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NKX2-5 Antibody (Center) Blocking Peptide
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
| Primary Accession | P52952 |
|---|---|
| Clone Names | 100507231 |
| Gene ID | 1482 |
|---|---|
| Other Names | Homeobox protein Nkx-25, Cardiac-specific homeobox, Homeobox protein CSX, Homeobox protein NK-2 homolog E, NKX2-5, CSX, NKX25, NKX2E |
| 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 | NKX2-5 |
|---|---|
| Synonyms | CSX, NKX2.5, NKX2E |
| Function | Transcription factor required for the development of the heart and the spleen (PubMed:22560297). During heart development, acts as a transcriptional activator of NPPA/ANF in cooperation with GATA4 (By similarity). May cooperate with TBX2 to negatively modulate expression of NPPA/ANF in the atrioventricular canal (By similarity). Binds to the core DNA motif of NPPA promoter (PubMed:22849347, PubMed:26926761). Together with PBX1, required for spleen development through a mechanism that involves CDKN2B repression (PubMed:22560297). Positively regulates transcription of genes such as COL3A1 and MMP2, resulting in increased pulmonary endothelial fibrosis in response to hypoxia (PubMed:29899023). |
| Cellular Location | Nucleus. |
| Tissue Location | Expressed only in the heart. |
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Provided below are standard protocols that you may find useful for product applications.
Background
This gene encodes a homeobox-containing transcriptionfactor. This transcription factor functions in heart formation anddevelopment. Mutations in this gene cause atrial septal defect withatrioventricular conduction defect, and also tetralogy of Fallot,which are both heart malformation diseases. Mutations in this genecan also cause congenital hypothyroidism non-goitrous type 5, anon-autoimmune condition. Alternative splicing results in multipletranscript variants.
References
Bailey, S.D., et al. Diabetes Care 33(10):2250-2253(2010)De Luca, A., et al. Clin. Genet. (2010) In press :Stallmeyer, B., et al. Clin. Genet. (2010) In press :Narumi, S., et al. J. Clin. Endocrinol. Metab. 95(4):1981-1985(2010)Joubert, B.R., et al. Genome Med 2 (3), 17 (2010) :
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