Atonal Homolog 1 (Drosophila) (ATOH1) Kits ELISA

Zebrafish Atonal Homolog 1 (Drosophila) (ATOH1) interaction partners

1. A genetic network of sensory determinant, Atoh1 (and Sox9a), play critical roles in otic neural development.

2. Sox2 and Fgf interact with Atoh1 to promote sensory competence throughout the zebrafish inner ear.

3. Atoh1a expression must be restricted by Notch signaling for effective morphogenesis of the posterior lateral line primordium in zebrafish.

4. in the zebrafish, two proneural genes are essential for differentiation of the hair cells, neuroD and atonal homolog 1

5. atoh1a and atoh1b are together necessary for hair cell development. These genes crossregulate each other but are differentially required during distinct developmental periods

6. atoh1.2 and beta3.1 are transcribed in distinct precursors.

Human Atonal Homolog 1 (Drosophila) (ATOH1) interaction partners

1. Atoh1 promotes ciliogenesis by transcriptionally regulating Cep131, which facilitates centriolar satellite clustering to the basal body

2. ATOH1 role in colon cancer.Positive ATOH1 expression in colon cancer tissues was significantly associated with lower grade and better overall survival.ATOH1 was the target mRNA of miR-613.

3. Data indicate that transcription factor atonal bHLH transcription factor 1 protein (Atoh1) is critical for hair cell development and regeneration [Review].

4. Our results suggest that KN promotes goblet cell differentiation by regulating Wnt, Notch, and AhR signals and expression of Hes1 and Hath1.

5. The authors discovered tyrosine 78 of Atoh1 is phosphorylated by a Jak2-mediated pathway only in tumor-initiating cells and in human Sonic Hedgehog-type medulloblastoma.

6. ATOH1 expression was detected consistently in recurrent and metastatic SHH medulloblastoma. Chromatin immunoprecipitation sequencing and gene expression profiling identified candidate ATOH1 targets in tumor cells involved in development and tumorigenesis.

7. These data indicate that the regulation of Atoh1 by the ubiquitin proteasome pathway is necessary for hair cell fate determination and survival.

8. ATOH1 is increased in advanced Merkel cell carcinoma (MCC) indicating that ATOH1 is involved in MCC progression.

9. Study provides evidence that Sox2 expression is required for the late stages of progenitor cell differentiation to hair cells and stimulates Atoh1 expression through a concentration dependent molecular interaction with the 3' enhancer of Atoh1.

10. mutation not found in group of children with sensorineural hearing loss

11. Downregulation of Hath1 expression promoted the proliferation and reduced the apoptosis of KUMA5 squamous cell carcinoma cells.

12. ATOH1 can induce the differentiation of gastric cancer stem cells.

13. ATOH1 acts in concert with other transcription factors to directly regulate the cochlear hair cell phenotype.

14. Testosterone-bovine serum albumin and Math1 treatment could promote an increase in hair-cell like cells in the lesser epithelial ridge through proliferation and transdifferentiation.

15. Atoh1 epigenetic regulation guides hair cell development in the mammalian cochlea

16. Atoh1 protein stabilization induced both a cancer stem cell phenotype and a mucinous phenotype, resulting in the acquisition of chemoresistance in colorectal cancer

17. Chicken Atoh1 might have intrinsic functional differences to mammalian Atoh1.

18. In this review, expression of the Atoh1 gene in supporting cells, results in their transformation into immature hair cells.

19. Data suggest that Atoh1 high expression correlates with a good prognosis and it may serve as a favorable prognostic factor for GIST.

20. Expression of Hath1, Muc2, cyclin D1 and p27 in the xenograft tumors was also detected.

Mouse (Murine) Atonal Homolog 1 (Drosophila) (ATOH1) interaction partners

1. Atoh1 (+) cells contributed minimally to other lineages during homeostasis, they displayed plasticity and contributed to epithelial repair during injury, independent of Lgr5 (+) cells

2. Progenitor plasticity maintains robust self-renewal in the intestinal epithelium, and the balance between stem and progenitor fate is directly coordinated by ATOH1 multisite phosphorylation.

3. Meis1 regulates degradation of Atoh1 via bone morphogenic protein signaling, contributing to granule cells differentiation in the inner external granule

4. Atoh1 thus promotes the development of the neural circuits governing hypoxic and hypercapnic chemoresponses.

5. Study identified 51 key reprogramming transcription factors that may increase the efficiency and completion of the regeneration process and confirmed that Isl1 in transgenic mice promotes Atoh1-mediated sensory regeneration as a co-reprogramming factor.

6. Sox4 promoted tuft and enteroendocrine cell lineage allocation independently of Atoh1. These results challenge the longstanding model in which Atoh1 is the sole regulator of secretory differentiation in the intestine and are relevant for understanding epithelial responses to parasitic infection.

7. The results of this study presented here from various Atoh1 mutants demonstrate that neither peripheral nor central target cell differentiation is necessary for cochlear afferent segregation from vestibular afferents or for some degree of a cochleotopic segregation

8. Atoh1 function in hair cell differentiation is modulated by interaction with other transcription factors, such as Gfi1 and Pou4f3. (Review)

9. The data suggest that ErbB3 restricts Paneth cells numbers through PI3K-mediated suppression of Atoh1 levels leading to inhibition of Paneth cells differentiation, with important implications for regulation of the intestinal stem cells niche.

10. This study illustrates a SHH-Stox1-Math1 regulatory axis in normal cerebellar development and medulloblastoma formation.

11. This work reveals a dynamic ATOH1-driven molecular cascade underlying medulloblastoma metastasis that offers possible therapeutic opportunities

12. The discovery that Atonal homolog 1 (Atoh1) governs the development of the sensory hair cells in the inner ear led to therapeutic efforts to restore these cells in cases of human deafness.

13. miR-183 family expression in combination with Atoh1 not only appears to fine tune gene expression in favor of hair cells fate, but is also required for the expression of some hair cell-specific genes.

14. These data illuminate a genetic pathway that initiates auditory HC regeneration and suggest p27(Kip1), GATA3, and POU4F3 as additional therapeutic targets for ATOH1-mediated auditory hair cells regeneration.

15. Study provides evidence that Sox2 expression is required for the late stages of progenitor cell differentiation to hair cells and stimulates Atoh1 expression through a concentration dependent molecular interaction with the 3' enhancer of Atoh1.

16. Hes/Hey signaling at the Atoh1 promoter has a role in selection of cell fate in the organ of Corti

17. The retrotrapezoid nucleus neurons expressing Atoh1 and Phox2b are essential for the respiratory response to CO2.

18. propose Atoh1 neurons tune the sequential activation of independent oscillators essential for the fine control of different muscles during breathing

19. our data indicate that beta-catenin and Atoh1 mediate synergistic effects on both proliferation and differentiation of a subset of neonatal cochlear Lgr5+ cells

20. Atoh1 expression is sufficient to produce new Merkel cells in the epidermis