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Merck
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主要文件

MAB5488

Sigma-Aldrich

Anti-CRABP2 Antibody

ascites fluid, Chemicon®

别名:

CRABPII

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About This Item

分類程式碼代碼:
12352203
eCl@ss:
32160702
NACRES:
NA.41

生物源

mouse

品質等級

抗體表格

ascites fluid

抗體產品種類

primary antibodies

無性繁殖

monoclonal

物種活性

mouse, human

製造商/商標名

Chemicon®

技術

ELISA: suitable
immunocytochemistry: suitable
western blot: suitable

同型

IgG2a

NCBI登錄號

UniProt登錄號

運輸包裝

wet ice

目標翻譯後修改

unmodified

基因資訊

human ... CRABP2(1382)

特異性

Reacts with Cellular Retinoic Acid Binding Protein II (CRABPII). No cross reactivity with CRABPI.

免疫原

Full length recombinant human CRABPII.

應用

Use Anti-CRABP2 Antibody (Mouse Monoclonal Antibody) validated in ELISA, WB, ICC to detect CRABP2 also known as Cellular Retinoic Acid Binding Protein II.

法律資訊

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

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儲存類別代碼

10 - Combustible liquids

水污染物質分類(WGK)

WGK 1

閃點(°F)

Not applicable

閃點(°C)

Not applicable


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Temporal blastemal cell gene expression analysis in the kidney reveals new Wnt and related signaling pathway genes to be essential for Wilms' tumor onset.
Maschietto, M; Trape, AP; Piccoli, FS; Ricca, TI; Dias, AA; Coudry, RA; Galante et al.
Cell Death & Disease null
L Delva et al.
Molecular and cellular biology, 19(10), 7158-7167 (1999-09-22)
Two sorts of proteins bind to, and mediate the developmental and homeostatic effects of, retinoic acid (RA): the RAR and RXR nuclear receptors, which act as ligand-dependent transcriptional regulators, and the cellular RA binding proteins (CRABPI and CRABPII). CRABPs are
Cutaneous clear cell squamous cell carcinoma in situ : clinical, histological and immunohistochemical characterization.
Munir Yahya Hussein Al-Arashi,H Randolph Byers
Journal of cutaneous pathology null
Epigenetic silencing of CRABP2 and MX1 in head and neck tumors.
Calmon MF, Rodrigues RV, Kaneto CM, Moura RP, Silva SD, Mota LD, Pinheiro DG, Torres C et al.
Neoplasia null
Shuiliang Yu et al.
Journal of experimental & clinical cancer research : CR, 41(1), 88-88 (2022-03-10)
Resistance to standard therapy is a major reason for the poor prognosis of pancreatic ductal adenocarcinoma (PDAC). Developing novel therapy to overcome PDAC drug-resistance is urgently needed. CRABP-II was highly expressed in all PDAC but not expressed in normal pancreatic

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