Difference between revisions of "Part:BBa K2976001"
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Toll-like receptor 1 (TLR1) is a transmembrane glycoprotein that participates in the innate immune response to microbial agents. TLR2 could form active heterodimers with TLR1 when exposed to some pathogen-associated molecular pattern molecules (PAMPs), and the heterodimers recognizes plenty of substance in lipoarabinomannan (LAM) biosynthesis with the help of CD14. | Toll-like receptor 1 (TLR1) is a transmembrane glycoprotein that participates in the innate immune response to microbial agents. TLR2 could form active heterodimers with TLR1 when exposed to some pathogen-associated molecular pattern molecules (PAMPs), and the heterodimers recognizes plenty of substance in lipoarabinomannan (LAM) biosynthesis with the help of CD14. | ||
| − | Usage In 2019 CPU_CHINA project, TLR1 is expressed along with TLR1 and CD14 to form the TLR1:TLR2: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. | + | ===Usage=== |
| + | <p> | ||
| + | In 2019 CPU_CHINA project, TLR1 is expressed along with TLR1 and CD14 to form the TLR1:TLR2: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. | ||
| + | <p> | ||
| − | Biology After being activated with Mtb, the activation cluster TLR1:TLR2: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 TLR1:TLR2: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. | + | ===Biology=== |
| + | <p> | ||
| + | After being activated with Mtb, the activation cluster TLR1:TLR2: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 TLR1:TLR2: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. | ||
| + | <p> | ||
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Revision as of 01:25, 5 September 2019
Toll-like receptor 1
Toll-like receptor 1 (TLR1) is a transmembrane glycoprotein that participates in the innate immune response to microbial agents. TLR2 could form active heterodimers with TLR1 when exposed to some pathogen-associated molecular pattern molecules (PAMPs), and the heterodimers recognizes plenty of substance in lipoarabinomannan (LAM) biosynthesis with the help of CD14.
Usage
In 2019 CPU_CHINA project, TLR1 is expressed along with TLR1 and CD14 to form the TLR1:TLR2: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. <p>
Biology
<p> After being activated with Mtb, the activation cluster TLR1:TLR2: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 TLR1:TLR2: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. <p>
Sequence and Features
- 10COMPATIBLE WITH RFC[10]
- 12COMPATIBLE WITH RFC[12]
- 21INCOMPATIBLE WITH RFC[21]Illegal BamHI site found at 788
- 23COMPATIBLE WITH RFC[23]
- 25COMPATIBLE WITH RFC[25]
- 1000INCOMPATIBLE WITH RFC[1000]Illegal BsaI site found at 103