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BCL2 antibody (B-Cell CLL/lymphoma 2) (AA 61-76)

Details for Product anti-BCL2 Antibody No. ABIN371613, Supplier: Login to see
Antigen
  • AW986256
  • Bcl-2
  • C430015F12Rik
  • D630044D05Rik
  • D830018M01Rik
  • PPP1R50
  • BCL-2
  • bcl-2
  • Bcl2
Alternatives
anti-Mouse (Murine) BCL2 antibody for Immunohistochemistry (Frozen Sections)
Epitope
AA 61-76
78
74
54
50
49
44
23
23
17
17
14
14
14
13
13
13
13
12
11
8
7
4
4
4
3
3
3
3
3
3
2
2
2
2
2
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
Reactivity
Mouse (Murine), Rat (Rattus)
681
199
149
17
9
7
4
3
2
2
1
1
Host
Mouse
498
241
20
6
2
2
2
Clonality (Clone)
Monoclonal ()
Conjugate
This BCL2 antibody is un-conjugated
37
33
27
24
18
14
11
10
8
6
6
6
6
6
6
3
1
1
1
1
Application
Enzyme Immunoassay (EIA), Western Blotting (WB)
485
275
241
145
139
136
118
68
49
42
36
11
10
9
8
8
5
1
1
1
1
1
Supplier
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Immunogen KLH-conjugated peptide corresponding to 61-76 amino acid sequence of murine Bcl-2. (Ref. 1)
Clone 10C2
Isotype IgG1
Specificity This antibody reacts with Bcl-2 (Mr. 26 kDa). The monoclonal antibody 10C2 reacts with an epitope between amino acids 61-76 of Mouse Bcl-2. The antibody also reacts with Rat Bcl-2 (Ref.1,14).
Characteristics Synonyms: BCL2, Bcl-2 alpha, Apoptosis regulator Bcl-2, B-Cell CLL/lymphoma 2
Purification Purified
Alternative Name Bcl-2 (BCL2 Antibody Abstract)
Background Bcl-2 is a 26 kDa member of the family of proteins involved in regulation of programmed cell death, or apoptosis. It is expressed in a variety of both normal and neoplastic tissues and appears to be membranebound since it is detectable in crude membrane and nuclear fractions, but not in the soluble fraction of cell lysates. Overexpression of Bcl-2 can prevent apoptosis, while formation of heterodimers with Bax, another Bcl-2-related protein, inhibits Bcl-2's ability to promote cell survival. Apoptosis, or programmed cell death, is a well-documented phenomenon in many cellular systems. (Ref.2) It plays a key role in tissue and organ development as well as in adult tissues during cell turnover. Apoptosis can be induced by a variety of internal and external stimuli including growth factor deprivation, cytokine treatment, antigen-receptor engagement, cell-cell interactions, irradiation and glucocorticoid treatment. (Ref.3) Bcl-2 is a widely studied protein that has been shown to be a potent inhibitor of programmed cell death. It has been localized to the outer mitochondrial membrane, perinuclear membrane, and endoplasmic reticulum. Bcl-2 is expressed in memory and resting, or other long-lived lymphoid cells, follicular mantle cells, medullary thymocytes, and lymphomas. Germical center cells and cortical thymocytes are negative for Bcl-2. Upregulation of Bcl-2 prevents or delays apoptosis induced by a variety of stimuli, including growth factor deprivation, gamma-irradiation, glucocorticoids, and chemotherapeutic agents. During lymphoid development, expression of the Bcl-2 protein appears to be regulated in a stage-specific manner, and is thought to be a survival signal for positive selection.Synonyms: Apoptosis regulator Bcl-2, B-Cell CLL/lymphoma 2, BCL2, Bcl-2 alpha
UniProt P10417
Research Area Cancer, Apoptosis/Necrosis
Pathways MAPK Signaling, PI3K-Akt Signaling, Apoptosis, Caspase Cascade in Apoptosis
Application Notes ELISA. Western Blot: < / = 1 μg/mL.
Other applications not tested.
Optimal dilutions are dependent on conditions and should be determined by the user.
Restrictions For Research Use only
Concentration 0.1 mg/mL
Buffer 100 mM Borate buffered saline, pH 8.2 without preservatives or amine-containing buffer salts.
Preservative Without preservative
Storage 4 °C
Storage Comment Store the antibody undiluted at 2-8 °C.
Shelf life: one year from despatch.
Expiry Date 12 months
Background publications Gottschalk, Boise, Oltvai et al.: "The ability of Bcl-x(L) and Bcl-2 to prevent apoptosis can be differentially regulated." in: Cell death and differentiation, Vol. 3, Issue 1, pp. 113-8, 2006 (PubMed).

Nuñez, Clarke: "The Bcl-2 family of proteins: regulators of cell death and survival." in: Trends in cell biology, Vol. 4, Issue 11, pp. 399-403, 2004 (PubMed).

Hsu, Youle: "Nonionic detergents induce dimerization among members of the Bcl-2 family." in: The Journal of biological chemistry, Vol. 272, Issue 21, pp. 13829-34, 1997 (PubMed).

Cheng, Levine, Boise et al.: "Bax-independent inhibition of apoptosis by Bcl-XL." in: Nature, Vol. 379, Issue 6565, pp. 554-6, 1996 (PubMed).

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

Yin, Oltvai, Korsmeyer: "BH1 and BH2 domains of Bcl-2 are required for inhibition of apoptosis and heterodimerization with Bax." in: Nature, Vol. 369, Issue 6478, pp. 321-3, 1994 (PubMed).

Shimizu, Eguchi, Kosaka et al.: "Prevention of hypoxia-induced cell death by Bcl-2 and Bcl-xL." in: Nature, Vol. 374, Issue 6525, pp. 811-3, 1995 (PubMed).

Kiefer, Brauer, Powers et al.: "Modulation of apoptosis by the widely distributed Bcl-2 homologue Bak." in: Nature, Vol. 374, Issue 6524, pp. 736-9, 1995 (PubMed).

Chittenden, Harrington, OConnor et al.: "Induction of apoptosis by the Bcl-2 homologue Bak." in: Nature, Vol. 374, Issue 6524, pp. 733-6, 1995 (PubMed).

Farrow, White, Martinou et al.: "Cloning of a bcl-2 homologue by interaction with adenovirus E1B 19K." in: Nature, Vol. 374, Issue 6524, pp. 731-3, 1995 (PubMed).

Cory: "Regulation of lymphocyte survival by the bcl-2 gene family." in: Annual review of immunology, Vol. 13, pp. 513-43, 1995 (PubMed).

Cohen: "Programmed cell death in the immune system." in: Advances in immunology, Vol. 50, pp. 55-85, 1991 (PubMed).