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tech@sbsbio.com
Beijing SBS Genetech Co.,Ltd.
Beijing SBS Genetech Co.,Ltd.

from China, for the World

for Superior Biology Services since 2000

  • Home
  • Product 
    • All Products
    • Custom Services
    • Catalog Products
    • Innovative Systems
    • Nucleic Acid Related
    • Natural Compounds
    • Synthetic Biology
    • Enzymes
  • POCT Solution 
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Human Bcl-xL, His tag

Human Bcl-xL, His tag

$168.00 - $448.00
$560.00
B-cell lymphoma-extra large (Bcl-xL) is a transmembrane molecule in the mitochondria. It is a member of the Bcl-2 family of proteins, and acts as an anti-apoptotic protein by preventing the release of mitochondrial contents such as cytochrome c, which leads to caspase activation and ultimately, programmed cell death. Bcl-xL dysfunction in mice can cause ineffective production of red blood cells, severe anemia, hemolysis, and death. This protein has also been shown as a requirement for heme production[6] and in erythroid lineage, Bcl-xL is a major survival factor responsible for an estimated half of the total survival "signal" proerythroblasts must receive in order to survive and become red cells. Similar to other Bcl-2 family members, Bcl-xL has been implicated in the survival of cancer cells by inhibiting the function of p53, a tumor suppressor. In cancerous mouse cells, those which contained Bcl-xL were able to survive while those that only expressed p53 died in a small period of time.
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Cat. No.: HBXLH-25 (for 25μg)

Cat. No.: HBXLH-50 (for 50μg)

Cat. No.: HBXLH-100 (for 100μg)

 

 

Description

B-cell lymphoma-extra large (Bcl-xL) is a transmembrane protein situated within the mitochondria, belonging to the esteemed Bcl-2 family of proteins. Functionally, it serves as a pivotal anti-apoptotic regulator, orchestrating cellular survival by impeding the release of mitochondrial contents, notably cytochrome c. By obstructing this crucial step, Bcl-xL effectively halts the activation of caspases, thereby thwarting the initiation of programmed cell death.

In murine models, dysfunction of Bcl-xL precipitates a cascade of detrimental consequences, including impaired production of red blood cells, culminating in severe anemia, hemolysis, and ultimately, mortality. Moreover, Bcl-xL emerges as an essential component in heme synthesis, further underscoring its indispensability in vital cellular processes.

Within the erythroid lineage, Bcl-xL assumes a paramount role as a survival factor, furnishing approximately half of the requisite survival "signal" crucial for proerythroblasts to navigate their developmental journey and mature into red blood cells. This underscores its pivotal function in maintaining erythroid homeostasis.

Similar to its counterparts in the Bcl-2 family, Bcl-xL is implicated in the survival machinery of cancer cells through its ability to antagonize the function of p53, a pivotal tumor suppressor. Experimental evidence in cancerous murine cells highlights the contrasting fate between cells harboring Bcl-xL, which evade demise, and those solely expressing p53, which succumb to cellular demise within a confined temporal window.

In summary, Bcl-xL stands as a central arbiter of cellular fate, regulating apoptosis, sustaining erythroid viability, and even fostering oncogenic survival pathways. Its multifaceted roles underscore its significance in both physiological and pathological contexts.

 

Species

Human

 

Molecular Alias

Bcl2-L-1, Apoptosis regulator Bcl-X, BCL2L1, BCLX, BCL2L

 

Accession

Q07817

 

Expression Sequence

Protein sequence(Q07817, Met1-Phe210, with C-10*His)

MSQSNRELVVDFLSYKLSQKGYSWSQFSDVEENRTEAPEGTESEMETPSAINGNPSWHLADSPAVNGATGHSSSLDAREVIPMAAVKQALREAGDEFELRYRRAFSDLTSQLHITPGTAYQSFEQVVNELFRDGVNWGRIVAFFSFGGALCVESVDKEMQVLVSRIAAWMATYLNDHLEPWIQENGGWDTFVELYGNNAAAESRKGQERFGGGGSHHHHHHHHHH

 

Expression Host

HEK293

 

Molecular Weight

Theoretical: 25.2kDa 

Actual: 29kDa

 

Purity

>95% by SDS-PAGE

 

Endotoxin content

<1 EU/μg

 

Label

Unconjugated

 

Tag

His Tag

 

Form

Lyophilized Powder

 

Buffer System

Lyophilized from a 0.2 μm filtered solution of 0.2M PBS, 1mM EDTA, pH7.4.

 

Reconstitution Method

Reconstitute at no more than 1 mg/mL according to the size in deionized water after rapid centrifugation.

 

Storage Conditions

12 months from the date of receipt when stored at -20 to -70 °C as supplied.

6 months at -20 to -70 °C under sterile conditions after reconstitution.

1 week at 2 to 8 °C under sterile conditions after reconstitution.

Please avoid repeated freeze-thaw cycles.


 

 

 

 
 
Only for research and not intended for treatment of humans or animals
 
 

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SBS Genetech is a long-term sponsor of Cold Spring Harbor Laboratory

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