Bcl-2 anticorps

N° du produit ABIN967441

Détail du produit anti-Bcl-2 anticorps

Antigène: Bcl-2 (BCL2) (B-Cell CLL/lymphoma 2 (BCL2))

Reactivité: Souris

Hôte: Hamster arménien

Clonalité: Monoclonal

Conjugué: Cet anticorp Bcl-2 est non-conjugé

Application: Western Blotting (WB), Flow Cytometry (FACS), Immunoprecipitation (IP), Immunohistochemistry (Frozen Sections) (IHC (fro)), Fluorescence Microscopy (FM)

Marque: BD Pharmingen™

Attributs du produit: 1. Since applications vary, each investigator should titrate the reagent to obtain optimal results.
2. Although hamster immunoglobulin isotypes have not been well defined, BD Biosciences Pharmingen has grouped Armenian and Syrian hamster IgG monoclonal antibodies according to their reactivity with a panel of mouse anti-hamster IgG mAbs.
3. Caution: Sodium azide yields highly toxic hydrazoic acid under acidic conditions. Dilute azide compounds in running water before discarding to avoid accumulation of potentially explosive deposits in plumbing.
4. Please refer to us for technical protocols.

Purification: The monoclonal antibody was purified from tissue culture supernatant or ascites by affinity chromatography.

Immunogène: Recombinant Mouse Bcl-2

Clone: 3F11

Isotype: IgG1

Information d'application

Indications d'application: Reported ranges for usage in western blot and IHC on frozen sections, is around 5 µg/ml. The antibody should be titrated for each application. Thymus and M1 mouse myeloma cells (ATCC TIB-192) are suggested as positive controls. For immunofluroescent staining and flow cytometry, the directly conjugated formats of this clone are recommended (Cat No. 554221 and 556537).

Commentaires:

Related Products: ABIN967311

Restrictions: For Research Use only

Stockage

Format: Liquid

Concentration: 0.5 mg/mL

Buffer: Aqueous buffered solution containing ≤0.09 % sodium azide.

Agent conservateur: Sodium azide

Précaution d'utilisation: This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.

Stock: 4 °C

Stockage commentaire: Store undiluted at 4°C.

Références pour anticorps anti-Bcl-2 (ABIN967441)

Miyashita, Krajewski, Krajewska, Wang, Lin, Liebermann, Hoffman, Reed: "Tumor suppressor p53 is a regulator of bcl-2 and bax gene expression in vitro and in vivo." dans: Oncogene, Vol. 9, Issue 6, pp. 1799-805, (1994) (PubMed).

Novack, Korsmeyer: "Bcl-2 protein expression during murine development." dans: The American journal of pathology, Vol. 145, Issue 1, pp. 61-73, (1994) (PubMed).

Veis, Sentman, Bach, Korsmeyer: "Expression of the Bcl-2 protein in murine and human thymocytes and in peripheral T lymphocytes." dans: Journal of immunology (Baltimore, Md. : 1950), Vol. 151, Issue 5, pp. 2546-54, (1993) (PubMed).

Oltvai, Milliman, Korsmeyer: "Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programmed cell death." dans: Cell, Vol. 74, Issue 4, pp. 609-19, (1993) (PubMed).

Veis, Sorenson, Shutter, Korsmeyer: "Bcl-2-deficient mice demonstrate fulminant lymphoid apoptosis, polycystic kidneys, and hypopigmented hair." dans: Cell, Vol. 75, Issue 2, pp. 229-40, (1993) (PubMed).

Hockenbery, Nuñez, Milliman, Schreiber, Korsmeyer: "Bcl-2 is an inner mitochondrial membrane protein that blocks programmed cell death." dans: Nature, Vol. 348, Issue 6299, pp. 334-6, (1991) (PubMed).

Williams: "Programmed cell death: apoptosis and oncogenesis." dans: Cell, Vol. 65, Issue 7, pp. 1097-8, (1991) (PubMed).

Reed, Tsujimoto, Alpers, Croce, Nowell: "Regulation of bcl-2 proto-oncogene expression during normal human lymphocyte proliferation." dans: Science (New York, N.Y.), Vol. 236, Issue 4806, pp. 1295-9, (1987) (PubMed).

Tsujimoto, Cossman, Jaffe, Croce: "Involvement of the bcl-2 gene in human follicular lymphoma." dans: Science (New York, N.Y.), Vol. 228, Issue 4706, pp. 1440-3, (1985) (PubMed).

Détails sur Bcl-2

Antigène: Bcl-2 (BCL2) (B-Cell CLL/lymphoma 2 (BCL2))

Autre désignation: Bcl-2 (BCL2 Produits)

Synonymes: anticorps Bcl-2, anticorps PPP1R50, anticorps bcl-2, anticorps AW986256, anticorps C430015F12Rik, anticorps D630044D05Rik, anticorps D830018M01Rik, anticorps BCL-2, anticorps Bcl2, anticorps BCL2, apoptosis regulator, anticorps B cell leukemia/lymphoma 2, anticorps B-cell CLL/lymphoma 2a, anticorps B-cell CLL/lymphoma 2 protein, anticorps BCL2, anticorps Bcl2, anticorps bcl2a, anticorps BCL-2

Sujet: Bcl-2 is considered to be novel among proto-oncogenes because it blocks apoptosis (programmed cell death) in many cell types. Apoptosis is an active form of cellular suicide that typically requires new RNA and protein synthesis and is associated with distinct morphological changes including cell shrinkage, cytoplasm membrane blebbing, nuclear fragmentation and DNA degradation. The Bcl-2 gene was first found in t(14:18) containing follicular B-cell lymphomas. A high proportion of these lymphomas contain t(14:18) chromosomal translocations involving the human Bcl-2 gene. Translocation of Bcl-2 sequences from chromosome 18 onto the transcriptionally active immunoglobulin locus at chromosome band 14q32 in B-cells deregulates Bcl-2 gene expression, resulting in high levels of Bcl-2 mRNA and protein expression. Because Bcl-2 blocks apoptosis it may contribute to tumorigenisis by prolonging cell survival rather than by accelerating the rate of cell proliferation. Mouse Bcl-2 migrates at a reduced molecular weight of ~26 kD. This antibody recognizes a 26 kD band representing the mouse p26-Bcl-2 protein. Additional minor bands at 27-31 kD and 18-21 kD may be visualized. The 27-31 kD upper band may represent a larger isoform, whereas the 18-21 kD lower band may be an internal translation or proteolytic product. 3F11 does not cross-react with human Bcl-2. For detection of human Bcl-2, refer to clone 6C8 (ABIN967311), or clone 4D7.

Poids moléculaire: 26 kDa

Pathways: Signalisation MAPK, Signalisation PI3K-Akt, Apoptose, Caspase Cascade in Apoptosis, Regulation of Muscle Cell Differentiation, Cell-Cell Junction Organization, Skeletal Muscle Fiber Development, Autophagy, Smooth Muscle Cell Migration, Negative Regulation of intrinsic apoptotic Signaling