Proteins Otx2, Human
- Known as:
- Proteins Otx2, Human
- Catalog number:
- C156
- Product Quantity:
- 10μg
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Proteins Otx2 Human
Related genes to: Proteins Otx2, Human
- Gene:
- OTX2 NIH gene
- Name:
- orthodenticle homeobox 2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 14q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-02-08
- Date modifiied:
- 2019-04-23
Related products to: Proteins Otx2, Human
Related articles to: Proteins Otx2, Human
- Anterior-posterior (AP) spatial regionalization is crucial for central nervous system development. Previous studies suggest that morphogen gradients can induce AP patterning in animal and organoid models. While self-organization in early embryogenesis and neurogenesis has been found using geometrically confined microtissues, spontaneously induced AP patterning has not been reported. Here, we show that circularly micropatterned human pluripotent stem cells self-organize into spatially distinct FOXG1-FOXA1+OTX2+ midbrain-like and HOXB4+ hindbrain/spinal cord-like regions. Notably, the tissue then folds inwardly to form a 3D annular structure, maintaining a distinct boundary between OTX2+ and HOXB4+ zones. The reaction-diffusion of BMP/Noggin plays a key role in the mechanism of AP patterning. Our model is validated by its capability to distinguish the teratogenic effects of valproic acid and isotretinoin. Our work suggests a novel regulatory mechanism for AP patterning and provides a tool for fast screening of teratogens. - Source: PubMed
Publication date: 2026/04/16
Xie TianfaJiang HanBrown Lauren EPak ChangHuiSun Yubing - While current pluripotency models capture discrete embryonic stages, they inadequately resolve transitional states during peri-implantation development. Here, we establish rosette-formative intermediate stem cells (rfISCs) from mouse embryonic stem cells using the MEK inhibitor PD0325901, the Wnt inhibitor IWR1, and the PKA activator Forskolin. These cells exhibit transcriptomic/epigenetic profiles mirroring those of E5.0‒5.5 epiblasts, bridging rosette-stage and formative pluripotency. rfISCs demonstrate developmental bipotency, retaining in vitro germline differentiation capacity while generating germline-competent chimeras in vivo. Mechanistically, we identified opposing signaling axes that govern rfISC identification through the regulation of lineage priming: IWR1 stabilizes Tcf7l1 to drive Otx2-mediated rfISC specification and neural priming, whereas Forskolin activates PKA to induce Id1-dependent neural suppression. This creates a bistable regulatory circuit in which Otx2/Id1 synergy maintains pluripotency plasticity under MEK inhibition. Notably, rfISCs can be directly derived from E5.25 epiblasts, confirming their physiological relevance. Our work bridges a fundamental gap in pluripotency modeling by capturing the RSC-to-FSC transition through dynamic signaling equilibria. - Source: PubMed
Publication date: 2026/04/17
Chen PengZhu ZhenhuaDong BaoxingJi JunxiangZhu YuqingDuan JunboWu LefanBan QianLiu WenqiangYe Shou-Dong - - Source: PubMed
Publication date: 2026/04/11
Song YaxiLiu CuifangWang Liping - The aim of this study was to gain insight into the molecular spectrum of anophthalmia and microphthalmia (A/M) in the Egyptian population. - Source: PubMed
Publication date: 2026/01/20
Elmakkawy GehadNabil AmiraNabil KarimAmin Asmaa KenawyMaskill DavidAli ManirSchorderet DanielBayoumi NaderShakankiri NihalAbdalla Ebtesam - Boys experience an overall increased incidence of several childhood cancers, including medulloblastoma, a clinically heterogeneous cerebellar tumor. In subtypes of Group 3 and Group 4 medulloblastoma, males are three times more prevalent than females. As medulloblastoma is suspected to initiate during fetal development, we hypothesized that this sex bias reflects a combination of prenatal, sex-specific developmental processes and somatic alterations. To test these hypotheses, we compiled a large multi-omics dataset from children with medulloblastoma, which revealed sex-specific alterations, including frequent loss of the inactive X chromosome in females with Group 4. Generation of a sex-matched single-cell transcriptome atlas of the developing murine cerebellum enabled investigation of putative developmental factors underlying sex bias. Progenitors giving rise to Group 3/4 subgroups were more abundant, more proliferative, and harbored more open chromatin for recruitment of LMX1A and OTX2, master transcription factors defining Group 3/4 idefntity. Advanced genetically engineered mouse models and human cerebellar organoids were leveraged to determine whether sexual dimorphism arises from intrinsic or extrinsic factors. These models showed that the XY genotype contributed to the phenotype, but the predominant effect was driven by presence of the male gonadal hormone testosterone. Our findings provide a sex-specific genetic and neurodevelopmental explanation for male bias in an aggressive pediatric brain tumor. Outcomes from this study may inform novel treatment strategies delivered according to sex and are likely to be broadly applicable to other sex-biased malignancies arising in early life. - Source: PubMed
Publication date: 2026/03/25
Bianchini LucaXu RuijieFilipovic Davidda Silva Patricia Benites GoncalvesSieber LauraAkçay VuslatArnskötter FrederikJoshi PiyushNolle JanaSoliman TahaTao RanScheuing AlexandraOkonechnikov KonstantinAtamian AlexanderZuckermann MarcRobinson Giles WQuadrato GiorgiaNorthcott Paul AKutscher Lena M