Shipping address. Our most popular JAX® Mice strains are readily available for ship- ment. Many unique specialty strains are maintained in breeding • Name and contact information (email and colonies sized to demand and may have limited immediate avail- telephone) of researcher using the mice ability. Orders for these strains often can be filled more quickly with • Name and contact information (email and some flexibility in requested age (include an age range or multiple telephone) of veterinarian or facility manager to acceptable ages), gender (either or both genders), or flexibility on receive animal health communications. delivery dates or partial shipments. • Name and contact information (email and Confirmation of Orders telephone) of veterinarian or facility manager to Order confirmations are sent by fax or email following order place- receive animal health communications. ment. Orders will ship as specified on confirmations. Please review all order confirmations to ensure the accuracy of order details. • Order type (one time order or standing order). • Purchase order number (and release number New Customers if applicable). If your institution does not currently have a customer account, • Strain information, including stock number, please complete and submit our online New Account and Credit Application before ordering (jax.org/customer-service). strain name, genotype, gender, age or age range, quantity desired. Privacy • Preferred delivery dates. We are committed to protecting the privacy of our customers. We do not sell, rent or distribute customer names or other information • Animal health requirements. to third party vendors. Please review our Privacy Policy at jax.org/ about/privacy for more information. Payment/Invoices Pricing Notice All payments (by check, money order, wire transfer, or credit card) Prices are effective June 1, 2019. Single orders placed prior should include the Customer Account Number of the institution making the payment and applicable invoice number(s). to June 1, 2019 will retain pricing quoted at time of order entry. Standing Orders will be charged the new prices for all shipments beginning June 1, 2019. Prices for JAX® Mice strains and cells are in U.S. dollars, F.O.B. shipping origin, with freight prepaid and invoiced. All prices are subject to change without notice. For the most current pricing infor- mation, visit our website at jax.org/jaxmice. 4 1-800-422-6423 or 1-207-288-5845 • jax.org/jax-mice-and-services Ordering Information U.S.A., Canada and Mexico Check and Money Order Payments Questions About Payment or Invoices We accept checks and U.S. or International Postal Money Orders,- For payment or invoice questions, please contact Accounts Receiv- made payable to The Jackson Laboratory. Please mail these pay- able: ment types to the following address: Tel: 1-207-288-6000 x1420 The Jackson Laboratory Fax: 1-207-288-6673 c/o Bank of America Mailing: The Jackson Laboratory Accounts Receivable 90260 Collection Center Drive 610 Main Street Chicago, IL 60693 U.S.A. Bar Harbor, ME 04609-1526 U.S.A. The Jackson Laboratory will assess a $25.00 USD fee for all check Email: [email protected] payments that are returned as “Non-Sufficient Funds.” Order Cancellations, Wire Transfer Payments Changes & Credit Policies We accept wire transfer payments. To ensure proper credit for your wire transfer payment, please send wire transfer information How to Cancel or Change Orders (including the Customer Account Number of the institution making We realize that research needs may change resulting in a need to the payment and applicable invoice number(s) by fax to 1-207-288- cancel or change orders. If order cancellations or changes become 6673, Attention: Accounts Receivable or by email to ar.notifications@ necessary, the policies, outlined on the following page, will apply at jax.org. Please DO NOT include bank account number information in our discretion. Cancellation policies are subject to change.For the email communications. most current information visit jaxmice.jax.org/support/orderchang- Credit Card Payments es. Order cancellations or order changes cannot be accepted on the day of shipment. For order cancellations or changes that meet We accept the following credit cards: MasterCard, Visa, and Ameri- the deadlines outlined below, requests must be made in writing, by can Express. Credit card information should only be communicated sending notifications by fax to 1-207-288-6150 or by email to via phone or fax. Please DO NOT email any credit card numbers [email protected]. Confirmation of cancellation or order change when placing your order. will be provided to confirm the request was received. Tax Exempt Employer Number We are a nonprofit research institution. Our tax-exempt Employer JAX® Mice or their shipping containers should Identification Number is 01-0211513. NOT be returned to The Jackson Laboratory. Payment Terms & Consequences of Non-Payment Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stat- ed terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings. Documentation Fees for International Shipments Documentation fees will be charged for preparation of special forms and certificates required for international shipments (outside the U.S.A. and Canada). If a customer cancels or changes an order for which documentation has already been processed, they are respon- sible for full payment of the documentation fees. 5 1-800-422-6423 or 1-207-288-5845 • jax.org/jax-mice-and-services Ordering Information U.S.A., Canada and Mexico Order Change and Cancellation Deadlines Shipping and Container Charges Order Type Order Cancellation/Change Freight charges are based on the number of containers shipped. Order confirmations will indicate an estimate of containers need- Deadline ed. However, actual numbers may vary depending on housing of Mice at Standard supply 7:30 PM ET (4:30 PM PT) one business day mice prior to shipment, and other welfare-related considerations. levels Readily Available prior to shipment Invoiced charges will reflect actual numbers shipped. and Available Now Availability Surgically modified mice or Prior to the mice being moved to the sur- The most popular JAX® Mice strains are readily available for ship- tissues gical or necropsy procedure area ment.
