Recombinant Human PHLDA2 Protein Catalog Number: ATGP0546

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Recombinant human PHLDA2 protein Catalog Number: ATGP0546 PRODUCT INPORMATION Expression system E.coli Domain 1-152aa UniProt No. Q53GA4 NCBI Accession No. NP_003302 Alternative Names Pleckstrin homology-like domain family A member 2, BRW1C, BWR1C, HLDA2, IPL, TSSC3, Pleckstrin homology- like domain family A member 2 Beckwith Wiedemann syndrome chromosome region 1 candidate protein C, BRW 1C, BWR 1C, HLDA 2, HLDA2, Imprinted in placenta and liver, Imprinted in placenta and liver protein, p17 Beckwith Wiedemann region 1C, p17 BWR1C, PHLDA 2, Pleckstrin homology like domain family A member 2, TSSC 3, Tumor supressing STF cDNA 3, Tumor suppressing STF cDNA 3 protein, Tumor suppressing subchromosomal transferable, fragment candidate gene 3 protein, Tumor suppressing subchromosomal transferable fragment cDNA 3, Tumor suppressing subtransferable candidate 3, PRODUCT SPECIFICATION Molecular Weight 19.2 kDa (172aa) confirmed by MALDI-TOF Concentration 0.5mg/ml (determined by Bradford assay) Formulation Liquid in. 20mM Tris-HCl buffer (pH 8.0) containing 20% glycerol, 0.1M NaCl,1mM DTT Purity > 80% by SDS-PAGE Tag His-Tag Application SDS-PAGE Storage Condition Can be stored at +2C to +8C for 1 week. For long term storage, aliquot and store at -20C to -80C. Avoid repeated freezing and thawing cycles. BACKGROUND 1 Recombinant human PHLDA2 protein Catalog Number: ATGP0546 Description PHLDA2, also known as Pleckstrin homology-like domain family A member 2, is a cytoplasmic protein that is involved in fetal and placental growth. It is an apoptosis-related protein that acts as a negative growth regulator and is expressed during normal human development. This protein is imprinted on placenta, liver and fetal tissues during embryogenesis and is removed once development is complete. Recombinant human PHLDA2 protein, fused to His-tag at N-terminus was expressed in E. coli and purified by using conventional chromatography techniques. Amino acid Sequence MGSSHHHHHH SSGLVPRGSH MKSPDEVLRE GELEKRSDSL FQLWKKKRGV LTSDRLSLFP ASPRARPKEL RFHSILKVDC VERTGKYVYF TIVTTDHKEI DFRCAGESCW NAAIALALID FQNRRALQDF RSRQERTAPA APAEDAVAAA AAAPSEPSEP SRPSPQPKPR TP General References Lee MP, et al. (1998) Cancer Res.. 58(5):1052-6. Frank D. et al. (2000) Mamm Genome. 10(12):1150-9.. DATA SDS-PAGE 3ug by SDS-PAGE under reducing condition and visualized by coomassie blue stain. 2.

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The Title of the Article
Mining the literature for genes associated with placenta-mediated maternal diseases Laritza M. Rodriguez, MD, PhD, Stephanie M. Morrison, MPH, Kathleen Greenberg, PhD, Dina Demner Fushman, MD, PhD Lister Hill National Center for Biomedical Communications, National Library of Medicine, National Institutes of Health, Bethesda, MD Abstract Automated literature analysis could significantly speed up understanding of the role of the placenta and the impact of its development and functions on the health of the mother and the child. To facilitate automatic extraction of information about placenta-mediated disorders from the literature, we manually annotated genes and proteins, the associated diseases, and the functions and processes involved in the development and function of placenta in a collection of PubMed/MEDLINE abstracts. We developed three baseline approaches to finding sentences containing this information: one based on supervised machine learning (ML) and two based on distant supervision: 1) using automated detection of named entities and 2) using MeSH. We compare the performance of several well-known supervised ML algorithms and identify two approaches, Support Vector Machines (SVM) and Generalized Linear Models (GLM), which yield up to 98% recall precision and F1 score. We demonstrate that distant supervision approaches could be used at the expense of missing up to 15% of relevant documents. Introduction The placenta is the most important organ in human pregnancy. It plays the role of lungs and kidneys for the developing fetus, supplies substrates for its development, and regulates complex immune functions to allow the cohabitation of two different organisms - the mother and the fetus- during the pregnancy. Defects in the placentation process are known to be associated with a wide range of pregnancy related complications such as preeclampsia, uterine growth restriction, and premature rupture of membranes, fetal growth retardation, placenta abruption, spontaneous abortion, and fetal death.
