RASA4 Rabbit Pab

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Leader in Biomolecular Solutions for Life Science RASA4 Rabbit pAb Catalog No.: A9860 Basic Information Background Catalog No. This gene encodes a member of the GAP1 family of GTPase-activating proteins that A9860 suppresses the Ras/mitogen-activated protein kinase pathway in response to Ca(2+). Stimuli that increase intracellular Ca(2+) levels result in the translocation of this protein Observed MW to the plasma membrane, where it activates Ras GTPase activity. Consequently, Ras is 100kDa converted from the active GTP-bound state to the inactive GDP-bound state and no longer activates downstream pathways that regulate gene expression, cell growth, and Calculated MW differentiation. Multiple transcript variants encoding different isoforms have been found 85kDa/90kDa for this gene. Category Primary antibody Applications WB Cross-Reactivity Human, Mouse, Rat Recommended Dilutions Immunogen Information WB 1:500 - 1:2000 Gene ID Swiss Prot 10156 O43374 Immunogen Recombinant fusion protein containing a sequence corresponding to amino acids 60-290 of human RASA4 (NP_008920.5). Synonyms RASA4;CAPRI;GAPL Contact Product Information www.abclonal.com Source Isotype Purification Rabbit IgG Affinity purification Storage Store at -20℃. Avoid freeze / thaw cycles. Buffer: PBS with 0.02% sodium azide,50% glycerol,pH7.3. Validation Data Western blot analysis of extracts of various cell lines, using RASA4 antibody (A9860) at 1:1000 dilution. Secondary antibody: HRP Goat Anti-Rabbit IgG (H+L) (AS014) at 1:10000 dilution. Lysates/proteins: 25ug per lane. Blocking buffer: 3% nonfat dry milk in TBST. Detection: ECL Basic Kit (RM00020). Exposure time: 90s. Antibody | Protein | ELISA Kits | Enzyme | NGS | Service For research use only. Not for therapeutic or diagnostic purposes. Please visit http://abclonal.com for a complete listing of recommended products..

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Genetic and Genomic Analysis of Hyperlipidemia, Obesity and Diabetes Using (C57BL/6J × TALLYHO/Jngj) F2 Mice
University of Tennessee, Knoxville TRACE: Tennessee Research and Creative Exchange Nutrition Publications and Other Works Nutrition 12-19-2010 Genetic and genomic analysis of hyperlipidemia, obesity and diabetes using (C57BL/6J × TALLYHO/JngJ) F2 mice Taryn P. Stewart Marshall University Hyoung Y. Kim University of Tennessee - Knoxville, [email protected] Arnold M. Saxton University of Tennessee - Knoxville, [email protected] Jung H. Kim Marshall University Follow this and additional works at: https://trace.tennessee.edu/utk_nutrpubs Part of the Animal Sciences Commons, and the Nutrition Commons Recommended Citation BMC Genomics 2010, 11:713 doi:10.1186/1471-2164-11-713 This Article is brought to you for free and open access by the Nutrition at TRACE: Tennessee Research and Creative Exchange. It has been accepted for inclusion in Nutrition Publications and Other Works by an authorized administrator of TRACE: Tennessee Research and Creative Exchange. For more information, please contact [email protected]. Stewart et al. BMC Genomics 2010, 11:713 http://www.biomedcentral.com/1471-2164/11/713 RESEARCH ARTICLE Open Access Genetic and genomic analysis of hyperlipidemia, obesity and diabetes using (C57BL/6J × TALLYHO/JngJ) F2 mice Taryn P Stewart1, Hyoung Yon Kim2, Arnold M Saxton3, Jung Han Kim1* Abstract Background: Type 2 diabetes (T2D) is the most common form of diabetes in humans and is closely associated with dyslipidemia and obesity that magnifies the mortality and morbidity related to T2D. The genetic contribution to human T2D and related metabolic disorders is evident, and mostly follows polygenic inheritance. The TALLYHO/ JngJ (TH) mice are a polygenic model for T2D characterized by obesity, hyperinsulinemia, impaired glucose uptake and tolerance, hyperlipidemia, and hyperglycemia.
