Human Bcl-xL Plasmids
Plasmids encoding wild-type human B-cell lymphoma-extra-large (Bcl-XL), as well as Bcl-xL variants that are targetd to cytosol, mitochondria or endoplasmic reticulum.
Available Plasmids:
- Bcl-xL (wild-type) - Wild-type human Bcl-xL cDNA cloned into mammalinan pEGFP-C1 vector to generate the plasmid pEGFP-C1-hBcl-xL (wild-type)
- Bcl-xL (ΔC) - The C-terminal transmembrane sequence of Bcl-xL in pEGFP-C1-hBcl-xL (wild-type) was deleted, which specifically confines Bcl-xL to the cytoplasm
- Bcl-xL (mitochondria) - The C-terminal transmembrane sequence of Bcl-xL in pEGFP-C1-hBcl-xL (wild-type) was replaced with membrane-targeting sequence of the listerial protein ActA, which specifically targets Bcl-xL at mitochondria
- Bcl-xL (ER) - The C-terminal transmembrane sequence of Bcl-xL in pEGFP-C1-hBcl-xL (wild-type) was replaced with cytochrome b5 (cb5) membrane-targeting sequence, which directs Bcl-xL specifically at the ER membrane
Bcl-2 protein family member Bcl-xL is a major regulator of cellular apoptotic signaling. Bcl-xL is a transmembrane molecule in the mitochondria and acts as a pro-survival protein by preventing the release of mitochondrial contents such as cytochrome c, which would lead to caspase inactivation. Tissue differentiation and homeostasis are regulated by apoptosis—a tightly controlled cellular suicide program. Dys-regulation of apoptosis has been implicated in many diseases. Evidence indicates that insufficient apoptosis can manifest as cancer or autoimmunity, while accelerated cell death is evident in acute and chronic degenerative diseases and immunodeficiency. Bcl-XL is a major regulator of cellular apoptotic signaling found to be localized at different subcellular compartments Bcl-XL targeted to different organelles are good tools to illustrate how dysregulation of apoptosis is involved in disease development, which could help lead to development of new therapeutic strategies for cancer and other diseases.
From the laboratory of Chi Li, PhD, University of Louisville.
Plasmids encoding wild-type human B-cell lymphoma-extra-large (Bcl-XL), as well as Bcl-xL variants that are targetd to cytosol, mitochondria or endoplasmic reticulum.
Available Plasmids:
- Bcl-xL (wild-type) - Wild-type human Bcl-xL cDNA cloned into mammalinan pEGFP-C1 vector to generate the plasmid pEGFP-C1-hBcl-xL (wild-type)
- Bcl-xL (ΔC) - The C-terminal transmembrane sequence of Bcl-xL in pEGFP-C1-hBcl-xL (wild-type) was deleted, which specifically confines Bcl-xL to the cytoplasm
- Bcl-xL (mitochondria) - The C-terminal transmembrane sequence of Bcl-xL in pEGFP-C1-hBcl-xL (wild-type) was replaced with membrane-targeting sequence of the listerial protein ActA, which specifically targets Bcl-xL at mitochondria
- Bcl-xL (ER) - The C-terminal transmembrane sequence of Bcl-xL in pEGFP-C1-hBcl-xL (wild-type) was replaced with cytochrome b5 (cb5) membrane-targeting sequence, which directs Bcl-xL specifically at the ER membrane
Bcl-2 protein family member Bcl-xL is a major regulator of cellular apoptotic signaling. Bcl-xL is a transmembrane molecule in the mitochondria and acts as a pro-survival protein by preventing the release of mitochondrial contents such as cytochrome c, which would lead to caspase inactivation. Tissue differentiation and homeostasis are regulated by apoptosis—a tightly controlled cellular suicide program. Dys-regulation of apoptosis has been implicated in many diseases. Evidence indicates that insufficient apoptosis can manifest as cancer or autoimmunity, while accelerated cell death is evident in acute and chronic degenerative diseases and immunodeficiency. Bcl-XL is a major regulator of cellular apoptotic signaling found to be localized at different subcellular compartments Bcl-XL targeted to different organelles are good tools to illustrate how dysregulation of apoptosis is involved in disease development, which could help lead to development of new therapeutic strategies for cancer and other diseases.
From the laboratory of Chi Li, PhD, University of Louisville.
| Catalog Number | Product | DataSheet | Size | AVAILABILITY | Price | Qty |
|---|
| Product Type: | Plasmid |
| Gene/insert name: | Bcl-xL (wild-type) |
| Accession ID: | Q07817 |
| Antibiotic Resistance: | Kanamycin |
| Fusion Tag(s): | GFP |
| Grow in E. coli at 37 C: | Yes |
| Selectable markers: | Neomycin |
| Cloning Site 5': | BspE1/Klenow |
| Cloning Site 3': | BamHI |
| Insert Size: | 700 bp |
| Vector Backbone and Size: | pEGFP-C1, 4700 bp |
| High or low copy: | High |
| Storage: | -80C |
| Shipped: | Ambient temperature |
Human Bcl-xL Plasmids
| Gene/Insert Name: | Bcl-xL (wild-type) | Bcl-xL (?C) | Bcl-xL (mitochondria) | Bcl-xL (ER) |
| Insert Size: | 700 bp | 600 bp | 700 bp | 700 bp |
| Species: | mammalian transfection | mammalian transfection | mammalian transfection | mammalian transfection |
| Fusion Proteins/Tags: | GFP | GFP | GFP | GFP |
| Vector Backbone and Size: | pEGFP-C1, 4700 bp | pEGFP-C1, 4700 bp | pEGFP-C1, 4700 bp | pEGFP-C1, 4700 bp |
| Cloning Site 5?: | BspE1/Klenow | BspE1/Klenow | BspE1/Klenow | BspE1/Klenow |
| Cloning Site 3?: | BamHI | BamHI | BamHI | BamHI |
| Antibiotic Resistance: | Kanamycin | Kanamycin | Kanamycin | Kanamycin |
| High or Low Copy: | High | High | High | High |
| Grow in Standard E. coli @ 37C?: | Yes | Yes | Yes | Yes |
| Selectable Markers: | Neomycin | Neomycin | Neomycin | Neomycin |
| Storage: | -80C | -80C | -80C | -80C |
| Shipped: | Stab agar at ambient temperature | Stab agar at ambient temperature | Stab agar at ambient temperature | Stab agar at ambient temperature |
- Eno CO, Eckenrode EF, Olberding KE, Zhao G, White C, Li C. Distinct roles of mitochondria- and ER-localized Bcl-xL in apoptosis resistance and Ca2+ homeostasis. Mol Biol Cell. 2012 Jul;23(13):2605-18.
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