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Maternal Diet During Pregnancy Induces Gene Expression and DNA Methylation Changes in Fetal Tissues in Sheep
CORE Metadata, citation and similar papers at core.ac.uk ORIGINAL RESEARCH ARTICLE Provided by Frontiers - Publisher Connector published: 05 April 2013 doi: 10.3389/fgene.2013.00049 Maternal diet during pregnancy induces gene expression and DNA methylation changes in fetal tissues in sheep Xianyong Lan1,2, Evan C. Cretney 2, Jenna Kropp 2, Karam Khateeb2, Mary A. Berg 2, Francisco Peñagaricano2, Ronald Magness 3, Amy E. Radunz 2* and Hasan Khatib2* 1 College of Animal Science and Technology, Northwest Agriculture and Forestry University, Yangling, China 2 Department of Animal Sciences, University of Wisconsin-Madison, Madison, WI, USA 3 Department of Obstetrics and Gynecology, University of Wisconsin-Madison, Madison, WI, USA Edited by: Studies in rats and mice have established that maternal nutrition induces epigenetic modifi- Peter Dovc, University of Ljubljana, cations, sometimes permanently, that alter gene expression in the fetus, which in turn leads Slovenia to phenotypic changes. However, limited data is available on the influence of maternal diet Reviewed by: Ikhide G. Imumorin, Cornell on epigenetic modifications and gene expression in sheep.Therefore, the objectives of this University, USA study were to investigate the impact of different maternal dietary energy sources on the Hsiao-Ching Liu, North Carolina State expression of imprinted genes in fetuses in sheep. Ewes were naturally bred to a single sire University, USA and from days 67 ± 3 of gestation until necropsy (days 130 ± 1), they were fed one of three *Correspondence: diets of alfalfa haylage (HY; fiber), corn (CN; starch), or dried corn distiller’s grains (DG; fiber Amy E. Radunz and Hasan Khatib, Department of Animal Sciences, plus protein plus fat).
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Supplementary Data
Supplemental figures Supplemental figure 1: Tumor sample selection. A total of 98 thymic tumor specimens were stored in Memorial Sloan-Kettering Cancer Center tumor banks during the study period. 64 cases corresponded to previously untreated tumors, which were resected upfront after diagnosis. Adjuvant treatment was delivered in 7 patients (radiotherapy in 4 cases, cyclophosphamide- doxorubicin-vincristine (CAV) chemotherapy in 3 cases). 34 tumors were resected after induction treatment, consisting of chemotherapy in 16 patients (cyclophosphamide-doxorubicin- cisplatin (CAP) in 11 cases, cisplatin-etoposide (PE) in 3 cases, cisplatin-etoposide-ifosfamide (VIP) in 1 case, and cisplatin-docetaxel in 1 case), in radiotherapy (45 Gy) in 1 patient, and in sequential chemoradiation (CAP followed by a 45 Gy-radiotherapy) in 1 patient. Among these 34 patients, 6 received adjuvant radiotherapy. 1 Supplemental Figure 2: Amino acid alignments of KIT H697 in the human protein and related orthologs, using (A) the Homologene database (exons 14 and 15), and (B) the UCSC Genome Browser database (exon 14). Residue H697 is highlighted with red boxes. Both alignments indicate that residue H697 is highly conserved. 2 Supplemental Figure 3: Direct comparison of the genomic profiles of thymic squamous cell carcinomas (n=7) and lung primary squamous cell carcinomas (n=6). (A) Unsupervised clustering analysis. Gains are indicated in red, and losses in green, by genomic position along the 22 chromosomes. (B) Genomic profiles and recurrent copy number alterations in thymic carcinomas and lung squamous cell carcinomas. Gains are indicated in red, and losses in blue. 3 Supplemental Methods Mutational profiling The exonic regions of interest (NCBI Human Genome Build 36.1) were broken into amplicons of 500 bp or less, and specific primers were designed using Primer 3 (on the World Wide Web for general users and for biologist programmers (see Supplemental Table 2) [1].
