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This locus encodes a member of the forked-head transcription factor family. Additionally we are shipping FOXG1 Proteins (8) and many more products for this protein.
Showing 10 out of 87 products:
Human Polyclonal FOXG1 Primary Antibody for IHC, WB - ABIN2780667
Tan, Couvineau, Laburthe: Diffuse pharmacophoric domains of vasoactive intestinal peptide (VIP) and further insights into the interaction of VIP with the N-terminal ectodomain of human VPAC1 receptor by photoaffinity labeling with [Bpa6]-VIP. in The Journal of biological chemistry 2004
Show all 2 references for 2780667
Cow (Bovine) Polyclonal FOXG1 Primary Antibody for WB - ABIN2780668
Tan, Shaw, Madsen, Jensen, Taylor-Papadimitriou, Freemont: Human PLU-1 Has transcriptional repression properties and interacts with the developmental transcription factors BF-1 and PAX9. in The Journal of biological chemistry 2003
Show all 2 references for 2780668
Human Polyclonal FOXG1 Primary Antibody for WB - ABIN2777412
Adesina, Nguyen, Mehta, Takei, Stangeby, Crabtree, Chintagumpala, Gumerlock: FOXG1 dysregulation is a frequent event in medulloblastoma. in Journal of neuro-oncology 2007
Human Polyclonal FOXG1 Primary Antibody for ELISA, WB - ABIN184820
Wiese, Murphy, Schlung, Burfeind, Schmundt, Schnülle, Mattei, Thies: The genes for human brain factor 1 and 2, members of the fork head gene family, are clustered on chromosome 14q. in Biochimica et biophysica acta 1995
Human Polyclonal FOXG1 Primary Antibody for IHC, WB - ABIN2792688
Murphy, Wiese, Burfeind, Schmundt, Mattei, Schulz-Schaeffer, Thies: Human brain factor 1, a new member of the fork head gene family. in Genomics 1994
Results suggest that foxg1b and foxg1c have undergone expression pattern divergence during evolution that has resulted in functional specialization.
These findings identify a key direct target of Foxg1, and uncover a simple molecular mechanism by which Foxg1 integrates two opposing signaling centers.
describe the initial design and characterizations of novel covalent BH3-based agents that potently target Bfl-1 (show BCL2A1 Antibodies)
findings demonstrate clear phenotype differences between FOXG1 and MECP2 (show MECP2 Antibodies) disorders.
Abnormal involuntary movements are a major feature of FOXG1 mutations. Our study delineates the spectrum of movement disorders and confirms an expanding clinical phenotype. Symptomatic treatment may be considered for severe or disabling cases, although further research regarding potential treatment strategies is necessary.
Report demonstrates the functional consequences of Foxg1 haploinsufficiency in the visual system of Foxg1+/Cre mice and a visual impairment in a cohort of Rett individuals presenting genetic alteration on FOXG1
Upregulated miR (show MLXIP Antibodies)-200b in cervical cancer was proven to show positive regulation on cervical cancer development by directly targeting FoxG1.
Rett syndrome with early epilepsy and the congenital variant are mainly due to variations in the CDKL5 (show CDKL5 Antibodies) and FOXG1 genes, respectively
FOXG1 mutations are associated with familial recurrence in FOXG1-related disorders.
these results implicate the overexpression of a group of neuropeptides in the basal ganglia, hypothalamus, cortex and hippocampus in the pathogenesis FOXG1 behavioral impairments.
These findings suggest a central AKT (show AKT1 Antibodies)-FOXG1-reelin (show RELN Antibodies) signaling pathway in focal malformations of cortical development and support pathway inhibitors as potential treatments or therapies for some forms of focal epilepsy.
We propose that the disruption of signaling pathways that promote mature neuronal differentiation by overexpressed FOXG1 is a contributing event in the neoplastic transformation of cerebellar stem cells.
The results presented here indicate that loss of Dlx5 (show DLX5 Antibodies) causes a down-modulation of miR (show MLXIP Antibodies)-9 and of miR (show MLXIP Antibodies)-200-class, which results in the over-expression of the Foxg1 protein.
Foxg1-Cre mediated Lrp2 (show LRP2 Antibodies) inactivation in developing mouse neural retina, ciliary and retinal pigment epithelia is a model of congenital high myopia
findings suggest that different subcellular localizations of Foxg1 control the machinery that brings about cell differentiation, replication, and bioenergetics, possibly linking mitochondrial functions to embryonic development and pathological conditions
EGFR (show EGFR Antibodies) mutations remodel the activated enhancer landscape of glioblastoma multiforme, promoting tumorigenesis through a SOX9 (show SOX9 Antibodies) and FOXG1-dependent transcriptional regulatory network in vitro and in vivo.
This study demonistrated that Celsr3 (show CELSR3 Antibodies)/Foxg1 mutation mice show the spinal motor network does not mature fully in the absence of corticofugal connections, and that some motor function is preserved despite congenital absence of the corticospinal tract.
Foxg1 as a key coordinator of the early transcriptional network during the course of cortical development.
target of Wnt (show WNT2 Antibodies)/beta-catenin (show CTNNB1 Antibodies) signalling, displayed significant upregulation of this pathway in Foxg1(-/-) nulls at embryonic days 12.5 and 14.5
Targets of RBPJ (show RBPJ Antibodies)/N1ICD in cortical neural stem cell at a genome-wide level, were identified
the dynamic expression of FoxG1 during migration within the intermediate zone is essential for the proper assembly of the cerebral cortex.
This locus encodes a member of the forked-head transcription factor family. The encoded protein, which functions as a repressor, may play a role in brain development. Mutations at this locus have been associated with Rett syndrome.
brain factor 1
, forkhead box G1
, forkhead box protein G1
, forkfead transcription factor G1
, brain factor 2
, forkhead-like 1
, forkhead-like 2
, forkhead-like 3
, forkhead-like 4
, oncogene QIN
, forkhead protein 4
, winged-helix transcription factor
, HNF-3/forkhead homolog, brain factor 1
, forkhead-related protein FKHL1
, forkhead-like transcription factor BF-1
, transcription factor BF-1
, CEQ 3-1
, brain factor-1
, proto-oncogene C-QIN