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Human Polyclonal FOXC1 Primary Antibody für ChIP, ELISA - ABIN249940
Dagenais, Hartsough, Erickson, Witte, Butler, Glover: Foxc2 is expressed in developing lymphatic vessels and other tissues associated with lymphedema-distichiasis syndrome. in Gene expression patterns : GEP 2004
Show all 11 Pubmed References
Human Polyclonal FOXC1 Primary Antibody für ChIP, EIA - ABIN5552874
Fatima, Wang, Uchida, Norden, Liu, Culver, Dietz, Culver, Millay, Mukouyama, Kume: Foxc1 and Foxc2 deletion causes abnormal lymphangiogenesis and correlates with ERK hyperactivation. in The Journal of clinical investigation 2017
Show all 3 Pubmed References
Human Polyclonal FOXC1 Primary Antibody für ELISA, WB - ABIN547104
Zhou, Kato, Asanoma, Kondo, Arima, Kato, Matsuda, Wake: Identification of FOXC1 as a TGF-beta1 responsive gene and its involvement in negative regulation of cell growth. in Genomics 2002
Human Polyclonal FOXC1 Primary Antibody für ELISA - ABIN547572
Berry, ONeill, Coca-Prados, Walter: FOXC1 transcriptional regulatory activity is impaired by PBX1 in a filamin A-mediated manner. in Molecular and cellular biology 2005
Human Polyclonal FOXC1 Primary Antibody für ICC, IF - ABIN4312329
DeGraff, Grabowska, Case, Yu, Herrick, Hayward, Strand, Cates, Hayward, Gao, Walter, Buttyan, Yi, Kaestner, Matusik: FOXA1 deletion in luminal epithelium causes prostatic hyperplasia and alteration of differentiated phenotype. in Laboratory investigation; a journal of technical methods and pathology 2014
FOXC1 expression was higher in colorectal cancer specimens than in benign tissue and correlated with poorer survival. Silencing FOXC1 expression in CRC cells inhibited proliferation and colony formation and decreased their glucose consumption and lactate production. Overexpression did the opposite and downregulated FBP1 by binding its promoter. The FOXC1/FBP1 axis induces CRC cell proliferation and reprograms metabolism.
Heterozygous pathogenic variants in the PITX2 and FOXC1 genes accounted for 66% (6/9) of the ARS/ASD cases. The absence of PAX6 or CYP1B1 abnormalities could reflect our small sample size, although their analysis could be justified in ARS/ASD patients that present with congenital glaucoma or aniridia.
FOXC1 can bind directly to the WNT5A promoter region to activate its expression. WNT5A activates NF-kappaB signaling to induce MMP7 expression. Collectively, this demonstrates a FOXC1-elicited non-canonical WNT5A signaling mechanism comprising NF-kappaB and MMP7 that is essential for triple negative breast cancer (TNBC) cell invasiveness, thereby providing implications toward developing an effective therapy for TNBC.
we identified forkhead box C1 (FOXC1) as a novel regulator of colorectal cancer metastases. FOXC1 directly binds its target genes integrin alpha7 (ITGA7) and fibroblast growth factor receptor 4 (FGFR4) and activates their expression
Study in Lebanese family reports the first documented human case with a mutation in FOXC1 regulating multi-organ developmental pathways that reflect a conserved mechanism in cell differentiation and proliferation.
We show the abrogation of latanoprost signalling when FOXC1 is knocked down via siRNA in a trabecular meshwork cell line. We propose that the lower levels of active FOXC1 in Axenfeld-Rieger syndrome patients with glaucoma account for the lack of response to prostaglandin-based medications.
The present study has successfully demonstrated that FOXC1 protein plays a crucial part in regulating VIC osteogenic differentiation. At the same time, we also proved that FOXC1 is a direct target gene of miR- 138 using dual-luciferase reporter assay. Our study also confirmed the function of FOXC1 in regulating osteogenic differentiation of human aortic valvular Interstitial Cells.
Study discovered that overexpression of FOXC1 significantly enhanced, whereas its knockdown significantly reduced, the capabilities of triple-negative breast cancer (TNBC) cell invasion and motility in vitro and metastasis to the lung in vivo. Also, FOXC1 enhanced the expression of CXCR4, probably through its transcriptional up-regulation in TNBC cells.
Targeting EZH2 reactivates a breast cancer subtype-specific anti-metastatic transcriptional program driven by FOXC1.
This study demonstrates that FOXC1 induces cancer stem cells (CSCs)-like properties in non-small cell lung cancer (NSCLC) by promoting beta-catenin expression. The findings indicate that FOXC1 is a potential molecular target for anti-CSC-based therapies in NSCLC
Foxc1 promoted cell proliferation by upregulation PI3K/AKT signaling, which was inflammation-dependent.
Knockdown of FOXC1 markedly suppressed cell migration and invasion in vitro, and resulted in downregulation of phosphorylatedRACalpha serine/threonineprotein kinase, protooncogene cMyc and Bcell lymphoma 2.
Results provide evidence that FOXC1 is not required for initiation of EMT events but rather participates in the specification of mesenchymal cell phenotype through regulation of FGF receptor switching from FGFR2-IIIb to FGFR1-IIIc in response to TGFb1-induced EMT.
In regulating cervical cancers metastasis by targeting FOXC1.
