Product Name	Bcl-2
Chinese Name	Bcl-2单克隆抗体
Alias	Apoptosis regulator Bcl 2; Apoptosis regulator Bcl2; AW986256; B cell CLL/lymphoma 2; B cell leukemia/lymphoma 2; B cell lymphoma 2; Bcl 2; Bcl-2; Bcl2; BCL2 protein; C430015F12Rik; D630044D05Rik; D830018M01Rik; Leukemia/lymphoma, B-cell, 2; Oncogene B-cell leukemia 2; BCL2_HUMAN.
Research Area	Tumour  Cardiovascular  Cell biology  Signal transduction  Apoptosis  The new supersedes the old  Mitochondrion
Immunogen Species	Mouse
Clonality	Monoclonal
Clone NO.	4D10
React Species	Mouse,  (predicted: Human, Rat, Dog, Pig, Cow, Horse, Rabbit, Sheep, Guinea Pig, )
Applications	WB=1:500-2000 ELISA=1:5000-10000 Flow-Cyt=1:100  not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user.
Theoretical molecular weight	26kDa
Cellular localization	The nucleus cytoplasmic The cell membrane Mitochondrion
Form	Liquid
Concentration	1mg/ml
immunogen	KLH conjugated synthetic peptide derived from human Bcl-2: 51-150/239
Lsotype	IgG
Purification	affinity purified by Protein G
Buffer Solution	0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
Storage	Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.
Attention	This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
PubMed	PubMed
Product Detail	The Bcl-2 gene was isolated at the chromosomal breakpoint of t(14;18)-bearing follicular B cell lymphomas(1,2).Bcl-2 blocks cell death following a variety of stimuli and confers a death-sparing effect to certain hematopoietic cell lines following growth factor withdrawal (3,5).Bcl-2 appears to function in several subcellular locations yet lacks any known motifs that would confer insight into its mechanism of action (6,7).A more recently identified protein,designated Bax p21(i.e., Bcl-associated X protein ),has extensive amino acid homology with Bcl-2 and both homodimerizes and forms heterodimers with Bcl-2(8). Overexpression of Bax accelerates apoptotic death induced by cytokine deprivation in an IL-3 dependent cell line and Bax also counters the death repressor activty of Bcl-2(8). Function: Suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. Regulates cell death by controlling the mitochondrial membrane permeability. Appears to function in a feedback loop system with caspases. 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). Subunit: Forms homodimers, and heterodimers with BAX, BAD, BAK and Bcl-X(L). Heterodimerization with BAX requires intact BH1 and BH2 motifs, and is necessary for anti-apoptotic activity. Interacts with EI24 (By similarity). Also interacts with APAF1, BBC3, BCL2L1, BNIPL, MRPL41 and TP53BP2. Binding to FKBP8 seems to target BCL2 to the mitochondria and probably interferes with the binding of BCL2 to its targets. Interacts with BAG1 in an ATP-dependent manner. Interacts with RAF1 (the 'Ser-338' and 'Ser-339' phosphorylated form). Interacts (via the BH4 domain) with EGLN3; the interaction prevents the formation of the BAX-BCL2 complex and inhibits the anti-apoptotic activity of BCL2. Interacts with G0S2; this interaction also prevents the formation of the anti-apoptotic BAX-BCL2 complex. Subcellular Location: Mitochondrion outer membrane; Single-pass membrane protein. Nucleus membrane; Single-pass membrane protein. Endoplasmic reticulum membrane; Single-pass membrane protein. Tissue Specificity: Expressed in a variety of tissues. Post-translational modifications: Phosphorylation/dephosphorylation on Ser-70 regulates anti-apoptotic activity. 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. In the absence of growth factors, BCL2 appears to be phosphorylated by other protein kinases such as ERKs and stress-activated kinases. Phosphorylated by MAPK8/JNK1 at Thr-69, Ser-70 and Ser-87, wich stimulates starvation-induced autophagy. Dephosphorylated by protein phosphatase 2A (PP2A). 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 PARK2, leading to increase its stability. DISEASE: Note=A chromosomal aberration involving BCL2 has been found in chronic lymphatic leukemia. Translocation t(14;18)(q32;q21) with immunoglobulin gene regions. BCL2 mutations found in non-Hodgkin lymphomas carrying the chromosomal translocation could be attributed to the Ig somatic hypermutation mechanism resulting in nucleotide transitions. Similarity: Belongs to the Bcl-2 family. SWISS: P49950 Gene ID: 596 Database links: Entrez Gene: 281020 Cow Entrez Gene: 596 Human Entrez Gene: 12043 Mouse Entrez Gene: 24224 Rat Omim: 151430 Human SwissProt: O02718 Cow SwissProt: P10415 Human SwissProt: P10417 Mouse SwissProt: P49950 Rat Unigene: 150749 Human Unigene: 257460 Mouse Unigene: 9996 Rat
Product Picture	Sample: Jurkat(Human) Cell Lysate at 30 ug Hela(Human) Cell Lysate at 30 ug HL60(Human) Cell Lysate at 30 ug Primary: Anti- Bcl-2 (SLM-33412M) at 1/1000 dilution Secondary: IRDye800CW Goat Anti-Mouse IgG at 1/20000 dilution Predicted band size: 26 kD Observed band size: 26 kD Blank control:Ctll-2. Primary Antibody (green line): Mouse Anti-Bcl-2 antibody (SLM-33412M) Dilution: 1:100; Secondary Antibody : Goat anti-mouse IgG-FITC Dilution: 0.5ug/Test. Protocol The cells were fixed with 4% PFA (10min at room temperature)and then permeabilized with 90% ice-cold methanol for 20 min at -20℃.The cells were then incubated in 5%BSA to block non-specific protein-protein interactions for 30 min at room temperature .Cells stained with Primary Antibody for 30 min at room temperature. The secondary antibody used for 40 min at room temperature. Acquisition of 20,000 events was performed.

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