Ask about this productRelated genes to: GRHL3 antibody
- Gene:
- GRHL3 NIH gene
- Name:
- grainyhead like transcription factor 3
- Previous symbol:
- TFCP2L4
- Synonyms:
- SOM
- Chromosome:
- 1p36.11
- Locus Type:
- gene with protein product
- Date approved:
- 2004-06-25
- Date modifiied:
- 2016-10-05
Related products to: GRHL3 antibody
Related articles to: GRHL3 antibody
- Mutations in BMP4 have been associated with malformations of the urinary tract in human patients. Genetic studies in mice have shown that these defects are linked to the expression of Bmp4 in the mesenchymal primordium of the ureter, where it acts as a critical signal for coordinated cytodifferentiation of the mesenchymal and epithelial tissues. Here, we used unbiased transcriptional profiling of ureters with genetic depletion of Bmp4 and pharmacological inhibition of BMP4 signaling to decipher the gene regulatory network controlled by BMP4 in the early ureter, focusing on transcription factors as possible drivers of cytodifferentiation. We show that in Bmp4-deficient ureters, expression of Grhl3, Msx2, Pparg, Trp63 and Foxa1 in the epithelial compartment, and of Gata6, Hopx, Id2, Id4, Myocd, Snai1 and Tbx18 in the mesenchymal primordium is reduced. Expression of Msx2, Pparg, Gata6, Id genes, Tbx18 and Snai1 requires direct BMP4 signaling input, whereas reduced expression of the other genes is likely due to secondary changes, including increased retinoic acid signaling. Conditional gene targeting of Smad4 revealed that BMP4-dependent activation of transcription factor genes is mediated in part by SMAD effectors in both ureteral tissues. Thus, our work links BMP4 (signaling) to known transcriptional regulators of ureteral cytodifferentiation and uncovers additional factors that may be relevant to this program. - Source: PubMed
Publication date: 2026/04/22
Deuper LenaHense NicolasBeckers AnjaThiesler HaukeMamo Tamrat MBergmann FlorianHildebrandt HerbertTrowe Mark-OliverKispert Andreas - The mesenchymal-to-epithelial transition (MET) is a critical and stepwise process in cellular reprogramming and development. Grhl3 has been implicated in MET, but its capacity to initiate epithelial programs in non-epithelial cells remains incompletely defined. Here, we demonstrate that Grhl3 overexpression in MEFs induces a transcriptional shift consistent with early MET, characterized by activation of epithelial genes and suppression of mesenchymal features. This response is accompanied by chromatin changes indicative of gene activation at epithelial loci and is reinforced through cooperative interactions with other MET-associated transcription factors. Grhl3 is associated with locus-specific changes in DNA methylation and with regulatory engagement at genes involved in epigenetic maintenance. Together, these findings position Grhl3 as a central coordinator of epithelial gene activation and epigenetic remodeling in a non-epithelial context, supporting its role in initiating early, transcriptionally and epigenetically primed MET states. - Source: PubMed
Publication date: 2026/02/26
Yaprak İnciAlotaibi Hani - The differentiation cascade that converts basal keratinocytes into suprabasal layers, including periderm, depends on the activity of transcription factors. Mutations in the genes encoding many of these transcription factors, including and , disrupt periderm development. Such mutations can also interfere with embryonic fusion and septation events that depend on periderm development, including palatogenesis, digit separation and the formation of temporary epithelial fusions between digits, between eyelids, and between pinnae and the scalp. ZNF750 (Zfp750 in the mouse) is a transcription factor required for keratinocyte differentiation, but whether mutations in contribute risk for orofacial cleft, and the role of Zfp750 in periderm development, are unknown. To address these questions we sequenced in 5,659 individuals including 2,125 with nonsyndromic OFC. We identify 33 rare missense variants with frequencies less than 0.1% in gnomAD. Of these, about half are predicted to be damaging with tools. Collectively, these missense variants are not overtransmitted from parents to children with OFCs. Two of the variants have lower activity than the reference variant in a zebrafish embryo-based assay but no phenotype in the