JavaScript is disabled in your browser. Please enable JavaScript to view this website.
AB290060

Recombinant Human BCL2 Protein

Be the first to review this product! Submit a review

|

(0 Publication)

Recombinant Human BCL2 Protein is a Human Fragment protein, in the 1 to 211 aa range, expressed in HEK 293 cells, with >95%, <0.005 EU/µg endotoxin level.

View Alternative Names

Apoptosis regulator Bcl-2, BCL2

3 Images
Mass Spectrometry - Recombinant Human BCL2 Protein (AB290060)
  • Mass Spec

Supplier Data

Mass Spectrometry - Recombinant Human BCL2 Protein (AB290060)

Mass determination by ESI-TOF.

Predicted MW is 23364.35 Da. (+/- 10 Da by ESI-TOF). Observed MW is 23364.81 Da.

SDS-PAGE - Recombinant Human BCL2 Protein (AB290060)
  • SDS-PAGE

Supplier Data

SDS-PAGE - Recombinant Human BCL2 Protein (AB290060)

SDS-PAGE analysis of ab290060

HPLC - Recombinant Human BCL2 Protein (AB290060)
  • HPLC

Supplier Data

HPLC - Recombinant Human BCL2 Protein (AB290060)

HPLC analysis of ab290060

Key facts

Purity

>95% HPLC

Endotoxin level

<0.005 EU/µg

Expression system

HEK 293 cells

Tags

Tag free

Biologically active

No

Accession

P10415

Animal free

No

Carrier free

No

Species

Human

Reconstitution

Reconstitute in PBS

Storage buffer

pH: 7.4 Constituents: 10.26% Trehalose, 0.727% Dibasic monohydrogen potassium phosphate, 0.248% Potassium phosphate monobasic

storage-buffer

You may be interested in:

AB119506

Human Bcl-2 ELISA Kit

0

0 Reviews

View product

We recommend this product because it’s often used in the same experiment or related research.

We advise that you always check the datasheet to ensure it fits your experiments, or contact ourtechnical teamfor help.

Sequence info

[{"sequence":"MAHAGRTGYDNREIVMKYIHYKLSQRGYEWDAGDVGAAPPGAAPAPGIFSSQPGHTPHPAASRDPVARTSPLQTPAAPGAAAGPALSPVPPVVHLTLRQAGDDFSRRYRRDFAEMSSQLHLTPFTARGRFATVVEELFRDGVNWGRIVAFFEFGGVMCVESVNREMSPLVDNIALWMTEYLNRHLHTWIQDNGGWDAFVELYGPSMRPLFD","proteinLength":"Fragment","predictedMolecularWeight":"26 kDa","actualMolecularWeight":null,"aminoAcidEnd":211,"aminoAcidStart":1,"nature":"Recombinant","expressionSystem":"HEK 293 cells","accessionNumber":"P10415","tags":[]}]

Properties and storage information

Shipped at conditions
Ambient - Can Ship with Ice
Appropriate short-term storage conditions
-20°C
Appropriate long-term storage conditions
-20°C
False

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

Bcl-2 also known as B-cell lymphoma 2 is an important protein involved in the regulation of apoptosis. It mechanically functions by inhibiting cell death and is a member of the Bcl-2 family of proteins. Bcl-2 has a molecular weight of approximately 26 kDa. It is expressed mainly in fetal and adult tissues including the immune system and is notably present in hematopoietic stem cells and various cell lines derived from lymphoid tissues. In laboratory practices scientists often assess Bcl-2 expression levels through techniques like western blotting using antibodies such as 10c4 for detection.
Biological function summary

The role of Bcl-2 extends to maintaining cell survival and balancing apoptotic signals. It functions as an anti-apoptotic molecule within the cell primarily involved in forming complexes with pro-apoptotic members of the Bcl-2 family like Bax and Bak. These interactions prevent mitochondrial membrane permeabilization which is an important step in apoptotic signal transduction. As an important regulator of apoptosis Bcl-2 helps in cellular homeostasis and appropriate immune responses under physiological conditions.

