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anti-Human GRHL2 Antibodies:
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Human Polyclonal GRHL2 Primary Antibody for ICC, IF - ABIN4316153
Varma, Cao, Tagne, Lakshminarayanan, Li, Friedman, Morell, Warburton, Kotton, Ramirez: The transcription factors Grainyhead-like 2 and NK2-homeobox 1 form a regulatory loop that coordinates lung epithelial cell morphogenesis and differentiation. in The Journal of biological chemistry 2012
Show all 8 Pubmed References
Human Polyclonal GRHL2 Primary Antibody for ELISA, WB - ABIN566411
Kang, Chen, Kim, Kang, Park: Regulation of the hTERT promoter activity by MSH2, the hnRNPs K and D, and GRHL2 in human oral squamous cell carcinoma cells. in Oncogene 2009
Show all 4 Pubmed References
Human Polyclonal GRHL2 Primary Antibody for IF, WB - ABIN529152
Dompe, Rivers, Li, Cordes, Schwickart, Punnoose, Amler, Seshagiri, Tang, Modrusan, Davis: A whole-genome RNAi screen identifies an 8q22 gene cluster that inhibits death receptor-mediated apoptosis. in Proceedings of the National Academy of Sciences of the United States of America 2011
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The data showed that midbrain-hindbrain boundary maintenance and morphogenesis are dissociable events regulated by grhl2b through diverse transcriptional targets.
This work reveals an evolutionarily conserved function of Grhl2 in otic development and provides a fish model for further studying mechanisms of Grhl2-related hearing loss.
recruited to a subset of estrogen receptor binding sites and regulates transcriptional output
The grainyhead-like-2 (GRHL2) genetic variants were reported in age-related hearing impairment (ARHI) susceptibility in several case-control studies
results demonstrated that GRHL2 was upregulated in colorectal cancer (CRC) cell lines. Knockdown of GRHL2 suppressed cell proliferation and induced apoptosis by inhibiting the PI3K/Akt pathway in CRC cell lines. Collectively, we concluded that GRHL2 act as an oncoprotein in CRC.
Mesenchymal-epithelial transition, NK-sensitization and ICAM-1 expression were promoted by GRHL2-KMT2C/D interactions and by GRHL2 inhibition of p300, revealing novel and potentially targetable epigenetic mechanisms connecting the epithelial phenotype with target cell susceptibility to NK killing.
Whole-genome sequencing identified a unique variant (c.20+544G>T) within an intronic regulatory region of GRHL2.
GRHL2 gene may have a role in orbital innervations and the defect in this gene (deletion) may be related to the Congenital fibrosis of the extraocular muscles type 1 phenotype.
In this study, we demonstrated for the first time that GRHL2 has a functional role in the regulation of epithelial plasticity of PDAC cells.
data analysis and modeling results highlight the relationships among multiple crucial Epithelial-to-Mesenchymal Transition /Mesenchymal-to-Epithelial Transition drivers including ZEB1, GRHL2, CD24, and ESRP1, particularly in basal-like breast cancers, which are most similar to triple-negative breast cancer (TNBC) and are considered the most dangerous subtype
Data indicate a 'phenotypic stability factors' (PSFs) such as GRHL2 that couple to the core epithelial-to-mesenchymal transition (EMT) decision-making circuit (miR-200/ZEB) and stabilize hybrid epithelial/mesenchymal (hybrid E/M) E/M phenotype.
All of these processes involve epithelial-mesencyhmal transition (EMT), MET or a sequence of both, suggesting that the GRHL factors((GRHL1, GRHL2 and GRHL3), could potentially affect tumor initiation and progression via EMT
Silencing of GRHL2 expression in non-tumorigenic kidney cell line results in increased cell proliferation, increased resistance to apoptosis, as well as changes in the levels of selected proteins involved in the pathogenesis of clear cell renal cell carcinoma (ccRCC). These changes support the potential role for GRHL2 as a suppressor of ccRCC.
Results demonstrate a mechanistic role for GRHL2 in promoting anoikis through metabolic alterations.
GRHL2 maintained AR expression in multiple prostate cancer model systems, was required for cell proliferation, enhanced AR's transcriptional activity, and colocated with AR at specific sites on chromatin to regulate genes relevant to disease progression.
Studies indicate that Grainyhead-like transcription factor 2 (GRHL2) controls the expression of E-cadherin (CDH1) required for adherens junctions and possibly regulates the expression of claudin-4 (CLDN4) in tight junctions.
results indicated GRHL2 might be a noise-induced hearing loss (NIHL) susceptibility gene, but the effect of POU4F3 on NIHL could only be detected when taking noise exposure into account and their effects were enhanced by higher levels of noise exposure
These data are indicative for a strong oncogenic potential of the GRHL2 gene in epithelial ovarian cancer cells displaying either epithelial (A2780s) or mesenchymal (SKOV3) phenotypes.
marked overlap of dyskeratosis congenita with four other genetic syndromes, confounding accurate diagnosis and subsequent management. Patients with clinical features of dyskeratosis congenita need to have genetic analysis of USB1, LIG4 and GRHL2 in addition to the classical dyskeratosis congenita genes and telomere length measurements.
