|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.|
|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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Provided below are standard protocols that you may find useful for product applications.
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.
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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