Rabbit Polyclonal Antibody – AP53853PU-N

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Rabbit Polyclonal Antibody – AP53853PU-N

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 AP53853PU-N SEPTIN5 (N-term) Rabbit Polyclonal Antibody Product data: Product Type: Primary Antibodies Applications: WB Recommended Dilution: ELISA: 1/1,000. Western blotting: 1/100-1/500. Reactivity: Human Host: Rabbit Isotype: Ig Clonality: Polyclonal Immunogen: KLH conjugated synthetic peptide between 1-30 amino acids from the N-terminal region of Human SEPT5 Specificity: Recognizes SEPT5 (N-term). Formulation: PBS with 0.09% (W/V) Sodium Azide as preservative State: Aff - Purified State: Liquid purified Ig fraction Concentration: lot specific Purification: Protein A column followed by peptide Affinity purification Conjugation: Unconjugated Storage: Store the antibody undiluted at 2-8°C for one month or (in aliquots) at -20°C for longer. Avoid repeated freezing and thawing. Stability: Shelf life: one year from despatch. Gene Name: Homo sapiens septin 5 (SEPT5), transcript variant 1 Database Link: Entrez Gene 5413 Human Q99719 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 SEPTIN5 (N-term) Rabbit Polyclonal Antibody – AP53853PU-N Background: This gene is a member of the septin gene family of nucleotide binding proteins, originally described in yeast as cell division cycle regulatory proteins. Septins are highly conserved in yeast, Drosophila, and mouse and appear to regulate cytoskeletal organization. Disruption of septin function disturbs cytokinesis and results in large multinucleate or polyploid cells. This gene is mapped to 22q11, the region frequently deleted in DiGeorge and velocardiofacial syndromes. A translocation involving the MLL gene and this gene has also been reported in patients with acute myeloid leukemia. Alternative splicing results in multiple transcript variants. The presence of a non-consensus polyA signal (AACAAT) in this gene also results in read-through transcription into the downstream neighboring gene (GP1BB; platelet glycoprotein Ib), whereby larger, non-coding transcripts are produced. [provided by RefSeq]. Synonyms: Peanut-like protein 1, PNUTL1, CDCrel-1 Note: Molecular Weight: 42777 Da Protein Families: Druggable Genome Protein Pathways: Parkinson's disease Product images: Western blot analysis of SEPT5 Antibody (N-term) in HepG2 cell line lysates (35ug/lane). This demonstrates the SEPT5 antibody detected the SEPT5 protein (arrow). 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.

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Diminished Dosage of 22Q11 Genes Disrupts Neurogenesis and Cortical Development in a Mouse Model of 22Q11 Deletion/Digeorge Syndrome
Diminished dosage of 22q11 genes disrupts neurogenesis and cortical development in a mouse model of 22q11 deletion/DiGeorge syndrome Daniel W. Meechana, Eric S. Tuckera, Thomas M. Maynarda, and Anthony-Samuel LaMantiaa,b,1 aDepartment of Cell and Molecular Physiology and bNeuroscience Center, University of North Carolina School of Medicine, Chapel Hill, NC 27599 Edited by Pasko Rakic, Yale University School of Medicine, New Haven, CT, and approved July 22, 2009 (received for review May 28, 2009) The 22q11 deletion (or DiGeorge) syndrome (22q11DS), the result of flect changes in cortical neurogenesis. We focused on two a 1.5- to 3-megabase hemizygous deletion on human chromosome 22, distinct classes of cortical progenitors: basal progenitors–transit results in dramatically increased susceptibility for ‘‘diseases of cortical amplifying progenitors in the cortical subventricular zone connectivity’’ thought to arise during development, including schizo- (SVZ)–and apical progenitors–self-renewing radial glial stem phrenia and autism. We show that diminished dosage of the genes cells present in the cortical VZ. Each class can be recognized deleted in the 1.5-megabase 22q11 minimal critical deleted region in with combinations of proliferative and molecular markers (Fig. a mouse model of 22q11DS speciﬁcally compromises neurogenesis 1). We found reduced frequency of mitotic basal progenitors, and subsequent differentiation in the cerebral cortex. Proliferation of identified by phosphohistone 3 labeling (PH3; a G2/M-phase basal, but not apical, progenitors is disrupted, and subsequently, the cell-cycle marker) as well as SVZ location, throughout the frequency of layer 2/3, but not layer 5/6, projection neurons is altered.
