anti-Atonal Homolog 7 (Drosophila) (ATOH7) Anticorps

Zebrafish Atonal Homolog 7 (Drosophila) (ATOH7) interaction partners

1. Atoh7 indirectly impacts amacrine-cell division modes to regulate the right number of Barhl2 (Montrer BARHL2 Anticorps)-expressing cells. Atoh7 itself influences the subtypes of Barhl2 (Montrer BARHL2 Anticorps)-dependent amacrine cells.

2. Observations suggest that Irx2 (Montrer IRX2 Anticorps) functions downstream of irx1a (Montrer IRX1 Anticorps) to control shh (Montrer SHH Anticorps) expression in the retina. Study proposed a novel transcriptional cascade of ath5-irx1a (Montrer IRX1 Anticorps)-irx2a in the regulation of hedgehog (Montrer SHH Anticorps) waves during vertebrate retinal development.

3. Staggered cell-intrinsic timing of ath5 expression underlies the wave of ganglion cell neurogenesis in the zebrafish retina.

Mouse (Murine) Atonal Homolog 7 (Drosophila) (ATOH7) interaction partners

1. The transient features of Atoh7 protein expression during retinal neurogenesis match the expected pattern at the tissue and cellular level.

2. Pou4f2 (Montrer POU4F2 Anticorps) and Isl1 (Montrer ISL1 Anticorps), are sufficient to specify the retinal ganglion cell fate in ATOH7 deficient mice

3. This study present evidence for a Pax6 (Montrer PAX6 Anticorps)-Atoh7-Eya2 (Montrer EYA2 Anticorps) pathway that acts downstream of Atoh7 but upstream of differentiation factor Pou4f2 (Montrer POU4F2 Anticorps).

4. Notch (Montrer NOTCH1 Anticorps) signaling controls the overall tempo of retinogenesis through Atoh7 and Neurog2 (Montrer NEUROG2 Anticorps), by integrating cell fate specification, the wave of neurogenesis and the developmental status of cells ahead of this wave

5. The level of basic helix-loop-helix factor Math5 expression may determine the ultimate number of retinal ganglion cells.

6. Atoh7 acts dominantly in Neurod1-expressing retina progenitor cells to activate the retinal ganglion cell genetic program.

7. Results suggest that Math5 is not sufficient to stimulate retinal ganglion cell (RGC)fate.

8. new insights into Math5 function, ganglion cell development, and the mechanism of retinal fate determination were provided.

9. The present data demonstrates that the loss of ganglion cells in the Math5(-/-) mice is associated with a lack of retinal vascular development.

10. Report Math5 expression/function in retinal ganglion cells.

Human Atonal Homolog 7 (Drosophila) (ATOH7) interaction partners

1. In conclusion, we have identified a homozygous mutation in the ATOH7 gene in a patient with nonsyndromic congenital retinal nonattachment.

2. We evaluated 21 consanguineous NCRNA pedigrees and identified the causal mutations in known retinal genes in 13 out of our 21 families. We found mutations in ATOH7 in three families.

3. We discovered a novel SNP, rs56238729 (P = 1.22 x 10-13), in the ATOH7-PBLD region that is significantly associated with VCDR in Latino individuals.

4. The genotype and allele frequencies of the polymorphism in ATOH7 did not show any statistically significant association with primary open angle glaucomacompared to controls.

5. Familial linkage studies for primary angle-closure glaucoma have been performed and identified ATOH7 causative primary angle-closure glaucoma disease

6. Single nucleotide polymorphism in ATOH7 gene is associated with primary open angle glaucoma.

7. The significant association of three common variants in TMCO1 (Montrer TMCO1 Anticorps), ATOH7, and CAV1 (Montrer CAV1 Anticorps) with primary open angle, primary angle closure, and pseudoexfoliation glaucoma was found in Pakistani cohorts.

8. Mutations within the ATOH7 gene are not implicated in the pathogenesis of optic nerve hypoplasia in our patient cohort.

9. This study finds that ATOH7 is associated with optic disc size but not independently with cup/disk ratio.

10. a bHLH mutation in ATOH7 causes recessive persistent hyperplasia of the primary vitreous