Recommended publications
  • Supplemental Information to Mammadova-Bach Et Al., “Laminin Α1 Orchestrates VEGFA Functions in the Ecosystem of Colorectal Carcinogenesis”
    Supplemental information to Mammadova-Bach et al., “Laminin α1 orchestrates VEGFA functions in the ecosystem of colorectal carcinogenesis” Supplemental material and methods Cloning of the villin-LMα1 vector The plasmid pBS-villin-promoter containing the 3.5 Kb of the murine villin promoter, the first non coding exon, 5.5 kb of the first intron and 15 nucleotides of the second villin exon, was generated by S. Robine (Institut Curie, Paris, France). The EcoRI site in the multi cloning site was destroyed by fill in ligation with T4 polymerase according to the manufacturer`s instructions (New England Biolabs, Ozyme, Saint Quentin en Yvelines, France). Site directed mutagenesis (GeneEditor in vitro Site-Directed Mutagenesis system, Promega, Charbonnières-les-Bains, France) was then used to introduce a BsiWI site before the start codon of the villin coding sequence using the 5’ phosphorylated primer: 5’CCTTCTCCTCTAGGCTCGCGTACGATGACGTCGGACTTGCGG3’. A double strand annealed oligonucleotide, 5’GGCCGGACGCGTGAATTCGTCGACGC3’ and 5’GGCCGCGTCGACGAATTCACGC GTCC3’ containing restriction site for MluI, EcoRI and SalI were inserted in the NotI site (present in the multi cloning site), generating the plasmid pBS-villin-promoter-MES. The SV40 polyA region of the pEGFP plasmid (Clontech, Ozyme, Saint Quentin Yvelines, France) was amplified by PCR using primers 5’GGCGCCTCTAGATCATAATCAGCCATA3’ and 5’GGCGCCCTTAAGATACATTGATGAGTT3’ before subcloning into the pGEMTeasy vector (Promega, Charbonnières-les-Bains, France). After EcoRI digestion, the SV40 polyA fragment was purified with the NucleoSpin Extract II kit (Machery-Nagel, Hoerdt, France) and then subcloned into the EcoRI site of the plasmid pBS-villin-promoter-MES. Site directed mutagenesis was used to introduce a BsiWI site (5’ phosphorylated AGCGCAGGGAGCGGCGGCCGTACGATGCGCGGCAGCGGCACG3’) before the initiation codon and a MluI site (5’ phosphorylated 1 CCCGGGCCTGAGCCCTAAACGCGTGCCAGCCTCTGCCCTTGG3’) after the stop codon in the full length cDNA coding for the mouse LMα1 in the pCIS vector (kindly provided by P.
