ZIC3 Antibody (N-term) Blocking Peptide
- Known as:
- ZIC3 Antibody (N-terminus) Blocking Peptide
- Catalog number:
- BP2761a
- Product Quantity:
- 2
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- ZIC3 Antibody (N-term) Blocking Peptide
Related genes to: ZIC3 Antibody (N-term) Blocking Peptide
- Gene:
- ZIC3 NIH gene
- Name:
- Zic family member 3
- Previous symbol:
- HTX1
- Synonyms:
- HTX, ZNF203
- Chromosome:
- Xq26.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-16
- Date modifiied:
- 2016-10-05
Related products to: ZIC3 Antibody (N-term) Blocking Peptide
Related articles to: ZIC3 Antibody (N-term) Blocking Peptide
- Distinct neuronal subtype specification involves a complex network of transcription factors (TF). Previous studies from our laboratory showed Zinc finger transcription factor of cerebellum (ZIC) 3 to regulate the expression of Tyrosine Hydroxylase (TH), a proxy marker for dopaminergic (DA) neurons, in mouse olfactory bulb (OB) and mid brain (MB) neurons by distinct mechanisms. In absence of ZIC3 consensus binding site in proximal region of mouse TH promoter, ZIC3 interacts with ER81 in OB and regulates TH expression whereas in absence of ER81 in midbrain, ZIC3 regulates TH by enhancing the expression of PITX3. To analyze whether this observation is evolutionarily conserved in humans, different human stem cell model systems were utilized to understand the role of ZIC3 in human DA generation. Differentiation of dental pulp stem cells (DPSCs) with proper cues resulted in the expression of TH. Gain and loss of function demonstrated ZIC3 to be essential for the expression of TH. ZIC3 activates the transcription of TH gene by binding to response element within the region of TH promoter. Addition of SHH, a known morphogen that facilitates dopaminergic differentiation, increased the expression of TH, however, this regulation was suppressed in the absence of ZIC3. Mechanistic insight demonstrated SHH influences ZIC3 expression by GLI protein binding to ZIC3 promoter. Similar role of ZIC3 in TH expression was observed in hiPSCs differentiated to DA like neurons. Conclusively, the present study for the first time demonstrates the undetermined importance of ZIC3 in SHH mediated TH specification in cells of human origin. - Source: PubMed
Publication date: 2026/09/06
Sheshadri PreethiBhaskar SmithaGowda JeevanBanerjee ShreetamaDuchen Michael RPrasanna JyothiKumar Anujith - IDH-wildtype glioblastoma exhibits substantial biological heterogeneity despite current molecular classification. Although dynamic malignant cell states have been described, molecular features that position tumors along these states remain incompletely defined. We investigated whether ZIC3 expression identifies a transcriptional state associated with clinical outcome in IDH-wildtype glioblastoma. - Source: PubMed
Publication date: 2026/08/06
Chung SuhmiLee SeungjooKim Jong HwiKim Jeong HoonHong Seok HoHong Chang-KiKim Young-HoonSong Sang WooChong SangjoonCho Young Hyun - Avian limbs have evolved precise digit lengths and shapes that are optimized for flight and locomotion, but the transcriptional regulators that regulate this architecture remain poorly defined. Although anteriorly biased Zic3 expression constrains digit outgrowth, whether other zinc finger of the cerebellum (Zic) factors-particularly Zic5-shape avian distal limb morphology remains unknown. Here, we define the spatiotemporal dynamics and developmental function of Zic5 expression in the chicken limb and evaluate its role in shaping avian limb and digit morphogenesis. Whole-mount in situ hybridization reveals that Zic5 shows a dynamic, stage-dependent shift from broad distal mesenchymal expression to digit-base-restricted domains in the chicken limb, consistent with a role in constraining digit elongation to shape fore-hind limb morphology. Overexpression of Zic5 in the chicken limb buds resulted in shortened digits and impaired limb ossification. These phenotypes were accompanied with altered expression of skeletal marker genes, including Sox9, Runx2, Col9a1, Col9a3, Ptch2 and Hhip, suggesting that elevated Zic5 expression is sufficient to impair skeletal maturation during limb development. Together, our results indicate that elevated Zic5 expression can impair limb skeletal growth and maturation, with effects on distal digit development that result in digit shortening or loss and suggest that Zic5 may contribute to the regulation of digit architecture during avian morphological diversification. - Source: PubMed
Publication date: 2026/07/12
Tang YiningLi ShanshanBai ShibinShang SongyangJia ZiqiuZhang JunpengIrwin David MZhang ShuyiWang Zhe - Defects in ZIC2, a member of the Zinc Finger of the Cerebellum family of transcription factors (TFs), cause holoprosencephaly, a congenital brain malformation characterized by the defective cleavage of cerebral hemispheres. However, the gene regulatory network (GRN) controlled by ZIC2 during neural development remains largely unexplored. Here, we combined a mouse embryonic stem cell (mESC) in vitro differentiation model toward anterior neural progenitors with genome editing and genomic methods to elucidate the ZIC2 GRN. We found that ZIC2 is dispensable in mESC due to compensation by ZIC3. In contrast, during neural induction ZIC2 directly controls the expression of master regulators implicated in the patterning and morphogenesis of specific brain regions (e.g. midbrain and roof plate). Mechanistically, ZIC2 plays a dual role in neural differentiation: during pluripotency exit, ZIC2 binds de novo to distal enhancers and increases their chromatin accessibility; during neural induction, ZIC2 is essential for the activation of a subset of the previously primed enhancers, which in turn control the expression of neural patterning regulators and signalling pathways (i.e. WNT) that prevent premature neuronal differentiation. Therefore, by sequentially acting as a promiscuous priming TF and selective enhancer activator, ZIC2 canalizes pluripotent cells toward neural progenitors with rostro-dorsal identities. - Source: PubMed
Mariner-Faulí MaríaSánchez-Gaya VíctorRobert Sarah MalikaRespuela Patriciade la Cruz-Molina SaraLobato-Moreno SaraTrovato MatteoPrummel Karin DNoh Kyung-MinZaugg Judith BRada-Iglesias Álvaro - Congenital heart disease (CHD) is the most common birth defect, and its pathogenesis is closely related to the abnormal establishment of the left-right (LR) bod axis, which highly depends on the ciliary function of the left-right organizer (LRO). This review systematically expounds the molecular pathways by which ciliary structural and functional abnormalities cause cardiac malformations by integrating multi-species model evidence. We believe that defects in multiple conserved genes (including , , , , , and microRNAs) disrupt ciliary assembly, motility, or signaling capacity, leading to the disappearance of the leftward nodal flow or mechanical sensing failure within the LRO. This further interrupts the left-specific calcium ion flicker and the activation of the Nodal-Pitx2 signaling cascade, ultimately resulting in failed cardiac looping and structural defects (such as ventricular septal defect and transposition of the great arteries). This review integrates transcriptional regulation, protein stability, miRNA-mediated fine regulation, and the planar cell polarity (PCP) pathway into a unified "cilia-LRO-heart" network and explores the molecular mechanisms of cilia in valve diseases and cardiac fibrosis. This not only deepens the understanding of the fundamental biological processes of heart development but also provides new molecular targets and theoretical frameworks for the genetic diagnosis and counseling of related congenital heart diseases. - Source: PubMed
Publication date: 2026/02/17
Ma WenqiZhang ZhuofengMa YunMa Chengxu