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Validated All-in-One™ qPCR Primer for SIX1(NM_005982.3) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
The protein encoded by this gene is a homeobox protein that is similar to the Drosophila 'sine oculis' gene product. This gene is found in a cluster of related genes on chromosome 14 and is thought to be involved in limb development. Defects in this gene are a cause of autosomal dominant deafness type 23 (DFNA23) and branchiootic syndrome type 3 (BOS3). [provided by RefSeq].
Gene References into function
- Six1 overexpression reinstates an embryonic pathway of proliferation in breast cancer by up-regulating cyclin A1
- Identification of SIX1 mutations as causing branchio-oto-renal syndrome offers insights into the molecular basis of otic and renal developmental diseases in humans
- SIX1 mutation may cause the enlargement of the vestibular aqueduct in patients diagnosed with branchio-oto syndrome.
- SALL1 is a likely target gene for SIX1 during kidney development
- Results showed that Six1 is frequently overexpressed in hepatocellular carcinoma (HCC) patients and elevated Six1 protein in HCC patients may be an indication of advanced stage and poor overall survival after hepatectomy.
- Cell cycle regulation of Six1 occurs both transcriptionally and post-translationally via phosphorylation
- CSRP3, MUSTN1, SIX1, and FBXO32 expression changes in response to lengthening and shortening contractions in human muscle
- A novel SIX1 mutation suggests a slightly different clinical profile compared to EYA1-related branchio-oto-renal syndrome.
- screen of 247 branchio-oto-renal syndrome families detected five novel SIX1 mutations (c.50T>A, c.218A>C, c.317T>G, c.329G>A, c.334C>T) and one previously reported mutation (c.328C>T) seen in 5 unrelated families
- Six1 overexpression is sufficient for malignant transformation of immortalized, nontumorigenic mammary epithelial cells, and suggest that the mechanism of this transformation involves inappropriate reexpression of cyclin A1 in the adult mammary gland.
- Microarray studies show that our in vitro model system reflects many cellular and molecular alterations characteristic of cervical cancer, and identified SIX1 and GDF15 as 2 novel potential biomarkers of cervical cancer progression.
- BOR and OAVS features are associated with duplication of SIX1, SIX6 and OTX2 resulting from a complex chromosomal rearrangement.
- Exposure to lithium chloride or sodium valproate elicited an increase in 936 changes in gene expression, with a 31.3-fold increase in the expression of Six1.
