anti-SIX3 (SIX3) Antikörper

Human Sine Oculis-Related Homeobox 3 (SIX3) Interaktionspartner

1. The authors demonstrate that the SIX3/LSD1/NuRD(MTA3) complex inhibits carcinogenesis in breast cancer cells and suppresses metastasis in breast cancer.

2. SIX3 deletions and incomplete penetrance in families affected by holoprosencephaly have been described.

3. 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.

4. SIX3 is a novel negative transcriptional regulator and acts as a tumor suppressor that directly represses the transcription of AURKA and AURKB in astrocytoma.

5. SIX2, SIX3, and SIX4 were correlated with higher TNM stages in lung neoplasms

6. High SIX3 expression is associated with Head and Neck Squamous Cell Carcinoma.

7. SIX3 may play an important role as a novel suppressor in human lung cancer.

8. Mutations in SIX3 is associated with holoprosencephaly.

9. There was a positive correlation between the severity of the brain malformation and facial features for SHH, SIX3, and TGIF, but no such correlation was found for ZIC2 mutations.

10. 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

11. SIX3 acts directly upstream of SHH, and the SHH pathway is a key regulator of ventral forebrain patterning and mutations are associated with schizencephaly.

12. A mutational screen was done to identify possible SIX3 mutations in a cohort of 149 (M:F 81:68) patients with hypopituitarism and/or midline abnormalities, falling within the spectrum of septo-optic dysplasia and holoprosencephaly.

13. The homeotic protein Six3 is a coactivator of the nuclear receptor NOR-1 and a corepressor of the fusion protein EWS/NOR-1 in human extraskeletal myxoid chondrosarcomas.

14. Six3 directly binds to geminin

15. Seven novel SIX3 mutations found in a cohort of Holoprosencephaly patinets.

16. different SIX3 mutations in HPE2 may affect different signaling pathways, and that one of these pathways may involve the nuclear receptor NOR1

17. Occurrence of aprosencephaly/atelencephaly and holoprosencephaly in a family with a SIX3 gene mutation.

18. Upregulation of Six3 expression in single progenitor cells of the embryonic telencephalon keeps them in an undifferentiated state; Six3 overexpression in mammalian brain depends strictly on the integrity of its DNA-binding domain.

19. role for the MTA1 as an upstream modifier of Six3 and indicate that Six3 is a direct stimulator of rhodopsin expression.

20. 89% of putative deleterious human SIX3 mutations are significant loss-of-function alleles; a systematic comparison of bioactivities of mutant six3 proteins is demonstrated that confirms a role for six3 in causation of holoprosencephaly.

Zebrafish Sine Oculis-Related Homeobox 3 (SIX3) Interaktionspartner

1. Lhx2 may mediate an alternative or parallel pathway for control of cellular proliferation in the developing forebrain via Six3b.

2. 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.

Mouse (Murine) Sine Oculis-Related Homeobox 3 (SIX3) Interaktionspartner

1. Six3 is haploinsufficient for main olfactory epithelium development, GnRH neuron migration, and fertility.

2. SP8 and SP9 coordinately promote D2-type medium spiny neuron production by activating Six3 expression

3. 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.

4. variations in Six3 dosage result in different forms of Holoprosencephaly

5. SIX3 and SIX6 play distinct but compensatory roles in regulating transcription of gonadotrope-specific genes as gonadotrope cells differentiate.

6. Sox2 directly activates the Six3 forebrain enhancer.

7. 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.

8. 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.

9. Neuroretina specification requires Six3-mediated suppression of Wnt8b a few hours later at the 6- to 8-somite stage.

10. Six3-mediated auto repression and eye development requires its interaction with members of the Groucho-related family of co-repressors.

11. role of expression with pax6 on haploinsufficient lens phenotype

12. Six 3 and Six 6 are differentially required during forebrain development; gene expression in brain

13. The Pax-Eya-Six-Dach network is at best only partly conserved during lens and nasal placode development.

14. Six3 directly activates Pax6 and probably also Sox2 in the PLE and regulates cell autonomously the earliest stages of mammalian lens induction.

15. role for the MTA1 as an upstream modifier of Six3 and indicate that Six3 is a direct stimulator of rhodopsin expression.

16. At the 15- to 17-somite stage, the prospective diencephalon is the most-anterior structure in the Six3-null brain, and Wnt1 expression is anteriorly expanded.

17. Six3-cre transgene is selectively expressed in layer 4 of sensory cortical areas.

18. These results identify Six3 as a direct regulator of Shh expression and reveal a crossregulatory loop between Shh and Six3 in the ventral forebrain.

19. Haploinsufficiency of both Six3 and Hesx1 leads to severe pituitary dysmorphogenesis during development, which results in hypopituitarism with dramatic postnatal growth retardation.

20. These data suggest a direct link between Six3 and Shh regulation during normal forebrain development and in the pathogenesis of holoprosencephaly.