A Genetic Variant in TGFBR3-CDC7 Is Associated with Visual Field Progression in Primary Open-Angle Glaucoma Patients from Singapore.
Singapore, Singapore. In Ophthalmology, 14 Oct 2015
Single nucleotide polymorphisms (SNPs) and their proxies from 10 POAG-associated loci (CAV1-CAV2, CDKN2B-AS1, SIX1-SIX6, an intergenic region on chromosome 8q22, ABCA1, GAS7, AFAP1, GMDS, PMM2, and TGFBR3-CDC7) identified from genome-wide association studies were tested for association with VF progression using logistic regression with an additive genetic model adjusting for age, gender, average intraocular pressure (IOP), central corneal thickness (CCT), and baseline vertical cup-to-disc ratio (VCDR).
Evolution and development of the adelphophagic, intracapsular Schmidt's larva of the nemertean Lineus ruber.
Bergen, Norway. In Evodevo, Dec 2014
The expression of evolutionarily conserved anterior (foxQ2, six3/6, gsc, otx), endomesodermal (foxA, GATA456-a, twi-a) and posterior (evx, cdx) markers demonstrate that the juvenile retains the molecular patterning of the Schmidt's larva.
Genetics of primary open angle glaucoma.
Tokyo, Japan. In Jpn J Ophthalmol, 2014
Several association studies have been conducted for candidate genes, and genome-wide association studies recently identified new susceptibility loci for POAG, namely, S1 RNA binding domain 1 region on chromosome 2p21, the caveolin 1 and caveolin 2 regions on 7q31, transmembrane and coiled-coil domain 1 region on 1q24, cyclin-dependent kinase inhibitor 2B antisense RNA on 9p21, the SIX1 and SIX6 regions on 14q24 and, possibly, the regulatory region of 8q22.
The bilaterian forebrain: an evolutionary chimaera.
Heidelberg, Germany. In Curr Opin Neurobiol, 2013
Here, we review recent comparative neurodevelopmental evidence indicating that these centres evolved from separate condensations of neurons on opposite body sides ('apical nervous system' versus 'blastoporal nervous system') and that their developmental specification involved distinct regulatory networks (apical six3 and rx versus mediolateral nk and pax gene-dependent patterning).
Six3 is required for ependymal cell maturation.
Memphis, United States. In Development, 2011
It was shown that Six3 is necessary for ependymal cell maturation during postnatal stages of brain development. In its absence, ependymal cells fail to suppress radial glia characteristics.
Eye development genes and known syndromes.
San Francisco, United States. In Mol Genet Metab, 2011
In addition, we briefly discuss the ocular and extraocular phenotypes associated with several other important eye developmental genes, including GDF6, VSX2, RAX, SHH, SIX6 and PAX6.
Etiopathogenetic advances and management of holoprosencephaly: from bench to bedside.
Novara, Italy. In Panminerva Med, 2010
Genetic causes are responsible for about 20% of cases: they are chromosomal abnormalities and gene mutations: up to date, nine genes (SHH, ZIC2, SIX3, TGIF, PATCHED1, TDGF1/CRIPTO, FAST1, GLI2 and DHCR) are definitely associated with HPE, but many others candidate gene are under investigation.
Seattle, United States. In Unknown Journal, 2004
Mutations in the following genes are associated with A/M: SIX3, HESX1, BCOR, SHH, PAX6, RAX, CHD7 (CHARGE syndrome), IKBKG (incontinentia pigmenti), NDP (Norrie disease), SOX2 (SOX2-related eye disorders), POMT1 (Walker-Warburg syndrome), and SIX6.