    [Show full text]
  • Brief Genetics Report Haplotype Structures and Large
    Brief Genetics Report Haplotype Structures and Large-Scale Association Testing of the 5؅ AMP-Activated Protein Kinase Genes PRKAA2, PRKAB1, and PRKAB2 With Type 2 Diabetes Maria W. Sun,1,2 Jennifer Y. Lee,1,2 Paul I.W. de Bakker,1,2,3 Noe¨l P. Burtt,2 Peter Almgren,4 Lennart Råstam,5 Tiinamaija Tuomi,6 Daniel Gaudet,7 Mark J. Daly,2,8 Joel N. Hirschhorn,2,3,9 David Altshuler,1,2,3,8,10 Leif Groop,4,6 and Jose C. Florez1,2,8,10 AMP-activated protein kinase (AMPK) is a key molecular plasma glucose, or insulin sensitivity. Several nominal asso- regulator of cellular metabolism, and its activity is induced ciations of variants in PRKAA2 and PRKAB1 with BMI appear by both metformin and thiazolidinedione antidiabetic med- to be consistent with statistical noise. Diabetes 55:849–855, ications. It has therefore been proposed both as a putative 2006 agent in the pathophysiology of type 2 diabetes and as a valid target for therapeutic intervention. Thus, the genes that encode the various AMPK subunits are intriguing ype 2 diabetes arises from the complex interplay candidates for the inherited basis of type 2 diabetes. We therefore set out to test for the association of common of various pathophysiologic mechanisms involv- variants in the genes that encode three selected AMPK ing peripheral insulin resistance and relative subunits with type 2 diabetes and related phenotypes. Of Tinsulin insufficiency. The final expression of the the seven genes that encode AMPK isoforms, we initially diabetic phenotype is strongly influenced by inheritance; chose PRKAA2, PRKAB1, and PRKAB2 because of their however, with the exception of rare monogenic forms of higher prior probability of association with type 2 diabetes, diabetes, common type 2 diabetes is thought to have a based on previous reports of genetic linkage, functional polygenic architecture (1).
    [Show full text]
  • A New Computational Approach to Evaluating Systemic Gene–Gene Interactions in a Pathway Affected by Drug LY294002
    processes Article A New Computational Approach to Evaluating Systemic Gene–Gene Interactions in a Pathway Affected by Drug LY294002 Shinuk Kim College of Kyedang General Education, Sangmyung University, Cheonan 31066, Korea; [email protected]; Tel.: +82-(41)-550-5452; Fax: +82-(41)-550-5439 Received: 14 August 2020; Accepted: 23 September 2020; Published: 1 October 2020 Abstract: In this study, we investigate how drugs systemically affect genes via pathways by integrating information from interactions between chemical compounds and molecular expression datasets, and from pathway information such as gene sets using mathematical models. First, we adopt drug-induced gene expression datasets; then, employ gene set enrichment analysis tools for selecting candidate enrichment pathways; and lastly, implement the inverse algorithm package for identifying gene–gene regulatory networks in a pathway. We tested LY294002-induced datasets of the MCF7 breast cancer cell lines, and found a CELL CYCLE pathway with 101 genes, ERBB signaling pathway consisting of 82 genes, and MTOR pathway consisting of 45 genes. We consider two interactions: quantity strength depending on number of interactions, and quality strength depending on weight of interaction as positive (+) and negative ( ) interactions. Our methods revealed ANAPC1-CDK6 ( 0.412) and − − ORC2L- CHEK1(0.951) for the CELL CYCLE pathway; INS-RPS6 ( 3.125) and PRKAA2-PRKAA2 − (+1.319) for the MTOR pathway; and CBLB-RPS6KB1 ( 0.141), RPS6KB1-CBLC (+0.238) for the ERBB − signaling pathway to be top quality interactions. Top quantity interactions discovered include 12; the CDC ( ,+) gene family for the CELL CYCLE pathway, 20; PIK3 ( ), 23; PIK3CG (+) for the MTOR − − pathway, 11; PAK ( ), 10; PIK3 (+) for the ERBB signaling pathway.
    [Show full text]
  • Association Study of AMP-Activated Protein Kinase Subunit Genes In
    European Journal of Endocrinology (2009) 161 405–409 ISSN 0804-4643 CLINICAL STUDY Association study of AMP-activated protein kinase subunit genes in polycystic ovary syndrome Kari Sproul1,2, Michelle R Jones3, Ricardo Azziz1,2,4 and Mark O Goodarzi1,3,4,5 1Department of Obstetrics and Gynecology, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA, 2Department of Obstetrics and Gynecology, the David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA, 3Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Room B-131, Los Angeles, California 90048, USA, 4Department of Medicine, the David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA and 5Medical Genetics Institute, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA (Correspondence should be addressed to M O Goodarzi at Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Cedars-Sinai Medical Center; Email: [email protected]) Abstract Objective: To examine the genes for AMP-activated protein kinase (AMPK) subunits a2(PRKAA2) and g3(PRKAG3) as candidates for polycystic ovary syndrome (PCOS) and its component traits. Design and methods: A total of 287 white PCOS women were recruited from the reproductive endocrinology clinic at the University of Alabama at Birmingham and 187 white control subjects were recruited from the surrounding community. Seven PRKAA2 single nucleotide polymorphisms (SNPs) and four PRKAG3 SNPs were genotyped in PCOS cases and controls. Genotyping and association analysis were performed at Cedars-Sinai Medical Center. Results: Nominal associations of PRKAA2 variants with insulin-related traits and the PRKAG3 Pro71Ala variant with PCOS were not statistically significant after multiple testing correction.
