(Mouse) Hopx Blocking Peptide (Center)
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Primary Accession | Q8R1H0 |
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Gene ID | 74318 |
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Other Names | Homeodomain-only protein, Homeobox-only protein, Odd homeobox protein 1, mOB1, Hopx, Hod, Hop, Ob1 |
Target/Specificity | The synthetic peptide sequence is selected from aa 22-34 of HUMAN Hopx |
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 | Hopx |
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Synonyms | Hod, Hop, Ob1 |
Function | Atypical homeodomain protein which does not bind DNA and is required to modulate cardiac growth and development. Acts via its interaction with SRF, thereby modulating the expression of SRF- dependent cardiac-specific genes and cardiac development. Prevents SRF- dependent transcription either by inhibiting SRF binding to DNA or by recruiting histone deacetylase (HDAC) proteins that prevent transcription by SRF. Overexpression causes cardiac hypertrophy (PubMed:12297045, PubMed:12297046). Acts as a co-chaperone for HSPA1A and HSPA1B chaperone proteins and assists in chaperone-mediated protein refolding (By similarity). |
Cellular Location | Nucleus. Cytoplasm. Note=According to PubMed:14516659 it is cytoplasmic. |
Tissue Location | Expressed in the embryonic and adult heart and in the adult brain, liver, lung, skeletal muscle, intestine and spleen Throughout embryonic and postnatal development, it is expressed in the myocardium. |
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Background
Atypical homeodomain protein which does not bind DNA and is required to modulate cardiac growth and development. Acts via its interaction with SRF, thereby modulating the expression of SRF-dependent cardiac-specific genes and cardiac development. Prevents SRF-dependent transcription either by inhibiting SRF binding to DNA or by recruiting histone deacetylase (HDAC) proteins that prevent transcription by SRF. Overexpression causes cardiac hypertrophy.
References
Chen F.,et al.Cell 110:713-723(2002).
Shin C.H.,et al.Cell 110:725-735(2002).
Adu J.,et al.Mech. Dev. 119:S43-S47(2002).
Carninci P.,et al.Science 309:1559-1563(2005).
Kook H.,et al.J. Clin. Invest. 112:863-871(2003).
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