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Taken together, this study suggests that the OVOL1-OVOL2 axis is a key modulator of c-Myc expression in the shift from in situ epidermal malignancy (Bowen's disease) to invasive squamous cell carcinoma.
OVOL2 antagonizes TGF-beta signaling to regulate epithelial to mesenchymal transition during mammary tumor metastasis.
the OVOL2 promoter variant c.-307T>C was herein identified in the original family that established the posterior polymorphous corneal dystrophy 1 locus.
OVOL2 maintains the transcriptional program of human corneal epithelium cells.
hOvol2 expression was restricted to the XY body of spermatocytes at the pachytene stage. This study demonstrates that hOvol2 is expressed in germ cells and may be involved in spermatogenesis.
Ovol2 can suppress migration and invasion ability of A549 cells, and prevent EMT by inhibition of Twist1 transcription directly.
congenital hereditary endothelial dystrophy 1 (CHED1) and CHED2 loci on chromosome 20 and the collagen, type VIII, alpha-2 (COL8A2) gene were excluded by linkage and haplotype analyses.
We report the absence of a presumed pathogenic coding region mutation in the common PPCD1 support interval.
that the OVOL1-OVOL2 axis may actively contribute to cell differentiation and proliferation in the hair bulb
OVOL2 is a colorectal tumor suppressor that blocks WNT signaling by facilitating the recruitment of histone deacetylase 1 to the TCF4-beta-catenin complex.
data demonstrate that all four mutated OVOL2 promoters exhibited more transcriptional activity than the corresponding wild-type promoter
Molecular phylogeny of OVOL1, OVOL2 and OVOL3 genes illustrates a conserved C2H2 zinc finger domain coupled by hypervariable unstructured regions in humans and other species
Ovol2 directly represses two critical downstream targets, c-Myc and Notch1, thereby suppressing keratinocyte transient proliferation and terminal differentiation, respectively
Association of a chromosomal rearrangement event with mouse posterior polymorphous corneal dystrophy and alterations in Csrp2bp, Dzank1, and Ovol2 gene expression have been reported.
a Grhl2/Ovol2 network controls Cldn4 and Rab25 expression that facilitates lumen expansion and barrier formation in subtypes of renal epithelia
We show that ER71 directly interacts with OVOL2 and that such interaction is critical for FLK1(+) cell generation and their differentiation into downstream cell lineages.
Deletion of Ovol2 blocks mammary ductal morphogenesis, depletes stem and progenitor cell reservoirs, and leads epithelial cells to undergo EMT .
Ovol2 acts downstream of the BMP pathway in the cell fate decision between neuroectoderm and mesendoderm to ensure proper germ layer development.
Ovol2/MOVO may play an important role in the XY body during spermatogenesis, possibly in the processes of XY body formation and meiotic sex chromosome inactivation.
Ovol2 transcription was dramatically reduced in testes from blind-sterile mice, suggesting that Ovol2 is expressed in male germ cells
Ovol2 is a key regulator of neural development and reveal a previously unexplored role for Ovo genes in mammalian embryogenesis.
Expression of Ovol2 was up-regulated in Ovol1-deficient epidermis; Ovol1 represses the activity of Ovol2 promoter in a DNA binding-dependent manner identifying Ovol2 as a downstream target of Ovol1.
Ovol2 may play a critical role in vascular angiogenesis during early embryogenesis
DNA-binding protein that binds to the 5'-GGGGGG-3' core sequence. Probably acts as a transcription regulator.
ovo-like 2 (Drosophila)
, ovo-like 2
, transcription factor Ovo-like 2
, zinc finger protein 339
, MOVO-B zinc finger protein
, MOVO-C zinc finger protein
, OVO homolog-like 2
, zinc finger OVO2
, zinc finger protein mOVO