    [Show full text]
  • Ahn Supp. Fig. 1 AB 1.5 ARRDC4 1.5 ARRDC4 * * * 1.0 1.0
    Ahn_Supp. Fig. 1 AB 1.5 ARRDC4 1.5 ARRDC4 * * * 1.0 1.0 * * 0.5 * 0.5 * * * Relative mRNA levels mRNA Relative Relative mRNA levels mRNA Relative 0.0 0.0 1.5 MLXIP (MondoA) 1.5 MLXIP (MondoA) 1.0 1.0 0.5 0.5 Relative mRNA levels mRNA Relative Relative mRNA levels mRNA Relative 0.0 0.0 MondoA MondoA 0124824 Starvation (6h) -++++++ Glucose Starvation (h) Refeeding (h) --0.51248 C 1.5 ARRDC4 1.5 MLXIP (MondoA) † Con # KD 1.0 1.0 0.5 0.5 * * * * Relative mRNA levels mRNA Relative Relative mRNA levels mRNA Relative * * 0.0 0.0 BasalStarvation Refeeding BasalStarvation Refeeding MondoA Con + + - - + + - - + + - - KD - - + + - - + + - - + + BasalStarvation Refeeding Supplemental Figure 1. Glucose-mediated regulation of ARRDC4 is dependent on MondoA in human skeletal myotubes. (A) (top) ARRDC4 and MLXIP (MondoA) mRNA levels were determined by qRT-PCR in human skeletal myotubes following deprivation of glucose at the indicated time (n=4). (bottom) Representative Western blot analysis of MondoA demonstrating the effect of glucose deprivation. *p<0.05 vs. 0h. (B) (top) ARRDC4 and MLXIP (MondoA) expression in human myotubes following a 6h glucose removal and refeeding at the times indicated (n=4). (bottom) Corresponding Western blot analysis. *p<0.05 vs Starvation 6h. (C) (top) Expression of ARRDC4 and MLXIP in human myotubes following deprivation and refeeding of glucose in the absence or presence of siRNA-mediated MondoA KD (n=4). (bottom) Corresponding Western blot analysis. *p<0.05 vs siControl. # p<0.05. § p<0.05. The data represents mean ± SD. All statistical significance determined by one-way ANOVA with Tukey multiple comparison post-hoc test.
    [Show full text]
  • The Study of Copy Number Variations in the Regions of PRKAB2 and PPM1K Among Congenital Heart Defects Patients
    The study of copy number variations in the regions of PRKAB2 and PPM1K among congenital heart defects patients Han-Quan Dong1 Yue-Xin Du2 1. Department of Pneumology, Tianjin Children’s Hospital, Tianjin, 300074–China 2. Department of Child Healthcare, Tianjin Municipal Women and Children health care center, Tianjin, 300070, China http://dx.doi.org/10.1590/1806-9282.65.6.786 SUMMARY OBJECTIVE: This study was to assess the genetic association of copy number variations in two genes (PRKAB2 and PPM1K) located in two regions (tetralogy of Fallot and ventricular septal defect) in a Chinese Han population. METHODS: A total of 200 congenital heart disease patients (100 tetralogy of Fallot patients and 100 ventricular septal defect patients) and 100 congenital heart defect-free controls were recruited, and quantitative real-time PCR analysis was used to replicate the asso- ciation of two copy number variations with congenital heart defects in a Chinese Han population. RESULTS: One deletion at PRKAB2 and one duplication at PPM1K were found in two of the tetralogy of Fallot patients, respectively; while all these regions were duplicated in both ventricular septal defect patients and in the 100 congenital heart defects-free controls. CONCLUSIONS: We replicated the copy number variations at the disease-candidate genes of PRKAB2 and PPM1K with tetralogy of Fallot in a Chinese Han population, and in patients with ventricular septal defect mutations in these two genes were not found. These results indicate the same molecular population genetics exist in these two genes with different ethnicity. This shows that these two genes are possibly specific pf tetralogy of Fallot candidates.