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Nº Ref Uniprot Proteína Péptidos Identificados Por MS/MS 1 P01024
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A Catalog of Hemizygous Variation in 127 22Q11 Deletion Patients
A catalog of hemizygous variation in 127 22q11 deletion patients. Matthew S Hestand, KU Leuven, Belgium Beata A Nowakowska, KU Leuven, Belgium Elfi Vergaelen, KU Leuven, Belgium Jeroen Van Houdt, KU Leuven, Belgium Luc Dehaspe, UZ Leuven, Belgium Joshua A Suhl, Emory University Jurgen Del-Favero, University of Antwerp Geert Mortier, Antwerp University Hospital Elaine Zackai, The Children's Hospital of Philadelphia Ann Swillen, KU Leuven, Belgium Only first 10 authors above; see publication for full author list. Journal Title: Human Genome Variation Volume: Volume 3 Publisher: Nature Publishing Group: Open Access Journals - Option B | 2016-01-14, Pages 15065-15065 Type of Work: Article | Final Publisher PDF Publisher DOI: 10.1038/hgv.2015.65 Permanent URL: https://pid.emory.edu/ark:/25593/rncxx Final published version: http://dx.doi.org/10.1038/hgv.2015.65 Copyright information: © 2016 Official journal of the Japan Society of Human Genetics This is an Open Access work distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/). Accessed September 28, 2021 7:41 PM EDT OPEN Citation: Human Genome Variation (2016) 3, 15065; doi:10.1038/hgv.2015.65 Ofﬁcial journal of the Japan Society of Human Genetics 2054-345X/16 www.nature.com/hgv ARTICLE A catalog of hemizygous variation in 127 22q11 deletion patients Matthew S Hestand1, Beata A Nowakowska1,2,Elﬁ Vergaelen1, Jeroen Van Houdt1,3, Luc Dehaspe3, Joshua A Suhl4, Jurgen Del-Favero5, Geert Mortier6, Elaine Zackai7,8, Ann Swillen1, Koenraad Devriendt1, Raquel E Gur8, Donna M McDonald-McGinn7,8, Stephen T Warren4, Beverly S Emanuel7,8 and Joris R Vermeesch1 The 22q11.2 deletion syndrome is the most common microdeletion disorder, with wide phenotypic variability.
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Supplementary Table S1. List of Differentially Expressed
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SEPT5 Antibody (N-Term) Affinity Purified Rabbit Polyclonal Antibody (Pab) Catalog # Ap14767a
10320 Camino Santa Fe, Suite G San Diego, CA 92121 Tel: 858.875.1900 Fax: 858.622.0609 SEPT5 Antibody (N-term) Affinity Purified Rabbit Polyclonal Antibody (Pab) Catalog # AP14767a Specification SEPT5 Antibody (N-term) - Product Information Application WB, IHC-P,E Primary Accession Q99719 Other Accession Q9JJM9, Q9Z2Q6, NP_002679.2 Reactivity Human Predicted Mouse, Rat Host Rabbit Clonality Polyclonal Isotype Rabbit Ig Calculated MW 42777 Antigen Region 1-30 SEPT5 Antibody (N-term) - Additional Information Gene ID 5413 Western blot analysis of lysate from human Other Names brain tissue lysate, using SEPT5 Antibody Septin-5, Cell division control-related (N-term)(Cat. #AP14767a). AP14767a was protein 1, CDCrel-1, Peanut-like protein 1, diluted at 1:1000 at each lane. A goat SEPT5, PNUTL1 anti-rabbit IgG H&L(HRP) at 1:5000 dilution was used as the secondary antibody. Lysate Target/Specificity at 35ug per lane. This SEPT5 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 1-30 amino acids from the N-terminal region of human SEPT5. Dilution WB~~1:1000 IHC-P~~1:10~50 Format Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. Storage Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw SEPT5 Antibody (N-term) cycles. (AP14767a)immunohistochemistry analysis in formalin fixed and paraffin embedded human Precautions cerebellum tissue followed by peroxidase Page 1/2 10320 Camino Santa Fe, Suite G San Diego, CA 92121 Tel: 858.875.1900 Fax: 858.622.0609 SEPT5 Antibody (N-term) is for research use conjugation of the secondary antibody and only and not for use in diagnostic or DAB staining.This data demonstrates the use therapeutic procedures.
