G2Cdb::Gene report

Gene id
G00000346
Gene symbol
Anxa3 (MGI)
Species
Mus musculus
Description
annexin A3
Orthologue
G00001595 (Homo sapiens)

Databases (8)

Gene
ENSMUSG00000029484 (Ensembl mouse gene)
11745 (Entrez Gene)
681 (G2Cdb plasticity & disease)
Gene Expression
NM_013470 (Allen Brain Atlas)
11745 (Genepaint)
Literature
106490 (OMIM)
Marker Symbol
MGI:1201378 (MGI)
Protein Sequence
O35639 (UniProt)

Synonyms (1)

  • Anx3

Literature (8)

Pubmed - other

  • A high-resolution anatomical atlas of the transcriptome in the mouse embryo.

    Diez-Roux G, Banfi S, Sultan M, Geffers L, Anand S, Rozado D, Magen A, Canidio E, Pagani M, Peluso I, Lin-Marq N, Koch M, Bilio M, Cantiello I, Verde R, De Masi C, Bianchi SA, Cicchini J, Perroud E, Mehmeti S, Dagand E, Schrinner S, Nürnberger A, Schmidt K, Metz K, Zwingmann C, Brieske N, Springer C, Hernandez AM, Herzog S, Grabbe F, Sieverding C, Fischer B, Schrader K, Brockmeyer M, Dettmer S, Helbig C, Alunni V, Battaini MA, Mura C, Henrichsen CN, Garcia-Lopez R, Echevarria D, Puelles E, Garcia-Calero E, Kruse S, Uhr M, Kauck C, Feng G, Milyaev N, Ong CK, Kumar L, Lam M, Semple CA, Gyenesei A, Mundlos S, Radelof U, Lehrach H, Sarmientos P, Reymond A, Davidson DR, Dollé P, Antonarakis SE, Yaspo ML, Martinez S, Baldock RA, Eichele G and Ballabio A

    Telethon Institute of Genetics and Medicine, Naples, Italy.

    Ascertaining when and where genes are expressed is of crucial importance to understanding or predicting the physiological role of genes and proteins and how they interact to form the complex networks that underlie organ development and function. It is, therefore, crucial to determine on a genome-wide level, the spatio-temporal gene expression profiles at cellular resolution. This information is provided by colorimetric RNA in situ hybridization that can elucidate expression of genes in their native context and does so at cellular resolution. We generated what is to our knowledge the first genome-wide transcriptome atlas by RNA in situ hybridization of an entire mammalian organism, the developing mouse at embryonic day 14.5. This digital transcriptome atlas, the Eurexpress atlas (http://www.eurexpress.org), consists of a searchable database of annotated images that can be interactively viewed. We generated anatomy-based expression profiles for over 18,000 coding genes and over 400 microRNAs. We identified 1,002 tissue-specific genes that are a source of novel tissue-specific markers for 37 different anatomical structures. The quality and the resolution of the data revealed novel molecular domains for several developing structures, such as the telencephalon, a novel organization for the hypothalamus, and insight on the Wnt network involved in renal epithelial differentiation during kidney development. The digital transcriptome atlas is a powerful resource to determine co-expression of genes, to identify cell populations and lineages, and to identify functional associations between genes relevant to development and disease.

    Funded by: Medical Research Council: MC_U127527203; Telethon: TGM11S03

    PLoS biology 2011;9;1;e1000582

  • Annexin A3 is associated with cell death in lactacystin-mediated neuronal injury.

    Chong KW, Chen MJ, Koay ES, Wong BS, Lee AY, Russo-Marie F and Cheung NS

    Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.

    Massive neuronal apoptosis and accumulation of protein aggregates in the cortex and hippocampus of the brain are hallmarks of several neurodegenerative disorders, indicating ubiquitin proteasome system (UPS) dysfunction. Lactacystin, a classical proteasome inhibitor, is used to simulate ubiquitin proteasome system dysfunction in neurons to mimic pathological features of neurodegenerative disorders. Based on Western blot analyses, we reported for the first time that annexin A3 (AnxA3) is not only endogenously expressed in mouse cortical neurons but also more importantly, by gene expression microarray and real-time RT-PCR that it is greatly transcriptional up-regulated to approximately 11- and 15-fold, respectively in murine primary cortical neurons with 1μM lactacystin for 24h. Up-regulation of AnxA3 expression occurred after 12-15h post-lactacystin treatment, which corresponded with the onset of neuronal injury, with approximately 25% of the neurons being non-viable by that time interval. Western blot analysis with anti-AnxA3 antibodies further validated that up-regulation of AnxA3 only occurs with onset of neuronal death, and not with the onset of proteasome inhibition, which occurs at 4.5h post-lactacystin treatment. Over-expression studies suggested AnxA3 might be involved in death promotion during lactacystin-mediated neuronal death, since caspase-3 activation was significantly stronger upon neuronal AnxA3 over-expression. We propose AnxA3 up-regulation may have significant relevance in the elucidation of neurodegenerative pathophysiology.