    [Show full text]
  • Table S1. Complete Gene List. Genbank Refseq and Description of Each Gene Were Provided By
    Document downloaded from http://www.elsevier.es, day 24/09/2021. This copy is for personal use. Any transmission of this document by any media or format is strictly prohibited. Table S1. Complete gene list. GenBank RefSeq and description of each gene were provided by the array supplier. Unigene GeneBank Symbol Description Gene Name/s Rn.11422 NM_033230 Akt1 V-akt murine thymoma viral oncogene homolog 1 Akt Rn.2104 NM_019288 App Amyloid beta (A4) precursor protein - Rn.23323 NM_001034933 Arsa Arylsulfatase A MGC125207 Rn.94004 NM_033443 Arsb Arylsulfatase B - Rn.6224 NM_001038495 Atg12 ATG12 autophagy related 12 Apg12l, MGC125080 Rn.101734NM_001108809 Atg16l1 ATG16 autophagy related 16-like 1 Apg16l, Wdr30 Rn.104199NM_001191560 Atg16l2 ATG16 autophagy related 16-like 2 RGD1311400 Rn.3084 NM_134394 Atg3 ATG3 autophagy related 3 Apg3l, PIG-1, Pig1 Rn.163086NM_001025711 Atg4b ATG4 autophagy related 4 homolog B Apg4b, MGC112887 Rn.23378 NM_001107948 Atg4c ATG4 autophagy related 4 homolog C - Rn.98385 NM_001014250 Atg5 ATG5 autophagy related 5 - Rn.162765NM_001012097 Atg7 ATG7 autophagy related 7 Apg7l Rn.35248 NM_001014218 Atg9a ATG9 autophagy related 9 homolog A MGC105908, RGD1310450 Rn.36696 NM_022698 Bad BCL2-associated agonist of cell death MGC72439 Rn.14598 NM_053812 Bak1 BCL2-antagonist/killer 1 MGC108627 Rn.10668 NM_017059 Bax Bcl2-associated X protein - Rn.9996 NM_016993 Bcl2 B-cell CLL/lymphoma 2 Bcl-2 Rn.10323 NM_031535 Bcl2l1 Bcl2-like 1 Bcl-xl, Bcl2l, Bclx, bcl-X Rn.2776 NM_053739 Becn1 Beclin 1, autophagy related - Rn.31142 NM_022684
    [Show full text]
  • (AMP)-Activated Protein Kinase: a New Target for Nutraceutical Compounds
    International Journal of Molecular Sciences Review Adenosine Monophosphate (AMP)-Activated Protein Kinase: A New Target for Nutraceutical Compounds Fabiola Marín-Aguilar 1, Luis E. Pavillard 1, Francesca Giampieri 2, Pedro Bullón 1 and Mario D. Cordero 1,* 1 Research Laboratory, Oral Medicine Department, University of Sevilla, Sevilla 41009, Spain; [email protected] (F.M.-A.); [email protected] (L.E.P.); [email protected] (P.B.) 2 Dipartimento di Scienze Cliniche Specialistiche ed Odontostomatologiche—Sez. Biochimica, Università Politecnica delle Marche, Ancona 60100, Italy; [email protected] * Correspondence: [email protected]; Tel.: +34-954-481-120; Fax: +34-954-486-784 Academic Editor: Rosa M. Lamuela-Raventós Received: 17 November 2016; Accepted: 23 January 2017; Published: 29 January 2017 Abstract: Adenosine monophosphate-activated protein kinase (AMPK) is an important energy sensor which is activated by increases in adenosine monophosphate (AMP)/adenosine triphosphate (ATP) ratio and/or adenosine diphosphate (ADP)/ATP ratio, and increases different metabolic pathways such as fatty acid oxidation, glucose transport and mitochondrial biogenesis. In this sense, AMPK maintains cellular energy homeostasis by induction of catabolism and inhibition of ATP-consuming biosynthetic pathways to preserve ATP levels. Several studies indicate a reduction of AMPK sensitivity to cellular stress during aging and this could impair the downstream signaling and the maintenance of the cellular energy balance and the stress resistance. However, several diseases have been related with an AMPK dysfunction. Alterations in AMPK signaling decrease mitochondrial biogenesis, increase cellular stress and induce inflammation, which are typical events of the aging process and have been associated to several pathological processes.