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Complete Hydatidiform Mole Retaining a Chromosome 11 of Maternal Origin: Molecular Genetic Analysis of a Case
Modern Pathology (2004) 17, 1155–1160 & 2004 USCAP, Inc All rights reserved 0893-3952/04 $30.00 www.modernpathology.org Complete hydatidiform mole retaining a chromosome 11 of maternal origin: molecular genetic analysis of a case Rosemary A Fisher1, Marisa R Nucci2, Harshwardhan M Thaker3, Stanislawa Weremowicz2, David R Genest2 and Diego H Castrillon2,* 1Department of Cancer Medicine, Faculty of Medicine, Imperial College London, Charing Cross Hospital, London, UK; 2Division of Women’s and Perinatal Pathology, Department of Pathology, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA and 3Department of Pathology, Columbia University College of Physicians & Surgeons, New York, NY, USA Hydatidiform moles are pregnancies characterized by abnormal development of both embryonic and extraembryonic tissues and are associated with the misexpression of imprinted genes. The vast majority of complete hydatidiform moles are diploid and androgenetic, whereas partial hydatidiform moles are triploid, with an extra set of chromosomes of paternal origin. Here, we present an unusual complete mole that showed strong expression of two imprinted, maternally transcribed genes, CDKN1C (encoding p57KIP2) and PHLDA2 (TSSC3/ IPL), both part of a large imprinted gene domain on chromosome 11. Using microsatellite genotyping and fluorescent in situ hybridization, we show that this paradoxical gene expression was due to retention of a maternal copy of chromosome 11 in addition to the two paternal copies normally present in complete moles. These findings demonstrate that, despite being predominantly androgenetic, some complete moles contain small amounts of DNA of maternal origin. Furthermore, these results provide an explanation for rare false negatives that can arise when p57KIP2 is used as a diagnostic marker for complete moles.
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Imprinted Gene Expression in Hybrids: Perturbed Mechanisms and Evolutionary Implications
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Developmental Biology ∎ (∎∎∎∎) ∎∎∎–∎∎∎ Contents lists available at ScienceDirect Developmental Biology journal homepage: www.elsevier.com/locate/developmentalbiology The imprinted Phlda2 gene modulates a major endocrine compartment of the placenta to regulate placental demands for maternal resources S.J. Tunster, H.D.J. Creeth, R.M. John n Cardiff School of Biosciences, Cardiff University, Cardiff, Wales CF10 3AX, UK article info abstract Article history: Imprinted genes, which are expressed from a single parental allele in response to epigenetic marks ﬁrst Received 4 August 2015 established in the germline, function in a myriad of processes to regulate mammalian development. Received in revised form Recent work suggests that imprinted genes may regulate the signalling function of the placenta by 2 October 2015 modulating the size of the endocrine compartment. Here we provide in vivo evidence that this hy- Accepted 11 October 2015 pothesis is well founded. Elevated expression of the imprinted Pleckstrin homology-like domain, family a, member 2 (Phlda2) gene drives a reduction of the spongiotrophoblast endocrine compartment, dimin- Keywords: ished placental glycogen and asymmetric foetal growth restriction. Using both loss-of-function and gain- Phlda2 in-expression mouse models, here we further show that Phlda2 exclusively modulates the spongio- Placenta trophoblast compartment of the placenta without signiﬁcantly altering the composition of the tropho- Hormones blast giant cell endocrine lineages that share a common progenitor with this lineage. Additionally, we Epigenetics Imprinting show that Phlda2 loss-of-function placentae contain nearly three times more placental glycogen than non-transgenic placentae. Remarkably, relative to a fully wild type scenario, wild type placentae also accumulate excessive glycogen.
