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This locus encodes a member of the forked-head transcription factor family. Zusätzlich bieten wir Ihnen FOXG1 Proteine (8) und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 86 products:
Human Polyclonal FOXG1 Primary Antibody für 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 Pubmed References
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.
The genetic etiology of Rett syndrome (RTT) without MECP2, CDKL5 (zeige CDKL5 Antikörper), and FOXG1 mutations is heterogeneous, overlaps with other NDDs, and complicated by a high mutation burden. Dysregulation of chromatin structure and abnormal excitatory synaptic signaling may form two common pathological bases of RTT.
FOXG1 and SOX2 (zeige SOX2 Antikörper) operate in complementary but distinct roles to fuel unconstrained self-renewal in Glioblastoma multiforme stem cells via transcriptional control of core cell cycle and epigenetic regulators.
phenotypes associated with FOXG1 mutations in Chinese Rett syndrome or Rett syndrome-like patients.
describe the initial design and characterizations of novel covalent BH3-based agents that potently target Bfl-1 (zeige BCL2A1 Antikörper)
findings demonstrate clear phenotype differences between FOXG1 and MECP2 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 (zeige MLXIP Antikörper)-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 (zeige CDKL5 Antikörper) and FOXG1 genes, respectively
FOXG1 mutations are associated with familial recurrence in FOXG1-related disorders.
Study reports a new role for Foxg1 as a critical upstream regulator of the development of cortical interneurons. Conditional inactivation of Foxg1 in the subpallium led to significant upregulation of transcription factors such as Dlx1/2, Mash1 (zeige ASCL1 Antikörper), and Prox1 (zeige C16orf35 Antikörper). Foxg1 plays a cell-autonomous role in regulating the development of cortical interneurons.
Foxg1 was found to play a role in promoting the closure of optic fissure.
The results presented here indicate that loss of Dlx5 (zeige DLX5 Antikörper) causes a down-modulation of miR (zeige MLXIP Antikörper)-9 and of miR (zeige MLXIP Antikörper)-200-class, which results in the over-expression of the Foxg1 protein.
Foxg1-Cre mediated Lrp2 (zeige LRP2 Antikörper) 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 (zeige EGFR Antikörper) mutations remodel the activated enhancer landscape of glioblastoma multiforme, promoting tumorigenesis through a SOX9 (zeige SOX9 Antikörper) and FOXG1-dependent transcriptional regulatory network in vitro and in vivo.
This study demonistrated that Celsr3 (zeige CELSR3 Antikörper)/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 (zeige WNT2 Antikörper)/beta-catenin (zeige CTNNB1 Antikörper) signalling, displayed significant upregulation of this pathway in Foxg1(-/-) nulls at embryonic days 12.5 and 14.5
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