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anti-Human GRHL2 Anticorps:
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Human Polyclonal GRHL2 Primary Antibody pour 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. dans The Journal of biological chemistry 2012
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Human Polyclonal GRHL2 Primary Antibody pour 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. dans Oncogene 2009
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Human Polyclonal GRHL2 Primary Antibody pour 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. dans 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.
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.
A novel connection between GRHL2 and miR-200 in oral cancer.Grainyhead-like 2 regulates epithelial plasticity and stemness in oral cancer cells.
GRHL2 genetic polymorphisms, rs611419 and rs10955255, have a protective role against sudden sensorineural hearing loss (SSHL) and reduce the risk of SSHL. However, rs6989650 is not associated with SSHL.
This study showed that Mendelian sensorineural hearing loss exhibits vestibular dysfunction, including DFNA9, DFNA11, DFNA15 and DFNA28.
study demonstrates that loss of GRHL2 increases the levels of histone mark H3K27me3 on promoters and GRHL2-binding sites at miR-200b/a and E-cadherin genes. These findings support GRHL2 as a pivotal gatekeeper of EMT in EOC via miR-200-ZEB1.
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