    [Show full text]
  • PRKAA2 (Human) Recombinant Protein (Q01)
    PRKAA2 (Human) Recombinant that monitors cellular energy status. In response to Protein (Q01) cellular metabolic stresses, AMPK is activated, and thus phosphorylates and inactivates acetyl-CoA carboxylase Catalog Number: H00005563-Q01 (ACC) and beta-hydroxy beta-methylglutaryl-CoA reductase (HMGCR), key enzymes involved in regulating Regulation Status: For research use only (RUO) de novo biosynthesis of fatty acid and cholesterol. Studies of the mouse counterpart suggest that this Product Description: Human PRKAA2 partial ORF ( catalytic subunit may control whole-body insulin NP_006243, 453 a.a. - 552 a.a.) recombinant protein sensitivity and is necessary for maintaining myocardial with GST-tag at N-terminal. energy homeostasis during ischemia. [provided by RefSeq] Sequence: MSLQLYLVDNRSYLLDFKSIDDEVVEQRSGSSTPQRS CSAAGLHRPRSSFDSTTAESHSLSGSLTGSLTGSTLS SVSPRLGSHTMDFFEMCASLITTLAR Host: Wheat Germ (in vitro) Theoretical MW (kDa): 36.74 Applications: AP, Array, ELISA, WB-Re (See our web site product page for detailed applications information) Protocols: See our web site at http://www.abnova.com/support/protocols.asp or product page for detailed protocols Preparation Method: in vitro wheat germ expression system Purification: Glutathione Sepharose 4 Fast Flow Storage Buffer: 50 mM Tris-HCI, 10 mM reduced Glutathione, pH=8.0 in the elution buffer. Storage Instruction: Store at -80°C. Aliquot to avoid repeated freezing and thawing. Entrez GeneID: 5563 Gene Symbol: PRKAA2 Gene Alias: AMPK, AMPK2, PRKAA Gene Summary: The protein encoded by this gene is a catalytic subunit of the AMP-activated protein kinase (AMPK). AMPK is a heterotrimer consisting of an alpha catalytic subunit, and non-catalytic beta and gamma subunits. AMPK is an important energy-sensing enzyme Page 1/1 Powered by TCPDF (www.tcpdf.org).
    [Show full text]
  • AMPK Causes Cell Cycle Arrest in LKB1-Deficient Cells Via Activation of CAMKK2
    Published OnlineFirst May 2, 2016; DOI: 10.1158/1541-7786.MCR-15-0479 Cell Cycle and Senescence Molecular Cancer Research AMPK Causes Cell Cycle Arrest in LKB1-Deficient Cells via Activation of CAMKK2 Sarah Fogarty, Fiona A. Ross, Diana Vara Ciruelos, Alexander Gray, Graeme J. Gowans, and D. Grahame Hardie Abstract The AMP-activated protein kinase (AMPK) is activated by also caused G1 arrest similar to that caused by expression of LKB1, phosphorylation at Thr172, either by the tumor suppressor kinase while expression of a dominant-negative AMPK mutant, or a þ LKB1 or by an alternate pathway involving the Ca2 /calmodulin- double knockout of both AMPK-a subunits, also prevented the dependent kinase, CAMKK2. Increases in AMP:ATP and ADP:ATP cell-cycle arrest caused by A23187. These mechanistic findings ratios, signifying energy deficit, promote allosteric activation and confirm that AMPK activation triggers cell-cycle arrest, and also net Thr172 phosphorylation mediated by LKB1, so that the LKB1– suggest that the rapid proliferation of LKB1-null tumor cells is due AMPK pathway acts as an energy sensor. Many tumor cells carry to lack of the restraining influence of AMPK. However, cell-cycle loss-of-function mutations in the STK11 gene encoding LKB1, but arrest can be restored by reexpressing LKB1 or a constitutively LKB1 reexpression in these cells causes cell-cycle arrest. Therefore, active CAMKK2, or by pharmacologic agents that increase intra- þ it was investigated as to whether arrest by LKB1 is caused by cellular Ca2 and thus activate endogenous CAMKK2. activation of AMPK or of one of the AMPK-related kinases, which are also dependent on LKB1 but are not activated by CAMKK2.
