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Merck
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主要文件

GR11

Sigma-Aldrich

Anti-IGF-IR (Ab-1) Mouse mAb (αIR3)

liquid, clone αIR3, Calbiochem®

别名:

Anti-IGF-R, Anti-Insulin-Like Growth Factor Receptor, Anti-Insulin-Like Growth Factor Receptor, Anti-IGF-R

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About This Item

分類程式碼代碼:
12352203
NACRES:
NA.43

生物源

mouse

品質等級

抗體表格

purified antibody

抗體產品種類

primary antibodies

無性繁殖

αIR3, monoclonal

形狀

liquid

包含

≤0.1% sodium azide as preservative

物種活性

human

製造商/商標名

Calbiochem®

儲存條件

do not freeze

同型

IgG1

運輸包裝

wet ice

儲存溫度

2-8°C

目標翻譯後修改

unmodified

基因資訊

human ... IGF1R(3480)

相关类别

一般說明

Purified mouse monoclonal antibody generated by immunizing SJL mice with the specified immunogen and fusing splenocytes with FO mouse myeloma cells (see application references). Recognizes the ~130 kDa α and the ~90 kDa β subunits of IGF-I receptor.
Recognizes the ~130 kDa α and the ~90 kDa β subunits of IGF-I receptor.
This Anti-IGF-IR (Ab-1) Mouse mAb (αIR3) is validated for use in Immunoblotting, IF, IP, Neutralization Studies, Paraffin Sections for the detection of IGF-IR (Ab-1).

免疫原

Human
partially purified, human placenta IGF-I receptor

應用

Immunoblotting (not recommended)

Immunofluorescence (1-5 µg/ml)

Immunoprecipitation (1-2 µg/sample)

Neutralization Studies (1 µg/ml; use Cat. No. GR11L)

Paraffin Sections (not recommended)

包裝

Please refer to vial label for lot-specific concentration.

警告

Toxicity: Standard Handling (A)

外觀

In 0.05 M sodium phosphate buffer, 0.2% gelatin.

分析報告

Negative Control
HS27 cells
Positive Control
HepG2 cells

其他說明

Anti-IGF-I Receptor (Ab-1) Mouse mAb (αIR3) immunoprecipitates the α and β subunits of the IGF-I receptor. Blocks IGF-I binding to its receptor and may bind weakly to the insulin receptor. It also inhibits the growth of MCF-7 cells in culture suggesting the IGF-I receptor may be involved in autocrine regulation of cell growth (see application references). Antibody should be titrated for optimal results in indvidual systems.
Roth, R. 1988. Science239, 1269.
Rohlik, Q.T., et al. 1987. Biochem. Biophy Res. Comm.149, 276.
Rosen, O.M., 1987. Science257, 1452.
Rechler, M.M. and Nissley, S.P., 1986. Hormone Res.24, 152.
Ullrich, A., et al. 1986. EMBO J.5, 2503.
Zapf, S. and Froesch, E.R., 1986. Hormone Res.24, 121.
Humbel, R.E., 1984. I. Chemistry; in Li Hormonal proteins and peptides. Vol 12, Chap. 4 (Academic Press, New York).
Kull, F.C., et al. 1983. J. Biol. Chem.258, 6561.

法律資訊

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

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儲存類別代碼

11 - Combustible Solids

水污染物質分類(WGK)

WGK 1

閃點(°F)

Not applicable

閃點(°C)

Not applicable


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Meletios Verras et al.
Molecular endocrinology (Baltimore, Md.), 19(2), 391-398 (2004-10-30)
The androgen-signaling pathway is important for the growth and progression of prostate cancer cells. IGF-I and other polypeptide growth factors have been shown to be capable of induction of androgen receptor (AR) activation in the absence of, or at low
K Kawamoto et al.
Cancer, 85(1), 18-25 (1999-01-28)
Insulin-like growth factor-2 (IGF-2) is considered one of the autocrine growth factors in colorectal carcinoma. In addition, it is well known that IGF-2 is produced in the liver. However, the role of IGF-2 in liver metastasis is not yet understood
Daniel Chesik et al.
Journal of neurochemistry, 113(5), 1319-1330 (2010-03-30)
In multiple sclerosis (MS), oligodendrocytes in lesions are lost, leaving damaged tissue virtually devoid of these myelin-producing cells. Our group has recently demonstrated enhanced expression of insulin-like growth factor (IGF) binding protein-1 (IGFBP-1) in oligodendrocytes (CNPase(+)) localized adjacent to MS
Y T Wang et al.
Neuron, 25(3), 635-647 (2000-04-25)
Cerebellar long-term depression (LTD) is a cellular model system of information storage that may underlie certain forms of motor learning. While cerebellar LTD is expressed as a selective modification of postsynaptic AMPA receptors, this might involve changes in receptor number/distribution
C Kuhn et al.
International journal of cancer, 80(3), 431-438 (1999-02-06)
The ultraviolet B (UVB) component of sunlight causes non-melanoma skin cancers due to the damage it inflicts on genomic DNA. The response of epidermal keratinocytes to sunlight depends on the dose of UVB received and the severity of the damage

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