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antibody from antibodies-online
Targeting: BCL2L1
Bcl-X, bcl-xL, bcl-xS, BCL2L, BCLX, PPP1R52
Western blotAntibody data
- Antibody Data
- Antigen structure
- References [10]
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- Product number
- ABIN264904 - Provider product page
- Provider
- antibodies-online
- Product name
- anti-BCL2-Like 1 (BCL2L1) antibody
- Antibody type
- Polyclonal
- Antigen
- Other
- Description
- Purified
- Reactivity
- Human
- Host
- Sheep
- Isotype
- IgG
- Vial size
- 0.1 mg
- Storage
- -20°C
- Handling
- Avoid repeated freezing and thawing.
Submitted references Bax deficiency prevents the increased cell death of immature neurons in bcl-x-deficient mice.
Identification of a novel regulatory domain in Bcl-X(L) and Bcl-2.
Apoptosis of human myeloid leukemia cells induced by an inhibitor of protein phosphatases (okadaic acid) is prevented by Bcl-2 and Bcl-X(L).
Bcl-x(L) forms an ion channel in synthetic lipid membranes.
Cytosol-to-membrane redistribution of Bax and Bcl-X(L) during apoptosis.
Bcl-xL rescues WEHI 231 B lymphocytes from oxidant-mediated death following diverse apoptotic stimuli.
Overexpression of Bcl-XL by cytotoxic drug exposure confers resistance to ionizing radiation-induced internucleosomal DNA fragmentation.
bcl-XL is the major bcl-x mRNA form expressed during murine development and its product localizes to mitochondria.
Immunohistochemical analysis of in vivo patterns of Bcl-X expression.
bcl-x, a bcl-2-related gene that functions as a dominant regulator of apoptotic cell death.
Shindler KS, Latham CB, Roth KA
The Journal of neuroscience : the official journal of the Society for Neuroscience 1997 May 1;17(9):3112-9
The Journal of neuroscience : the official journal of the Society for Neuroscience 1997 May 1;17(9):3112-9
Identification of a novel regulatory domain in Bcl-X(L) and Bcl-2.
Chang BS, Minn AJ, Muchmore SW, Fesik SW, Thompson CB
The EMBO journal 1997 Mar 3;16(5):968-77
The EMBO journal 1997 Mar 3;16(5):968-77
Apoptosis of human myeloid leukemia cells induced by an inhibitor of protein phosphatases (okadaic acid) is prevented by Bcl-2 and Bcl-X(L).
Benito A, Lerga A, Silva M, Leon J, Fernandez-Luna JL
Leukemia 1997 Jul;11(7):940-4
Leukemia 1997 Jul;11(7):940-4
Bcl-x(L) forms an ion channel in synthetic lipid membranes.
Minn AJ, Vélez P, Schendel SL, Liang H, Muchmore SW, Fesik SW, Fill M, Thompson CB
Nature 1997 Jan 23;385(6614):353-7
Nature 1997 Jan 23;385(6614):353-7
Cytosol-to-membrane redistribution of Bax and Bcl-X(L) during apoptosis.
Hsu YT, Wolter KG, Youle RJ
Proceedings of the National Academy of Sciences of the United States of America 1997 Apr 15;94(8):3668-72
Proceedings of the National Academy of Sciences of the United States of America 1997 Apr 15;94(8):3668-72
Bcl-xL rescues WEHI 231 B lymphocytes from oxidant-mediated death following diverse apoptotic stimuli.
Fang W, Rivard JJ, Ganser JA, LeBien TW, Nath KA, Mueller DL, Behrens TW
Journal of immunology (Baltimore, Md. : 1950) 1995 Jul 1;155(1):66-75
Journal of immunology (Baltimore, Md. : 1950) 1995 Jul 1;155(1):66-75
Overexpression of Bcl-XL by cytotoxic drug exposure confers resistance to ionizing radiation-induced internucleosomal DNA fragmentation.
Datta R, Manome Y, Taneja N, Boise LH, Weichselbaum R, Thompson CB, Slapak CA, Kufe D
Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research 1995 Apr;6(4):363-70
Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research 1995 Apr;6(4):363-70
bcl-XL is the major bcl-x mRNA form expressed during murine development and its product localizes to mitochondria.
González-García M, Pérez-Ballestero R, Ding L, Duan L, Boise LH, Thompson CB, Núñez G
Development (Cambridge, England) 1994 Oct;120(10):3033-42
Development (Cambridge, England) 1994 Oct;120(10):3033-42
Immunohistochemical analysis of in vivo patterns of Bcl-X expression.
Krajewski S, Krajewska M, Shabaik A, Wang HG, Irie S, Fong L, Reed JC
Cancer research 1994 Nov 1;54(21):5501-7
Cancer research 1994 Nov 1;54(21):5501-7
bcl-x, a bcl-2-related gene that functions as a dominant regulator of apoptotic cell death.
Boise LH, González-García M, Postema CE, Ding L, Lindsten T, Turka LA, Mao X, Nuñez G, Thompson CB
Cell 1993 Aug 27;74(4):597-608
Cell 1993 Aug 27;74(4):597-608
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