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Supplemental Information
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RASA4 Antibody Cat
RASA4 Antibody Cat. No.: 23-946 RASA4 Antibody Specifications HOST SPECIES: Rabbit SPECIES REACTIVITY: Human, Mouse, Rat Recombinant fusion protein containing a sequence corresponding to amino acids 60-290 IMMUNOGEN: of human RASA4 (NP_008920.5). TESTED APPLICATIONS: WB APPLICATIONS: WB: ,1:500 - 1:2000 POSITIVE CONTROL: 1) SH-SY5Y 2) 293T 3) Mouse thymus 4) Mouse spleen PREDICTED MOLECULAR Observed: 100kDa WEIGHT: Properties PURIFICATION: Affinity purification CLONALITY: Polyclonal September 24, 2021 1 https://www.prosci-inc.com/rasa4-antibody-23-946.html ISOTYPE: IgG CONJUGATE: Unconjugated PHYSICAL STATE: Liquid BUFFER: PBS with 0.02% sodium azide, 50% glycerol, pH7.3. STORAGE CONDITIONS: Store at -20˚C. Avoid freeze / thaw cycles. Additional Info OFFICIAL SYMBOL: RASA4 CAPRI, GAPL, ras GTPase-activating protein 4, Ca2+-promoted Ras inactivator, calcium- ALTERNATE NAMES: promoted Ras inactivator, rasGAP-activating-like protein 2 GENE ID: 10156 USER NOTE: Optimal dilutions for each application to be determined by the researcher. Background and References This gene encodes a member of the GAP1 family of GTPase-activating proteins that suppresses the Ras/mitogen-activated protein kinase pathway in response to Ca(2+). Stimuli that increase intracellular Ca(2+) levels result in the translocation of this protein to the plasma membrane, where it activates Ras GTPase activity. Consequently, Ras is BACKGROUND: converted from the active GTP-bound state to the inactive GDP-bound state and no longer activates downstream pathways that regulate gene expression, cell growth, and differentiation. Multiple transcript variants encoding different isoforms have been found for this gene. ANTIBODIES FOR RESEARCH USE ONLY. For additional information, visit ProSci's Terms & Conditions Page.
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Supplementary Table S1. List of Differentially Expressed
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RASA4 Sirna (Human)
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Genome-Wide Hydroxymethylation Tested Using the HELP-GT Assay
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RASA4 CRISPR/Cas9 KO Plasmid (M): Sc-424802
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Foxc1 and Foxc2 Deletion Causes Abnormal Lymphangiogenesis and Correlates with ERK Hyperactivation
Foxc1 and Foxc2 deletion causes abnormal lymphangiogenesis and correlates with ERK hyperactivation Anees Fatima, … , Yoh-suke Mukouyama, Tsutomu Kume J Clin Invest. 2016;126(7):2437-2451. https://doi.org/10.1172/JCI80465. Research Article Angiogenesis Vascular biology The lymphatic vasculature is essential for maintaining interstitial fluid homeostasis, and dysfunctional lymphangiogenesis contributes to various pathological processes, including inflammatory disease and tumor metastasis. Mutations in FOXC2 are dominantly associated with late-onset lymphedema; however, the precise role of FOXC2 and a closely related factor, FOXC1, in the lymphatic system remains largely unknown. Here we identified a molecular cascade by which FOXC1 and FOXC2 regulate ERK signaling in lymphatic vessel growth. In mice, lymphatic endothelial cell–specific (LEC-specific) deletion of Foxc1, Foxc2, or both resulted in increased LEC proliferation, enlarged lymphatic vessels, and abnormal lymphatic vessel morphogenesis. Compared with LECs from control animals, LECs from mice lacking both Foxc1 and Foxc2 exhibited aberrant expression of Ras regulators, and embryos with LEC-specific deletion ofF oxc1 and Foxc2, alone or in combination, exhibited ERK hyperactivation. Pharmacological ERK inhibition in utero abolished the abnormally enlarged lymphatic vessels in FOXC-deficient embryos. Together, these results identify FOXC1 and FOXC2 as essential regulators of lymphangiogenesis and indicate a new potential mechanistic basis for lymphatic-associated diseases. Find the latest version: https://jci.me/80465/pdf The Journal of Clinical Investigation RESEARCH ARTICLE Foxc1 and Foxc2 deletion causes abnormal lymphangiogenesis and correlates with ERK hyperactivation Anees Fatima,1 Ying Wang,2 Yutaka Uchida,3 Pieter Norden,1 Ting Liu,1 Austin Culver,1 William H. Dietz,1 Ford Culver,1 Meredith Millay,1 Yoh-suke Mukouyama,3 and Tsutomu Kume1 1Feinberg Cardiovascular Research Institute, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
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