In this review, we summarized recent progress on grainyhead-like 2 in development and cancer in order to get an insight into the regulation network of grainyhead-like 2 and understand the roles of grainyhead-like 2 in various cancers.
A loss or strong reduction in GRHL2 expression appears to be a characteristic of cervical cancer, suggesting that GRHL2 down-regulation is a necessary step during cervical carcinogenesis.
In skin from psoriasis patients, the effect of miR-194 on cell proliferation and differentiation was significantly reversed by overexpression of GRHL2. Moreover, the expression of miR-194 and GRHL2 was inversely correlated in psoriasis lesional skin. Taken together, our results suggest that miR-194 inhibits the proliferation and promotes the differentiation of keratinocytes through targeting GRHL2.
The GRHL2 assumes control over a subset of the naive network via enhancer switching to maintain expression of epithelial genes upon exit from naive pluripotency.
These data indicated that GRHL2 directly controls expression levels of genes that encode tight junction-associated proteins in the CD. The study thus identifies a novel role of the GRHL2-mediated collecting duct epithelial barrier in renal osmoregulation.
Findings suggest that Grhl2 plays a crucial role in regulating biomechanical properties of the surface ectoderm that are essential for spinal neurulation.
we observed a striking additive genetic interaction between Grhl2 and Grhl3 gain-of-function alleles. moderate Grhl3 overexpression also interacted with the Vangl2Lp allele to cause SB, demonstrating genetic interaction with the planar cell polarity signalling pathway that is implicated in mouse and human neural tube defects.
Results indicate GRHL2 as a novel progenitor cell maker in the developing pituitary that may contribute to progenitor cell function and maintenance.
GRHL2 promotes the epithelial nature of non-neural ectoderm during dynamic events of neural tube formation by both activating key epithelial genes and actively suppressing epithelial-mesenchymal (EMT) transition through novel downstream EMT suppressors.
a Grhl2/Ovol2 network controls Cldn4 and Rab25 expression that facilitates lumen expansion and barrier formation in subtypes of renal epithelia
Our findings reveal important pathophysiological differences between human pulmonary fibrosis and specific mouse models of fibrosis and support a crucial role of GRHL2 in epithelial activation in lung fibrosis and perhaps also in epithelial plasticity.
expression of GRHL2 is directly suppressed by the ZEB1, which in turn is a direct target for repression by GRHL2, suggesting that the EMT transcription factors GRHL2 and ZEB1 form a double negative regulatory feedback loop
Grhl2 plays an essential role in the determination of epithelial phenotype of breast cancers, EMT and tumor progression
the results indicate that Grhl2 regulates epithelial morphogenesis through transcriptional up-regulation of Cldn3 and Cldn4, as well as of Rab25, which increases the Cldn4 protein and its localization at TJs
Grhl2 and Nkx2-1 bind to each other's promoter in vivo, forming a positive feedback regulatory loop.
Over-expression of Grhl2 causes spina bifida in the Axial defects mutant mouse
tissue closure defects in Grhl2 mutants are similar to that of AP-2alpha null mutants and AP-2alpha has been shown to bind to the promoter of E-cadherin
Both GRHL2 and GRHL3 bind to and regulate expression of the wound repair gene Rho GEF 19, but regulation of the barrier forming gene, Transglutaminase 1 (TGase1), is unique to GRHL3.
Study showed that Grhl2 functions to regulate epithelial differentiation in different types of epithelia both in vivo and in vitro and found that Grhl2 deficiency in mice results in defective neural tube closure and in embryonic lethality by E11.5.
deletion of Grhl2 results in failed closure 3, with mutants exhibiting a split-face malformation and exencephaly, associated with failure of neuro-epithelial folding at the dorso-lateral hinge points
Grhl genes are highly expressed in the developing epidermis.
The protein encoded by this gene is a transcription factor that can act as a homodimer or as a heterodimer with either GRHL1 or GRHL3. Defects in this gene are a cause of non-syndromic sensorineural deafness autosomal dominant type 28 (DFNA28).
, grainyhead-like 2b protein
, grainyhead-like protein 2 homolog
, grainyhead-like 2 (Drosophila)
, brother of mammalian grainyhead
, transcription factor CP2-like 3
, grainyhead like 2
, grainyhead-like 2a
, grainyhead-like transcription factor 2a