Difference between revisions of "Part:BBa K364301:Design"

 
 
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__NOTOC__
 
__NOTOC__
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<partinfo>BBa_K364301 short</partinfo>
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<partinfo>BBa_K364301 short</partinfo>PUMA (p53 upregulated modulator of apoptosis) is a Bcl-2 homology 3 (BH3)-only Bcl-2 family member and a critical mediator of p53-dependent and -independent apoptosis induced by a wide variety of stimuli, including genotoxic stress, deregulated oncogene expression, toxins, altered
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redox status, growth factor/cytokine withdrawal and infection. It serves as a proximal signaling
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molecule whose expression is regulated by transcription factors in response to these stimuli.
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PUMA transduces death signals primarily to the mitochondria, where it acts indirectly on the
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Bcl-2 family members Bax and/or Bak by relieving the inhibition imposed by antiapoptotic
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members. It directly binds and antagonizes all known antiapoptotic Bcl-2 family members to
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induce mitochondrial dysfunction and caspase activation. PUMA ablation or inhibition leads to
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apoptosis deficiency underlying increased risks for cancer development and therapeutic resistance.
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Although elevated PUMA expression elicits profound chemo- and radio-sensitization in cancer
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cells, inhibition of PUMA expression may be useful for curbing excessive cell death associated
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with tissue injury and degenerative diseases.
 
<partinfo>BBa_K364301 SequenceAndFeatures</partinfo>
 
<partinfo>BBa_K364301 SequenceAndFeatures</partinfo>
  
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===References===
 
===References===
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'''PUMA, a potent killer with or without p53'''
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''J Yu and L Zhang,  Oncogene. ''2008 December ; 27(Suppl 1): S71–S83. doi:10.1038/onc.2009.45.
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'''PUMA, a Novel Proapoptotic Gene Is Induced by p53'''''''Katsunori Nakanoa and Karen H Vousden'', Molecular Cell, Vol. 7, 683–694, March, 2001, Copyright ã2001 by Cell Press''

Latest revision as of 10:17, 13 August 2010

hPUMA PUMA (p53 upregulated modulator of apoptosis) is a Bcl-2 homology 3 (BH3)-only Bcl-2 family member and a critical mediator of p53-dependent and -independent apoptosis induced by a wide variety of stimuli, including genotoxic stress, deregulated oncogene expression, toxins, altered redox status, growth factor/cytokine withdrawal and infection. It serves as a proximal signaling molecule whose expression is regulated by transcription factors in response to these stimuli. PUMA transduces death signals primarily to the mitochondria, where it acts indirectly on the Bcl-2 family members Bax and/or Bak by relieving the inhibition imposed by antiapoptotic members. It directly binds and antagonizes all known antiapoptotic Bcl-2 family members to induce mitochondrial dysfunction and caspase activation. PUMA ablation or inhibition leads to apoptosis deficiency underlying increased risks for cancer development and therapeutic resistance. Although elevated PUMA expression elicits profound chemo- and radio-sensitization in cancer cells, inhibition of PUMA expression may be useful for curbing excessive cell death associated with tissue injury and degenerative diseases.


Assembly Compatibility:
  • 10
    COMPATIBLE WITH RFC[10]
  • 12
    COMPATIBLE WITH RFC[12]
  • 21
    COMPATIBLE WITH RFC[21]
  • 23
    COMPATIBLE WITH RFC[23]
  • 25
    COMPATIBLE WITH RFC[25]
  • 1000
    COMPATIBLE WITH RFC[1000]


Design Notes

Compatible with RFC-10 and RFC-25.


Source

Human.

References

PUMA, a potent killer with or without p53 J Yu and L Zhang, Oncogene. 2008 December ; 27(Suppl 1): S71–S83. doi:10.1038/onc.2009.45.

PUMA, a Novel Proapoptotic Gene Is Induced by p53''Katsunori Nakanoa and Karen H Vousden, Molecular Cell, Vol. 7, 683–694, March, 2001, Copyright ã2001 by Cell Press