Laser capture microdissection and cDNA array analysis for identification of mouse KIAA/FLJ genes differentially expressed in the embryonic dorsal spinal cord

Masuda, Tomoyuki; Kai, Norihisa; Sakuma, Chie; Kobayashi, Kazuto; Koga, Hisashi; Yaginuma, Hiroyuki

doi:10.1016/j.brainres.2008.10.028

Cited by 16 publications

(20 citation statements)

References 21 publications

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“…In adult mouse brains, FSTL5 is selectively expressed at high levels in the olfactory system, hippocampal CA3 area, and granular cell layer of the cerebellum [32]. In humans, FSTL5 has been associated with the prognosis of medulloblastoma, and it is highly expressed in a specific cell population during neuronal development [33,34]. The SNP rs148809765 is located in the intron region of KIAA1751 and upstream of gamma-aminobutyric acid (GABA) A receptor, delta ( GABRD ).…”

Section: Discussionmentioning

confidence: 99%

Genome-Wide Association Analysis of the Sense of Smell in U.S. Older Adults: Identification of Novel Risk Loci in African-Americans and European-Americans

et al. 2016

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The human sense of smell decreases with age, and a poor sense of smell are among the most important prodromal symptoms of several neurodegenerative diseases. Recent evidence further suggests a racial difference in the sense of smell among U.S. older adults. However, no genome-wide association study (GWAS) on the sense of smell has been conducted in African-Americans (AAs). We performed the first genome-wide meta-analysis of the sense of smell among 1,979 AAs and 6,582 European-Americans (EAs) from three U.S. aging cohorts. In the AA population, we identified nine novel regions (KLF4-ACTL7B, RAPGEF2-FSTL5, TCF4-LOC100505474, PCDH10, KIAA1751, MYO5B, MIR320B1-CD2, NR5A2-LINC00862, SALL1-C16orf97) that were associated with the sense of smell (P < 5 × 10−8). Many of these regions have been previously linked to neuropsychiatric (schizophrenia or epilepsy) or neurodegenerative (Parkinson’s or Alzheimer’s disease) diseases associated with a decreased sense of smell. In the EA population, we identified two novel loci in or near RASGRP1 and ANXA2P3 associated with sense of smell. In conclusion, this study identified several ancestry-specific loci that are associated with the sense of smell in older adults. While these findings need independent confirmation, they may lead to novel insights into the biology of the sense of smell in older adults and its relationships to neuropsychological and neurodegenerative diseases.

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Section: Discussionmentioning

confidence: 99%

Genome-Wide Association Analysis of the Sense of Smell in U.S. Older Adults: Identification of Novel Risk Loci in African-Americans and European-Americans

et al. 2016

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“…This is in agreement with proposals of previous studies [13], [14] that very large CNVs might have a high prior probability of being associated with schizophrenia phenotypes when observed almost exclusively in patients with schizophrenia. One of the new deleted genes identified, follistatin-like 5 ( FSTL5 ) located in the 4q32.1–32.2 region, encodes for the follistatin-related protein 5 precursor, an extracellular protein mainly expressed in B lymphoblasts, cerebellum and cerebellum peduncles, and possibly involved [24] in the early development of chemoattraction events responsible for the projection of the axons of the dorsal root ganglion neurons toward the dorsal spinal cord. A further new deletion, at 5q14.3, involved the EGF-like repeats and Discoidin I-Like domains 3 ( EDIL3 ) gene, which encodes an integrin-ligand promoting adhesion of endothelial cells, inhibits formation of vascular-like structures and might be involved in regulation of vascular morphogenesis of remodelling during embryonic development [25].…”

Section: Discussionmentioning

confidence: 99%

New Copy Number Variations in Schizophrenia

et al. 2010

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Genome-wide screenings for copy number variations (CNVs) in patients with schizophrenia have demonstrated the presence of several CNVs that increase the risk of developing the disease and a growing number of large rare CNVs; the contribution of these rare CNVs to schizophrenia remains unknown. Using Affymetrix 6.0 arrays, we undertook a systematic search for CNVs in 172 patients with schizophrenia and 160 healthy controls, all of Italian origin, with the aim of confirming previously identified loci and identifying novel schizophrenia susceptibility genes. We found five patients with a CNV occurring in one of the regions most convincingly implicated as risk factors for schizophrenia: NRXN1 and the 16p13.1 regions were found to be deleted in single patients and 15q11.2 in 2 patients, whereas the 15q13.3 region was duplicated in one patient. Furthermore, we found three distinct patients with CNVs in 2q12.2, 3q29 and 17p12 loci, respectively. These loci were previously reported to be deleted or duplicated in patients with schizophrenia but were never formally associated with the disease. We found 5 large CNVs (>900 kb) in 4q32, 5q14.3, 8q23.3, 11q25 and 17q12 in five different patients that could include some new candidate schizophrenia susceptibility genes. In conclusion, the identification of previously reported CNVs and of new, rare, large CNVs further supports a model of schizophrenia that includes the effect of multiple, rare, highly penetrant variants.

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“…Bcr is among a set of genes expressed very early in development (171). Full-length Bcr contributes to NGF-independent neurite formation in PC12 cells (172), while a fusion construct including the GEF domain but not the RhoGAP domain suppresses neurite outgrowth (172).…”

Section: Introductionmentioning

confidence: 99%

Synaptic Plasticity, a Symphony in GEF

Kiraly

Eipper-Mains

Mains

et al. 2010

ACS Chem. Neurosci.

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Dendritic spines are the postsynaptic sites for the majority of excitatory synapses in the mammalian forebrain. While many spines display great stability, others change shape in a matter of seconds to minutes. These rapid alterations in dendritic spine number and size require tight control of the actin cytoskeleton, the main structural component of dendritic spines. The ability of neurons to alter spine number and size is essential for the expression of neuronal plasticity. Within spines, guanine nucleotide exchange factors (GEFs) act as critical regulators of the actin cytoskeleton by controlling the activity of Rho-GTPases. In this review we focus on the Rho-GEFs expressed in the nucleus accumbens and localized to the postsynaptic density, and thus positioned to effect rapid alterations in the structure of dendritic spines. We review literature that ties these GEFs to different receptor systems and intracellular signaling cascades and discuss the effects these interactions are likely to have on synaptic plasticity.

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Laser capture microdissection and cDNA array analysis for identification of mouse KIAA/FLJ genes differentially expressed in the embryonic dorsal spinal cord

Cited by 16 publications

References 21 publications

Genome-Wide Association Analysis of the Sense of Smell in U.S. Older Adults: Identification of Novel Risk Loci in African-Americans and European-Americans

Genome-Wide Association Analysis of the Sense of Smell in U.S. Older Adults: Identification of Novel Risk Loci in African-Americans and European-Americans

New Copy Number Variations in Schizophrenia

Synaptic Plasticity, a Symphony in GEF

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