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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.


This gene is the human ortholog of the Drosophila melanogaster 'abnormal spindle' gene (asp), which is essential for normal mitotic spindle function in embryonic neuroblasts. Studies in mouse also suggest a role of this gene in mitotic spindle regulation, with a preferential role in regulating neurogenesis. Mutations in this gene are associated with microcephaly primary type 5. Multiple transcript variants encoding different isoforms have been found for this gene.[provided by RefSeq, May 2011] (from NCBI)
Top mentioned proteins: MCPH1, CAN, C48, LAP, ACID
Papers on ASPM
Identification and biochemical characterization of polyamine oxidases in amphioxus: Implications for emergence of vertebrate-specific spermine and acetylpolyamine oxidases.
Zhang et al., Qingdao, China. In Gene, Feb 2016
Generally, plant PAOs oxidize spermine (Spm), spermidine (Spd) and their acetylated derivatives, N(1)-acetylspermine (N(1)-Aspm) and N(1)-acetylspermidine (N(1)-Aspd), while yeast PAOs oxidize Spm, N(1)-Aspm and N(1)-Aspd, but not Spd.
A candidate gastric stem/progenitor cell marker revealed by genome-wide analysis.
Gao et al., Shanghai, China. In J Pathol, Jan 2016
In a recent paper in The Journal of Pathology, Vange et al suggest ASPM as a candidate stem/progenitor cell marker for oxyntic glands.
Microcephaly protein Asp focuses the minus ends of spindle microtubules at the pole and within the spindle.
Goshima et al., Nagoya, Japan. In J Cell Biol, Jan 2016
Depletion of Drosophila melanogaster Asp, an orthologue of microcephaly protein ASPM, causes spindle pole unfocusing during mitosis.
Aspm sustains postnatal cerebellar neurogenesis and medulloblastoma growth in mice.
Gershon et al., Chapel Hill, United States. In Development, Dec 2015
Here, we report that Aspm, a gene that is mutated in familial microcephaly, regulates postnatal neurogenesis in the cerebellum and supports the growth of medulloblastoma, the most common malignant pediatric brain tumor.
Accurate Prediction and Validation of Response to Endocrine Therapy in Breast Cancer.
Dixon et al., London, United Kingdom. In J Clin Oncol, Aug 2015
RESULTS: The molecular response to letrozole was characterized and a four-gene classifier of clinical response was established (accuracy of 96%) on the basis of the level of two genes before treatment (one gene [IL6ST] was associated with immune signaling, and the other [NGFRAP1] was associated with apoptosis) and the level of two proliferation genes (ASPM, MCM4) after 2 weeks of therapy.
MCPH1: a window into brain development and evolution.
Nardelli et al., Sydney, Australia. In Front Cell Neurosci, 2014
In this context, causative genes of human autosomal recessive primary microcephaly, such as ASPM and MCPH1, are attractive candidates, as many of them show positive selection during primate evolution.
Molecular genetics of human primary microcephaly: an overview.
Saleh Jamal et al., In Bmc Med Genomics, 2014
Twelve MCPH loci (MCPH1-MCPH12) have been mapped to date from various populations around the world and contain the following genes: Microcephalin, WDR62, CDK5RAP2, CASC5, ASPM, CENPJ, STIL, CEP135, CEP152, ZNF335, PHC1 and CDK6.
ASPM regulates symmetric stem cell division by tuning Cyclin E ubiquitination.
Pozner et al., Salt Lake City, United States. In Nat Commun, 2014
We generate a mouse model for the human microcephaly syndrome by mutating the ASPM locus, and demonstrate a premature exhaustion of the neuronal progenitor pool due to dysfunctional self-renewal processes.
The microcephaly protein Asp regulates neuroepithelium morphogenesis by controlling the spatial distribution of myosin II.
Basto et al., Paris, France. In Nat Cell Biol, 2013
Here, we characterized the function of the Drosophila ASPM orthologue, Asp, and found that asp mutants present severe defects in brain size and neuroepithelium morphogenesis.
ASPM influences DNA double-strand break repair and represents a potential target for radiotherapy.
