Difference between revisions of "Part:BBa K2976003"
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After being activated with Mtb, the activation cluster TLR2:TLR1:CD14 triggers NF-kappa-B signaling pathways via MYD88 and TRAF6. NF-κB proteins exist in the cytoplasm in an inactive form because of their association with the IκB proteins. IκB proteins mask the nuclear-localization sequences (NLSs) of NF-κB subunits and retain it in the cytoplasm. Activation of TLR2:TLR1:CD14 cluster cause the degradation of IκB proteins by proteasomes. Then, NF-κB subunits could pass through the nuclear pore complex (NPC) and cause the expression of an array of pro-inflammatory cytokines and chemokines. Similarly, NF-κB subunits also can bind the NF-κB induced promoter and initiate transcription of the downstream genes behind these promoters. | After being activated with Mtb, the activation cluster TLR2:TLR1:CD14 triggers NF-kappa-B signaling pathways via MYD88 and TRAF6. NF-κB proteins exist in the cytoplasm in an inactive form because of their association with the IκB proteins. IκB proteins mask the nuclear-localization sequences (NLSs) of NF-κB subunits and retain it in the cytoplasm. Activation of TLR2:TLR1:CD14 cluster cause the degradation of IκB proteins by proteasomes. Then, NF-κB subunits could pass through the nuclear pore complex (NPC) and cause the expression of an array of pro-inflammatory cytokines and chemokines. Similarly, NF-κB subunits also can bind the NF-κB induced promoter and initiate transcription of the downstream genes behind these promoters. | ||
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Revision as of 01:36, 5 September 2019
Cluster of differentiation 14 (CD14)
CD14 is a glycosylphosphatidylinositol (GPI)-anchored cell surface glycoprotein, which preferentially expresses on monocytes and macrophages. It cooperates with other proteins to mediate the innate immune response to pathogen-associated molecular pattern molecules (PAMPs). For example, CD14 cooperates with TLR1/2 heterodimers and acts as a co-receptor for recognizing lipopolysaccharide.
Usage
In 2019 CPU_CHINA project, we express CD14 to form the TLR2:TLR1:CD14 cluster on the designer cell membrane. As a Mtb sensor, the complex could recognize the substances of Mtb and then stimulate the downstream signaling pathway. Then, activated NF-κB initiates transcription of the gene circuits to express other proteins in our project.
Biology
After being activated with Mtb, the activation cluster TLR2:TLR1:CD14 triggers NF-kappa-B signaling pathways via MYD88 and TRAF6. NF-κB proteins exist in the cytoplasm in an inactive form because of their association with the IκB proteins. IκB proteins mask the nuclear-localization sequences (NLSs) of NF-κB subunits and retain it in the cytoplasm. Activation of TLR2:TLR1:CD14 cluster cause the degradation of IκB proteins by proteasomes. Then, NF-κB subunits could pass through the nuclear pore complex (NPC) and cause the expression of an array of pro-inflammatory cytokines and chemokines. Similarly, NF-κB subunits also can bind the NF-κB induced promoter and initiate transcription of the downstream genes behind these promoters.
Sequence and Features
- 10COMPATIBLE WITH RFC[10]
- 12INCOMPATIBLE WITH RFC[12]Illegal NheI site found at 336
- 21INCOMPATIBLE WITH RFC[21]Illegal XhoI site found at 367
- 23COMPATIBLE WITH RFC[23]
- 25INCOMPATIBLE WITH RFC[25]Illegal NgoMIV site found at 181
- 1000INCOMPATIBLE WITH RFC[1000]Illegal BsaI site found at 187