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Original Article Placental Expression of PHLDA2 and IGF2 in Selective Intrauterine Growth Restriction in Monozygotic Twins
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Table S1. 103 Ferroptosis-Related Genes Retrieved from the Genecards
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Anti-PHLDA2 Monoclonal Antibody, Clone 6F5 (CAB-4194MH) This Product Is for Research Use Only and Is Not Intended for Diagnostic Use
Anti-PHLDA2 Monoclonal antibody, clone 6F5 (CAB-4194MH) This product is for research use only and is not intended for diagnostic use. PRODUCT INFORMATION Product Overview Mouse Anti-PHLDA2 Monoclonal Antibody Antigen Description This gene is one of several genes in the imprinted gene domain of 11p15.5 which is considered to be an important tumor suppressor gene region. Alterations in this region may be associated with the Beckwith-Wiedemann syndrome, Wilms tumor, rhabdomyosarcoma, adrenocortical carcinoma, and lung, ovarian, and breast cancer. Studies of the mouse gene, however, which is also located in an imprinted gene domain, have shown that the product of this gene regulates placental growth. Target PHLDA2 Immunogen PHLDA2 (NP_003302, 1 a.a.~111 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa. Isotype IgG2a Source/Host Mouse Species Reactivity Human Clone 6F5 Conjugate Unconjugated Applications ELISA, WB Format Clear, colorless solution in phosphate buffered saline, pH 7.2. Size 100 μg Preservative None Storage Maintain refrigerated at 2~8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. GENE INFORMATION 45-1 Ramsey Road, Shirley, NY 11967, USA Email: [email protected] Tel: 1-631-624-4882 Fax: 1-631-938-8221 1 © Creative Diagnostics All Rights Reserved Gene Name PHLDA2 pleckstrin homology-like domain, family A, member 2 [ Homo sapiens ] Official Symbol PHLDA2 Synonyms PHLDA2; pleckstrin homology-like domain, family A, member 2; TSSC3,
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bioRxiv preprint doi: https://doi.org/10.1101/2021.09.02.458742; this version posted September 3, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. 1 Single-cell transcriptome analysis reveals mesenchymal stem cells 2 in cavernous hemangioma 3 Fulong Ji1$, Yong Liu2$, Jinsong Shi3$, Chunxiang Liu1, Siqi Fu1 4 Heng Wang1, Bingbing Ren1, Dong Mi4, Shan Gao2*, Daqing Sun1* 5 1 Department of Paediatric Surgery, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China. 6 China. 7 2 College of Life Sciences, Nankai University, Tianjin, Tianjin 300071, P.R. China; 8 3 National Clinical Research Center of Kidney Disease, Jinling Hospital, Nanjing University School of 9 Medicine, Nanjing, Jiangsu 210016, P.R. China; 10 4 School of Mathematical Sciences, Nankai University, Tianjin, Tianjin 300071, P.R. China; 11 12 13 $ These authors contributed equally to this paper. 14 * Corresponding authors. 15 SG：[email protected] 16 DS：[email protected] 17 bioRxiv preprint doi: https://doi.org/10.1101/2021.09.02.458742; this version posted September 3, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. 18 Abstract 19 A cavernous hemangioma, well-known as vascular malformation, is present at birth, grows 20 proportionately with the child, and does not undergo regression.
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