Pathways

Bcl-2 plays a critical role in the intrinsic or mitochondrial pathway of apoptosis. Within this pathway Bcl-2 interacts with other proteins such as cytochrome c and APAF-1 to inhibit apoptosis. This pathway involves a network of Bcl-2 family proteins where Bcl-2's anti-apoptotic role counteracts the pro-apoptotic activity of proteins like Bax. These interactions help fine-tune the apoptotic response to various internal stimuli maintaining cellular integrity and function.

The dysregulation of Bcl-2 expression has been implicated in cancer and autoimmune diseases. Overexpression of Bcl-2 is associated with several types of cancer including lymphomas and breast cancer where its anti-apoptotic property leads to tumor cell survival and resistance to chemotherapy. Bcl-2 also connects to disorders such as autoimmune diseases due to its regulation of cell survival with proteins like Bim playing an opposite role in promoting apoptosis. Understanding Bcl-2's functionality within these contexts is essential for developing targeted therapies.

Specifications

Form

Lyophilized

General info

Function

Suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells (PubMed : 1508712, PubMed : 8183370). Regulates cell death by controlling the mitochondrial membrane permeability (PubMed : 11368354). Appears to function in a feedback loop system with caspases (PubMed : 11368354). Inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF-1) (PubMed : 11368354). Also acts as an inhibitor of autophagy : interacts with BECN1 and AMBRA1 during non-starvation conditions and inhibits their autophagy function (PubMed : 18570871, PubMed : 20889974, PubMed : 21358617). May attenuate inflammation by impairing NLRP1-inflammasome activation, hence CASP1 activation and IL1B release (PubMed : 17418785).

Sequence similarities

Belongs to the Bcl-2 family.

Post-translational modifications

Phosphorylation/dephosphorylation on Ser-70 regulates anti-apoptotic activity (PubMed:11368354). Growth factor-stimulated phosphorylation on Ser-70 by PKC is required for the anti-apoptosis activity and occurs during the G2/M phase of the cell cycle (PubMed:11368354). In the absence of growth factors, BCL2 appears to be phosphorylated by other protein kinases such as ERKs and stress-activated kinases (PubMed:11368354). Phosphorylated by MAPK8/JNK1 at Thr-69, Ser-70 and Ser-87, which stimulates starvation-induced autophagy (PubMed:10567572, PubMed:18570871). Dephosphorylated by protein phosphatase 2A (PP2A) (By similarity).. Proteolytically cleaved by caspases during apoptosis. The cleaved protein, lacking the BH4 motif, has pro-apoptotic activity, causes the release of cytochrome c into the cytosol promoting further caspase activity.. Monoubiquitinated by PRKN, leading to an increase in its stability (PubMed:20889974). Ubiquitinated by SCF(FBXO10), leading to its degradation by the proteasome (PubMed:23431138). Ubiquitinated by XIAP, leading to its degradation by the proteasome (PubMed:29020630).

Subcellular localisation

Mitochondrion outer membrane

Product protocols

Target data

Suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells (PubMed : 1508712, PubMed : 8183370). Regulates cell death by controlling the mitochondrial membrane permeability (PubMed : 11368354). Appears to function in a feedback loop system with caspases (PubMed : 11368354). Inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF-1) (PubMed : 11368354). Also acts as an inhibitor of autophagy : interacts with BECN1 and AMBRA1 during non-starvation conditions and inhibits their autophagy function (PubMed : 18570871, PubMed : 20889974, PubMed : 21358617). May attenuate inflammation by impairing NLRP1-inflammasome activation, hence CASP1 activation and IL1B release (PubMed : 17418785).
See full target information BCL2

Product promise

We are committed to supporting your work with high-quality reagents, and we're here for you every step of the way. In the unlikely event that one of our products does not perform as expected, you're protected by our Product Promise.
For full details, please see our Terms & Conditions

Please note: All products are 'FOR RESEARCH USE ONLY. NOT FOR USE IN DIAGNOSTIC OR THERAPEUTIC PROCEDURES'.

For licensing inquiries, please contact partnerships@abcam.com