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Parkin Promotes Degradation of the Mitochondrial Pro- Apoptotic ARTS Protein
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Mirna and Parkinson's Disease Protein PARK2
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Parkin and Relatives: the RBR Family of Ubiquitin Ligases
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Expression of Sept3, Sept5a and Sept5b in the Developing and Adult Nervous System of the Zebrafish (Danio Rerio)
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PRODUCT SPECIFICATION Product Datasheet
Product Datasheet QPrEST PRODUCT SPECIFICATION Product Name QPrEST SEPT5 Mass Spectrometry Protein Standard Product Number QPrEST34942 Protein Name Septin-5 Uniprot ID Q99719 Gene SEPT5 Product Description Stable isotope-labeled standard for absolute protein quantification of Septin-5. Lys (13C and 15N) and Arg (13C and 15N) metabolically labeled recombinant human protein fragment. Application Absolute protein quantification using mass spectrometry Sequence (excluding QQMTSKLTQDSRMESPIPILPLPTPDAETEKLIRMKDEELRRMQEMLQRM fusion tag) KQ Theoretical MW 24055 Da including N-terminal His6ABP fusion tag Fusion Tag A purification and quantification tag (QTag) consisting of a hexahistidine sequence followed by an Albumin Binding Protein (ABP) domain derived from Streptococcal Protein G. Expression Host Escherichia coli LysA ArgA BL21(DE3) Purification IMAC purification Purity >90% as determined by Bioanalyzer Protein 230 Purity Assay Isotopic Incorporation >99% Concentration >5 μM after reconstitution in 100 μl H20 Concentration Concentration determined by LC-MS/MS using a highly pure amino acid analyzed internal Determination reference (QTag), CV ≤10%. Amount >0.5 nmol per vial, two vials supplied. Formulation Lyophilized in 100 mM Tris-HCl 5% Trehalose, pH 8.0 Instructions for Spin vial before opening. Add 100 μL ultrapure H2O to the vial. Vortex thoroughly and spin Reconstitution down. For further dilution, see Application Protocol. Shipping Shipped at ambient temperature Storage Lyophilized product shall be stored at -20°C. See COA for expiry date. Reconstituted product can be stored at -20°C for up to 4 weeks. Avoid repeated freeze-thaw cycles. Notes For research use only Product of Sweden. For research use only. Not intended for pharmaceutical development, diagnostic, therapeutic or any in vivo use.
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Interplay of Placental DNA Methylation and Maternal Insulin Sensitivity in Pregnancy
484 Diabetes Volume 69, March 2020 Interplay of Placental DNA Methylation and Maternal Insulin Sensitivity in Pregnancy Marie-France Hivert,1,2,3 Andres Cardenas,4 Catherine Allard,5 Myriam Doyon,5 Camille E. Powe,2 Patrick M. Catalano,6 Patrice Perron,3,5 and Luigi Bouchard5,7,8 Diabetes 2020;69:484–492 | https://doi.org/10.2337/db19-0798 The placenta participates in maternal insulin sensitivity Insulin sensitivity decreases drastically in the 2nd half of changes during pregnancy; however, mechanisms remain pregnancy to levels that are similar to those in individuals unclear. We investigated associations between maternal with early type 2 diabetes (T2D) (1). It is hypothesized that insulin sensitivity and placental DNA methylation markers this dramatic decrease in insulin sensitivity is meant to help across the genome. We analyzed data from 430 mother- provide nutrients from maternal sources to the growing offspring dyads in the Gen3G cohort. All women under- fetus. The placenta likely plays a role in this physiologic ∼ went 75-g oral glucose tolerance tests at 26 weeks of adaptation, but the exact mechanisms remain unclear. gestation; we used glucose and insulin measures to es- The placenta is a unique organ of fetal origin that lies at timate insulin sensitivity (Matsuda index). At delivery, we the maternal and fetal interface with primary roles to collected samples from placenta (fetal side) and mea- optimize fetal growth, protect the fetus against infections, sured DNA methylation using Illumina EPIC arrays. Using and produce key hormones to maintain pregnancy; these linear regression models to quantify associations at 720,077 hormones profoundly inﬂuence maternal physiology.
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Structural Studies on Mammalian Septins – New Insights Into Filament Formation
Structural studies on mammalian septins – New insights into filament formation Inaugural-Dissertation zur Erlangung des Doktorgrades des Fachbereiches Chemie der Universität Dortmund vorgelegt von Minhajuddin Sirajuddin aus Ranipet / Indien Dortmund 2007 ii Die vorliegende Arbeit wurde im Zeitraum October 2003 bis August 2007 in der Abteilung I (Structurelle Biologie) des Max-Planck-Instituts für Molekulare Physiologie in Dortmund unter der Anleitung von Prof. Dr. Alfred Wittinghofer angefertigt. 1. Gutachter: Prof. Dr. Alfred Wittinghofer 2. Gutachter: Prof. Dr. Herbert Waldmann iii iv Contents Contents 1 Introduction.................................................................................................... 1 1.1 Cytoskeleton ...................................................................................................1 1.1.1 Components of the cytoskeleton................................................................................ 1 1.1.2 Polymerization and dynamics of cytoskeletal systems.............................................. 4 1.2 An overview of the cell cycle .........................................................................5 1.3 Guanine nucleotide binding proteins ..............................................................7 1.3.1 Classification of GTPase superclass.......................................................................... 8 1.3.2 Characteristic features of the G domain .................................................................... 9 1.4 Septins identification ....................................................................................11
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