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KCTD11 Blocking Peptide (N-Term)
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
| Primary Accession | Q693B1 |
|---|---|
| Other Accession | Q8K485 |
| Gene ID | 147040 |
|---|---|
| Other Names | BTB/POZ domain-containing protein KCTD11, KCTD11, C17orf36, REN |
| Target/Specificity | The synthetic peptide sequence is selected from aa 41-53 of HUMAN KCTD11 |
| Format | Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed. |
| Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C. |
| Precautions | This product is for research use only. Not for use in diagnostic or therapeutic procedures. |
| Name | KCTD11 |
|---|---|
| Synonyms | C17orf36, REN |
| Function | Plays a role as a marker and a regulator of neuronal differentiation; Up-regulated by a variety of neurogenic signals, such as retinoic acid, epidermal growth factor/EGF and NGFB/nerve growth factor. Induces apoptosis, growth arrest and the expression of cyclin- dependent kinase inhibitor CDKN1B. Plays a role as a tumor repressor and inhibits cell growth and tumorigenicity of medulloblastoma (MDB). Acts as a probable substrate-specific adapter for a BCR (BTB-CUL3-RBX1) E3 ubiquitin-protein ligase complex towards HDAC1. Functions as antagonist of the Hedgehog pathway on cell proliferation and differentiation by affecting the nuclear transfer of transcription factor GLI1, thus maintaining cerebellar granule cells in undifferentiated state, this effect probably occurs via HDAC1 down- regulation, keeping GLI1 acetylated and inactive. When knock-down, Hedgehog antagonism is impaired and proliferation of granule cells is sustained. Activates the caspase cascade. |
| Tissue Location | Higher expression in cerebellum than in whole brain and lower expression in medulloblastoma. |
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Background
Plays a role as a marker and a regulator of neuronal differentiation; Up-regulated by a variety of neurogenic signals, such as retinoic acid, epidermal growth factor/EGF and NGFB/nerve growth factor. Induces apoptosis, growth arrest and the expression of cyclin-dependent kinase inhibitor CDKN1B. Plays a role as a tumor repressor and inhibits cell growth and tumorigenicity of medulloblastoma (MDB). Acts as an E3 ubiquitin-protein ligase towards HDAC1, leading to its proteasomal degradation. Functions as antagonist of the Hedgehog pathway on cell proliferation and differentiation by affecting the nuclear transfer of transcrition factor GLI1, thus maintaining cerebellar granule cells in undifferentiated state, this effect probably occurs via HDAC1 down-regulation, keeping GLI1 acetylated and inactive. When knock- down, Hedgehog antagonism is impaired and proliferation of granule cells is sustained. Activates the caspase cascade.
References
Di Marcotullio L.,et al.Proc. Natl. Acad. Sci. U.S.A. 101:10833-10838(2004).
Correale S.,et al.Biochimie 93:715-724(2011).
Ota T.,et al.Nat. Genet. 36:40-45(2004).
Mural R.J.,et al.Submitted (SEP-2005) to the EMBL/GenBank/DDBJ databases.
Canettieri G.,et al.Nat. Cell Biol. 12:132-142(2010).
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