Forkhead box C1 protein (FOXC1) promotes melanoma cell function by regulating macrophage stimulating 1 receptor (MST1R) and activating MST1R/PI3K/AKT pathway.
expression of FOXC1 in BRCA1 mutant cell lines correlates with sensitivity to olaparib. Whether this is due to rates of proliferation or another mechanism is yet to be explored, but this, and the specificity of FOXC1 in BRCA1-mutant tumors, suggests a possible role for FOXC1 as a marker for targeted therapy.
novel EGFR-NF-kappaB-FOXC1 signaling axis that is critical for BLBC cell function
Taken together, these data indicate that FOXC1 is a novel hypoxia-induced transcription factor and plays a critical role in tumor microenvironment-promoted lung cancer progression.
Genomic analysis of blood and excised valve tissue showed down-regulation of FOXC1 but also FOXC2 expression in the diseased aortic valve. This allows us to speculate on the potential role of FOXC1 in aortic valve anomalies.
Results showed a significant higher FOXC1 expression in estrogen receptor-negative breast cancer than that in estrogen receptor-positive. Its overexpression reduced expression of ERalpha and cellular responses to tamoxifen suggesting that FOXC1 regulated expression of ERalpha and affected sensitivity of tamoxifen treatment in breast cancer
siRNA-mediated knockdown of FOXC1 was confirmed to decrease the proliferation rate, migration, and invasion in a model Basal-like breast cancer-like cell line (4T1).
These findings suggest that Foxc1 is an important regulator to further chondrogenesis and initiate the ossification of the presphenoid and basisphenoid bones.
Lineage tracing experiments in Foxc1 mutant mouse cerebella indicate that aberrant migration of granule cell progenitors destined to form the posterior-most lobule causes this cerebellar malformation phenotype.
Foxc1 regulates both early cardiomyogenesis and the functional properties of embryonic stem cell-derived cardiomyocytes.
FOXC1 and FOXC2 are essential regulators of lymphangiogenesis and may have roles in lymphatic-associated diseases
These data indicate that Foxc1 expression is regulated by BMP4 and FOXC1 functions in the commitment of progenitor cells to the osteoblast fate and its expression is reduced when differentiation proceeds.
Foxc1 regulates sweat duct luminal cell differentiation and mimic apocrine miliaria.
Compound, NC-specific Foxc1; Foxc2 homozygous mutant mice have more severe defects in structures of the ocular surface, such as the cornea and eyelids, accompanied by significant declines in the expression of another key developmental factor, Pitx2, and its downstream effector Dkk2, which antagonizes canonical Wnt signaling.
These findings offer the first evidence for a role of the meninges in brain vascular development and provide new insight into potential causes of cerebrovascular defects in patients with FOXC1 mutations.
Foxc1 and Foxc2 maintain glomerular podocyte integrity by regulating the gene expression.
Foxc1 and Foxc2 have a role in kidney and axial skeleton development.
FOXC1 maintains the hair follicle stem cell niche and governs stem cell quiescence to preserve long-term tissue-regenerating potential.FOXC1 is necessary to establish a multiple-bulge hair follicle architecture.
deletion of Foxc1 and Foxc2 specifically in Pax3-positive cells affects cell fate choices in the dermomyotome of somites at forelimb level, promoting the myogenic cell fate at the expense of endothelial cells that migrate to the limb
Foxc1 is an important transcriptional partner of Ihh-Gli2 signalling during endochondral ossification, and that disruption of the Foxc1-Gli2 interaction causes skeletal abnormalities observed in the Axenfeld-Rieger syndrome.
In self-renewing stem cells (SCs), Foxc1 activates Nfatc1 and bone morphogenetic protein (BMP) signaling, two key mechanisms that govern quiescence. These findings reveal a dynamic, cell-intrinsic mechanism used by hair follicle SCs to reinforce quiescence upon self-renewal and suggest a unique ability of SCs to maintain cell identity.
These observations reveal an essential role for Foxc1 in the early stage of vascular formation in the telencephalon.
loss of Foxc1 non-autonomously induces a rapid and devastating decrease in embryonic cerebellar ventricular zone radial glial proliferation and concurrent increase in cerebellar neuronal differentiation
A loss of Foxc1 function affects skull bone formation of the apical region.
Together our data demonstrates that Foxc1 - Fgf8 signaling regulates mammalian jaw patterning and provides a mechanistic basis for the pathogenesis of syngnathia.
Identify mesodermal foxc1a/b as a direct upstream regulator of etsrp in angioblasts. This establishes a new molecular link in the process of mesoderm specification into angioblast.
This study reveals an important role for FOXC1 in the direct regulation of the FGF19-FGFR4-MAPK pathway to promote both the development and maintenance of anterior segment structures within the eye.
This gene belongs to the forkhead family of transcription factors which is characterized by a distinct DNA-binding forkhead domain. The specific function of this gene has not yet been determined\; however, it has been shown to play a role in the regulation of embryonic and ocular development. Mutations in this gene cause various glaucoma phenotypes including primary congenital glaucoma, autosomal dominant iridogoniodysgenesis anomaly, and Axenfeld-Rieger anomaly.
forkhead box protein C1
, forkhead, drosophila, homolog-like 7
, forkhead-related activator 3
, forkhead-related protein FKHL7
, forkhead-related transcription factor 3
, forkhead/winged helix-like transcription factor 7
, myeloid factor-delta
, forkhead box C1
, forkhead box protein C1-B
, Forkhead box protein C1
, congenital hydrocephalus
, mesoderm/mesenchyme forkhead 1
, transcription factor FKH-1
, winged helix protein CWH-6
, winged-helix transcription factor
, forkhead box C1-B