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anti-Human SIX3 Antikörper:
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SIX3 deletions and incomplete penetrance in families affected by holoprosencephaly have been described.
Results demonstrate that Six3 silence or loss in glioma is induced by its promoter hypermethylation and Six3 down-regulation contributes to proliferation and invasion of glioma. And this process is involved in activation of Wnt/beta-catenin pathway. Six3 play a suppressor role in the initiation and progression of human glioma and potentially serve as a target for the diagnosis and treatment of human glioma.
SIX3 is a novel negative transcriptional regulator and acts as a tumor suppressor that directly represses the transcription of AURKA (zeige AURKA Antikörper) and AURKB (zeige AURKB Antikörper) in astrocytoma.
SIX2 (zeige SIX2 Antikörper), SIX3, and SIX4 (zeige SIX4 Antikörper) were correlated with higher TNM (zeige ODZ1 Antikörper) stages in lung neoplasms
High SIX3 expression is associated with Head and Neck Squamous Cell Carcinoma.
SIX3 may play an important role as a novel suppressor in human lung cancer.
Mutations in SIX3 is associated with holoprosencephaly.
There was a positive correlation between the severity of the brain malformation and facial features for SHH (zeige SHH Antikörper), SIX3, and TGIF (zeige IL10 Antikörper), but no such correlation was found for ZIC2 (zeige ZIC2 Antikörper) mutations.
screened four known HPE genes in a Dutch cohort of 86 non-syndromic HPE index cases, including 53 family members. We detected 21 mutations (24.4%), 3 in SHH, 9 in ZIC2 and 9 in SIX3
SIX3 acts directly upstream of SHH (zeige SHH Antikörper), and the SHH (zeige SHH Antikörper) pathway is a key regulator of ventral forebrain patterning and mutations are associated with schizencephaly.
Lhx2 (zeige LHX2 Antikörper) may mediate an alternative or parallel pathway for control of cellular proliferation in the developing forebrain via Six3b.
lmo4b has an essential role in forebrain development as a modulator of six3 and rx3 expression, and thus indirectly influences neural cell fate commitment, cell proliferation and tissue growth in the anterior CNS.
SP8 and SP9 coordinately promote D2-type medium spiny neuron production by activating Six3 expression
Six3 in a small population of progenitors expressing Six3-Cre at E8.5 is required for neuroretinal specification via regulating cell signaling and survival in mice.
variations in Six3 dosage result in different forms of Holoprosencephaly
SIX3 and SIX6 (zeige SIX6 Antikörper) play distinct but compensatory roles in regulating transcription of gonadotrope-specific genes as gonadotrope cells differentiate.
Sox2 directly activates the Six3 forebrain enhancer.
Six3OS regulates Six3 activity in developing retina by a mechanism via which promoter-associated long non-coding RNAs can modulate the activity of their associated protein coding genes during development.
It was shown that Six3 is necessary for ependymal cell maturation during postnatal stages of brain development. In its absence, ependymal cells fail to suppress radial glia characteristics.
Neuroretina specification requires Six3-mediated suppression of Wnt8b a few hours later at the 6- to 8-somite stage.
Six3-mediated auto repression and eye development requires its interaction with members of the Groucho-related family of co-repressors.
role of expression with pax6 (zeige PAX6 Antikörper) on haploinsufficient lens phenotype
This gene encodes a member of the sine oculis homeobox transcription factor family. The encoded protein plays a role in eye development. Mutations in this gene have been associated with holoprosencephaly type 2.
homeobox protein SIX3
, sine oculis homeobox homolog 3
, sine oculis homeobox homolog 6
, sine oculis-related homeobox 3 homolog
, sine oculis homeobox 3-like protein
, Sine oculis homeobox homolog 3