Fujimori et al., Chiba, Japan. In Int J Radiat Biol, 2011
Results show for the first time that ASPM is required for efficient non-homologous end-joining in mammalian cells.
The derived allele of ASPM is associated with lexical tone perception.
Zheng et al., Evanston, United States. In Plos One, 2011
the association between the recently derived allele of ASPM is likely to be specific and is tied to higher level brain functions in the temporal cortex related to human communication.
ASPM regulates Wnt signaling pathway activity in the developing brain.
Tsai et al., Cambridge, United States. In Genes Dev, 2011
knockdown of Aspm results in decreased Wnt-mediated transcription
In vivo fate analysis reveals the multipotent and self-renewal features of embryonic AspM expressing cells.
Muzio et al., Milano, Italy. In Plos One, 2010
AspM is expressed by proliferating cells of the adult mouse SVZ that can generate neuroblasts fated to become olfactory bulb neurons
Angelman syndrome protein UBE3A interacts with primary microcephaly protein ASPM, localizes to centrosomes and regulates chromosome segregation.
Kumar et al., Bengaluru, India. In Plos One, 2010
Study links Angelman syndrome protein UBE3A to ASPM, centrosome and mitosis.
Autosomal Recessive Primary Microcephaly (MCPH): clinical manifestations, genetic heterogeneity and mutation continuum.
Hassan et al., Lahore, Pakistan. In Orphanet J Rare Dis, 2010
So far, seven genetic loci (MCPH1-7) for this condition have been mapped with seven corresponding genes (MCPH1, WDR62, CDK5RAP2, CEP152, ASPM, CENPJ, and STIL) identified from different world populations.
WDR62 is associated with the spindle pole and is mutated in human microcephaly.
Woods et al., Cambridge, United Kingdom. In Nat Genet, 2010
In human cell lines, we found that WDR62 is a spindle pole protein, as are ASPM and STIL, the MCPH7 and MCHP7 proteins.
Many roads lead to primary autosomal recessive microcephaly.
Gressens et al., Paris, France. In Prog Neurobiol, 2010
Genetic causes of MCPH subtypes 1-7 include mutations in genes encoding microcephalin, cyclin-dependent kinase 5 regulatory associated protein 2 (CDK5RAP2), abnormal spindle-like, microcephaly associated protein (ASPM), centromeric protein J (CENPJ), and SCL/TAL1-interrupting locus (STIL) as well as linkage to the two loci 19q13.1-13.2 and 15q15-q21.
Primary Autosomal Recessive Microcephalies and Seckel Syndrome Spectrum Disorders
Passemard et al., Seattle, United States. In Unknown Journal, 2009
The genes in which biallelic mutation is known to cause MCPH-SCKS spectrum disorders are separated into those that are currently known to be associated with: MCPH phenotype only: MCPH1 (locus name MCPH1), WDR62 (MCPH2), CDK5RAP2 (MCPH3), CASC5 (MCPH4), ASPM (MCPH5), STIL (MCPH7), CEP135 (MCPH8), and CDK6 (MCPH12); SCKS phenotype only: ATR (locus name SCKL1), NIN (SCKL7), and ATRIP ; and MCPH, SCKS, and/or intermediate phenotypes: RBBP8 (locus name SCKL2), CEP152 (MCPH9/SCKL5), CENPJ (MCPH6/SCKL4), CEP63 (SCKL6), and PHC1 (MCPH11).
NuMA-related LIN-5, ASPM-1, calmodulin and dynein promote meiotic spindle rotation independently of cortical LIN-5/GPR/Galpha.
van den Heuvel et al., Utrecht, Netherlands. In Nat Cell Biol, 2009
Here we identify ASPM-1 (abnormal spindle-like, microcephaly-associated) as a novel LIN-5 binding partner.
Mutations in the pericentrin (PCNT) gene cause primordial dwarfism.
Reis et al., Erlangen, Germany. In Science, 2008
Mutations in related genes are known to cause primary microcephaly (MCPH1, CDK5RAP2, ASPM, and CENPJ).
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