    Neuroscience letters 2010;485;2;129-33

  • Identification of transcripts with enriched expression in the developing and adult pancreas.

    Hoffman BG, Zavaglia B, Witzsche J, Ruiz de Algara T, Beach M, Hoodless PA, Jones SJ, Marra MA and Helgason CD

    Department of Cancer Endocrinology, BC Cancer Research Center, West 10th Ave, Vancouver, BC V5Z 1L3, Canada. bhoffman@bccrc.ca

    Background: Despite recent advances, the transcriptional hierarchy driving pancreas organogenesis remains largely unknown, in part due to the paucity of comprehensive analyses. To address this deficit we generated ten SAGE libraries from the developing murine pancreas spanning Theiler stages 17-26, making use of available Pdx1 enhanced green fluorescent protein (EGFP) and Neurog3 EGFP reporter strains, as well as tissue from adult islets and ducts.

    Results: We used a specificity metric to identify 2,536 tags with pancreas-enriched expression compared to 195 other mouse SAGE libraries. We subsequently grouped co-expressed transcripts with differential expression during pancreas development using K-means clustering. We validated the clusters first using quantitative real time PCR and then by analyzing the Theiler stage 22 pancreas in situ hybridization staining patterns of over 600 of the identified genes using the GenePaint database. These were then categorized into one of the five expression domains within the developing pancreas. Based on these results we identified a cascade of transcriptional regulators expressed in the endocrine pancreas lineage and, from this, we developed a predictive regulatory network describing beta-cell development.

    Conclusion: Taken together, this work provides evidence that the SAGE libraries generated here are a valuable resource for continuing to elucidate the molecular mechanisms regulating pancreas development. Furthermore, our studies provide a comprehensive analysis of pancreas development, and insights into the regulatory networks driving this process are revealed.

    Genome biology 2008;9;6;R99

  • Identification of FGF10 targets in the embryonic lung epithelium during bud morphogenesis.

    Lü J, Izvolsky KI, Qian J and Cardoso WV

    Pulmonary Center, Boston University School of Medicine, Boston, Massachusetts 02118, USA.

    Genetic studies implicate Fgf10-Fgfr2 signaling as a critical regulator of bud morphogenesis in the embryo. However, little is known about the transcriptional targets of Fgf10 during this process. Here we identified global changes in gene expression in lung epithelial explants undergoing FGF10-mediated budding in the absence of other growth factors and mesenchyme. Targets were confirmed by their localization at sites where endogenous Fgf10 signaling is active in embryonic lungs and by demonstrating their induction in intact lungs in response to local application of FGF10 protein. We show that the initial stages of budding are characterized by marked up-regulation of genes associated with cell rearrangement and cell migration, inflammatory process, and lipid metabolism but not cell proliferation. We also found that some genes implicated in tumor invasion and metastatic behavior are epithelial targets of Fgf10 in the lung and other developing organs that depend on Fgf10-Fgfr2 signaling to properly form. Our approach identifies Fgf10 targets that are common to multiple biological processes and provides insights into potential mechanisms by which Fgf signaling regulates epithelial cell behavior.

    Funded by: NHLBI NIH HHS: (P01) HL47049

    The Journal of biological chemistry 2005;280;6;4834-41

  • Amelogenesis imperfecta in a new animal model--a mutation in chromosome 5 (human 4q21).

    Seedorf H, Springer IN, Grundner-Culemann E, Albers HK, Reis A, Fuchs H, Hrabe de Angelis M and Açil Y

    Department of Prosthetic Dentistry, University Hospital Hamburg-Eppendorf, Martinistr. 52, D-20246 Hamburg, Germany.

    Candidate genes for amelogenesis imperfecta (AI) and dentinogenesis imperfecta (DI) are located on 4q21 in humans. We tested our hypothesis that mutations in the portion of mouse chromosome 5 corresponding to human chromosome 4q21 would cause enamel and dentin abnormalities. Male C3H mice were injected with ethylnitrosourea (ENU). Within a dominant ENU mutagenesis screen, a mouse mutant was isolated with an abnormal tooth enamel (ATE) phenotype. The structure and ultrastructure of teeth were studied. The mutation was located on mouse chromosome 5 in an interval of 9 cM between markers D5Mit18 and D5Mit10. Homozygotic mutants showed total enamel aplasia with exposed dentinal tubules, while heterozygotic mutants showed a significant reduction in enamel width. Dentin of mutant mice showed a reduced content of mature collagen cross-links. We were able to demonstrate that a mutation on chromosome 5 corresponding to human chromosome 4q21 can cause amelogenesis imperfecta and changes in dentin composition.

    Journal of dental research 2004;83;8;608-12

  • Large-scale screen for genes controlling mammalian embryogenesis, using high-throughput gene expression analysis in mouse embryos.