    [Show full text]
  • Association of AMP-Activated Protein Kinase with Risk and Progression of Non–Hodgkin Lymphoma
    Published OnlineFirst February 8, 2013; DOI: 10.1158/1055-9965.EPI-12-1014 Cancer Epidemiology, Research Article Biomarkers & Prevention Association of AMP-Activated Protein Kinase with Risk and Progression of Non–Hodgkin Lymphoma Aaron E. Hoffman1, Kathryn Demanelis1, Alan Fu2, Tongzhang Zheng2, and Yong Zhu2 Abstract Background: Metabolic dysregulation has been identified as an "emerging hallmark" of cancer. The heterotrimeric AMP-activated protein kinase (AMPK) complex is a central regulator of the metabolic system and an important component of the mTOR pathway and the p53 axis, making it uniquely positioned to influence carcinogenesis through its canonical functions in the metabolic arena, as well as through more traditional mechanisms such as regulation of apoptosis and angiogenesis. Methods: We conducted a population-based genetic association study to examine the impact of mutations in AMPK subunit genes on risk of non–Hodgkin lymphoma (NHL). We also analyzed public microarray data to determine the expression of AMPK in NHL cells and to assess the influence of AMPK expression on overall survival in patients with NHL. Results: We identified an AMPK subunit haplotype, which was significantly associated with NHL [OR, 5.44, 95% confidence interval (CI), 2.15–13.75] in women with no family history of cancer. Haplotypes in two subunits, PRKAA2 and PRKAG3, were nominally associated with the follicular and diffuse large B-cell lymphoma histologic subtypes, respectively, although these associations did not retain statistical significance after correction for multiple comparisons. Further, both of these subunits were differentially expressed (P < 0.05) in one or more lymphoma cell type, and higher expression of two versions of the AMPK-b subunit was significantly associated with increased 5-year survival among patients with NHL (P ¼ 0.001 and P ¼ 0.021).
    [Show full text]
  • Therapeutic Inhibition of Mir-802 Protects Against Obesity Through
    Supporting Information Therapeutic inhibition of miR-802 protects against obesity through AMPK-mediated regulation of hepatic lipid metabolism Yangyue Ni †, Zhipeng Xu †, Chen Li †, Yuxiao Zhu, Ran Liu, Fan Zhang, Hao Chang, Maining Li, Liang Sheng, Zhong Li, Min Hou, Lin Chen, Hong You, Donald P. McManus, Wei Hu, Yinong Duan, Yu Liu, Minjun Ji * † Yangyue Ni, Zhipeng Xu and Chen Li contributed equally to this work. 1 Figure S1. Schistosoma japonicum infection improves lipid metabolism in HFD mice. (A) Sixteen 10-week-old male C57BL/6 mice were separated equally into two groups and fed a normal diet. Each mouse in the ND-inf group was infected with 10 ± 1 S. 2 japonicum cercariae and the ND-con group was established as the normal control group. Sixteen 6-week-old male C57BL/6 mice that had been maintained on a high-fat diet for 1 month were randomly divided into two groups: a high-fat diet-chronic infection group (HFD-inf) and the control group (HFD-con). Mice were sacrificed 9 weeks after the infection. (B) Dynamic changes in body weight of ND- and HFD-fed mice after infection with Schistosoma japonicum. (C) Cholesterol, TG, HDL-C, LDL-C levels in sera of HFD mice upon infection. (D, E) Representative images of liver sections from ND-con, HFD-con, ND-inf or HFD-inf mice stained with Oil red O. (F) qRT-PCR quantification of lipid-related genes expression in livers of four groups of mice (ND- con, HFD-con, ND-inf or HFD-inf). (G) qRT-PCR quantification of lipid-related gene expression in adipose tissues of three groups of mice (ND-con, HFD-con and HFD-inf).
    [Show full text]