corresponding murine model. However, in murine embryos homozygous for a frame-shift mutation in ( ) that we generated, palatal shelves are fused but intra-oral adhesions are present, a phenotype seen in murine mutants of several OFC genes. In addition, temporary epithelial fusions are absent in neonates. RNA sequencing of forelimbs from embryos reveals decreased expression of epidermal terminal differentiation genes, and both increased and decreased expression of distinct periderm genes. Immunofluorescence shows the consistent presence of periderm proteins within the oral adhesions in embryos. Together these studies suggest that while mutations in are not a major contributor to OFC risk, Zfp750 does contribute to periderm-dependent morphogenic events. - Source: PubMed
Publication date: 2026/02/13
Singh SAdelizzi EHeffner CCurtis SDuncan KAwotoye WOlotu JBusch TAdeyemo W LGowans L JjNaicker TMurray S AButali ALeslie-Clarkson E JDunnwald MCornell R A - Keratinocyte stem cells (KSCs) are the principal drivers of epidermal renewal, barrier maintenance, and wound repair. Their ability to alternate between self-renewal and differentiation is orchestrated by tightly integrated extrinsic and intrinsic programs that ensure tissue stability while enabling rapid regeneration after injury. This review synthesizes current understanding of KSC homeostasis through a unified framework of three interdependent "fate locks"-the identity switch (ΔNp63 ↔ Notch/IRF6-KLF4/GRHL3/OVOL), the cell-cycle lock (E2F/MYC ↔ p21/p27-RB), and the mechanotransduction lock (YAP/TAZ ↔ Hippo/LATS). We summarize how niche-derived cues-integrins/ECM, EGFR, Wnt, Notch, Ca /CaSR, and TGF--interface with intrinsic timers such as asymmetric division, DNMT1-UHRF1-mediated epigenetic memory, the DNA-damage response, proteostasis/autophagy, and redox signaling to steer keratinocyte fate. Building on this biological foundation, we categorize current methods for isolation and xeno-free expansion of primary human keratinocytes, emphasizing advances in defined media, feeder-free substrates, and biomimetic culture surfaces. We further review 3D and organotypic models, hydrogel-based delivery systems, and the growing portfolio of keratinocyte-derived clinical products used in wound healing. Finally, we highlight emerging applications extending beyond cutaneous repair-including immunomodulation, pigment restoration, ocular and mucosal regeneration, and acellular exosome-based therapeutics. - Source: PubMed
Publication date: 2026/02/06
Uddin AdnanRahmani MohamadSajini Abdulrahim - Epithelial-to-mesenchymal transition (EMT) is a fundamental process in development and disease; however, its study is often complicated by the intrinsic heterogeneity of commonly used epithelial cell models. Here, we show that pre-existing heterogeneity contributes to divergent outcomes following transforming growth factor-beta 3 (TGFβ3) treatment. Flow cytometry, gene expression profiling and imaging revealed persistent variability in E-cadherin (E-cad) and epithelial cell adhesion molecule (EpCAM) expression, with differentially sorted subpopulations displaying distinct transcriptional responses. Remarkably, some single-cell-derived clones exhibited paradoxical CDH1 upregulation during EMT, coinciding with GRHL3 induction and reflecting context-specific regulatory plasticity. Additionally, forskolin-mediated cyclic adenosine monophosphate (cAMP) activation enhanced epithelial stability and modulated EMT dynamics by preserving membrane-localised E-cadherin without preventing transcriptional repression of CDH1. Comparison with an epithelial subclone model further demonstrated how baseline identity shapes EMT trajectories. Moreover, in vivo analysis using zebrafish xenografts revealed that intrinsic epithelial features were associated with differential dissemination potential, reinforcing the connection between cellular identity and metastatic behaviour. These findings underline the importance of accounting for inherent heterogeneity in EMT models and demonstrate how intrinsic regulatory states and extrinsic signals intersect to shape epithelial plasticity. - Source: PubMed
Publication date: 2026/02/17
Ozkuru Sekeroglu EsinYıldız Şeyma NYetkin SerayKafaz Gkamze ImpraimoglouSengez BurcuErez OzlemErsöz Gülseven EsraCakan-Akdogan GulcinBatur TugceAlotaibi Hani