    Neidhardt L, Gasca S, Wertz K, Obermayr F, Worpenberg S, Lehrach H and Herrmann BG

    Max-Planck-Institut für Immunbiologie, Abt. Entwicklungsbiologie, Stübeweg 51, 79108, Freiburg, Germany.

    We have adapted the whole-mount in situ hybridization technique to perform high-throughput gene expression analysis in mouse embryos. A large-scale screen for genes showing specific expression patterns in the mid-gestation embryo was carried out, and a large number of genes controlling development were isolated. From 35760 clones of a 9.5 d.p.c. cDNA library, a total of 5348 cDNAs, enriched for rare transcripts, were selected and analyzed by whole-mount in situ hybridization. Four hundred and twenty-eight clones revealed specific expression patterns in the 9.5 d.p.c. embryo. Of 361 tag-sequenced clones, 198 (55%) represent 154 known mouse genes. Thirty-nine (25%) of the known genes are involved in transcriptional regulation and 33 (21%) in inter- or intracellular signaling. A large number of these genes have been shown to play an important role in embryogenesis. Furthermore, 24 (16%) of the known genes are implicated in human disorders and three others altered in classical mouse mutations. Similar proportions of regulators of embryonic development and candidates for human disorders or mouse mutations are expected among the 163 new mouse genes isolated. Thus, high-throughput gene expression analysis is suitable for isolating regulators of embryonic development on a large-scale, and in the long term, for determining the molecular anatomy of the mouse embryo. This knowledge will provide a basis for the systematic investigation of pattern formation, tissue differentiation and organogenesis in mammals.

    Mechanisms of development 2000;98;1-2;77-94

  • Genome-wide expression profiling of mid-gestation placenta and embryo using a 15,000 mouse developmental cDNA microarray.

    Tanaka TS, Jaradat SA, Lim MK, Kargul GJ, Wang X, Grahovac MJ, Pantano S, Sano Y, Piao Y, Nagaraja R, Doi H, Wood WH, Becker KG and Ko MS

    Laboratory of Genetics and DNA Array Unit, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224-6820, USA.

    cDNA microarray technology has been increasingly used to monitor global gene expression patterns in various tissues and cell types. However, applications to mammalian development have been hampered by the lack of appropriate cDNA collections, particularly for early developmental stages. To overcome this problem, a PCR-based cDNA library construction method was used to derive 52,374 expressed sequence tags from pre- and peri-implantation embryos, embryonic day (E) 12.5 female gonad/mesonephros, and newborn ovary. From these cDNA collections, a microarray representing 15,264 unique genes (78% novel and 22% known) was assembled. In initial applications, the divergence of placental and embryonic gene expression profiles was assessed. At stage E12.5 of development, based on triplicate experiments, 720 genes (6.5%) displayed statistically significant differences in expression between placenta and embryo. Among 289 more highly expressed in placenta, 61 placenta-specific genes encoded, for example, a novel prolactin-like protein. The number of genes highly expressed (and frequently specific) for placenta has thereby been increased 5-fold over the total previously reported, illustrating the potential of the microarrays for tissue-specific gene discovery and analysis of mammalian developmental programs.

    Proceedings of the National Academy of Sciences of the United States of America 2000;97;16;9127-32

  • Mouse annexin III cDNA, genetic mapping and evolution.

    Fernández MP, Copeland NG, Gilbert DJ, Jenkins NA and Morgan RO

    Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Oviedo, Spain. mpff@dwarf1.quimica.uniovi.es

    Mouse annexin III cDNA was characterized from I.M.A.G.E. Consortium (LLNL) expressed sequence tag clones by molecular sequencing, chromosomal mapping and systematic analysis. cDNA sequences extended the known 5' and 3' untranslated regions and confirmed the location of intron 7 with respect to the human gene. The Anx3 locus mapped to the middle of mouse chromosome 5 between Areg and Fgf5. Protein-coding regions were compared with homologous annexins to establish subfamily identity, structural conservation and divergence pattern. Annexin III exhibited low functional constraint against structural change and weak phylogenetic association with known annexins. The rapid, constant divergence of human and rodent annexins III from each other and from other annexin subfamilies was used to estimate gene separation times. Phylogenetic, phenetic and structural data suggested a possible direct or indirect separation of annexin III from XI approximately 317 million years ago.

    Gene 1998;207;1;43-51

Gene lists (2)

Gene List Source Species Name Description Gene count
L00000001 G2C Mus musculus Mouse PSD Mouse PSD adapted from Collins et al (2006) 1080
L00000008 G2C Mus musculus Mouse PSP Mouse PSP adapted from Collins et al (2006) 1121
© G2C 2014. The Genes to Cognition Programme received funding from The Wellcome Trust and the EU FP7 Framework Programmes:
EUROSPIN (FP7-HEALTH-241498), SynSys (FP7-HEALTH-242167) and GENCODYS (FP7-HEALTH-241995).

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