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Mouse DCC Affinity Purified Polyclonal Ab (25 UG)

货号: AF844-SP 基本售价: 1378.1 元 规格: -

产品信息

概述
货号AF844-SP
别名Colorectal cancer suppressor; CRC18; CRCR1; deleted in colorectal cancer protein; deleted in colorectal carcinoma; IGDCC1colorectal tumor suppressor; Immunoglobulin superfamily DCC subclass member 1; immunoglobulin superfamily, DCC subclass, member 1; netrin receptor DCC; Tumor suppressor protein DCC
全称Deleted in Colorectal Cancer
反应种属Mouse
应用Western Blot(0.1 µg/mL)
目标/特异性Detects mouse DCC in direct ELISAs and Western blots.
使用方法Western Blot: 0.1 µg/mL
Blockade of Receptor-ligand Interaction: In a functional ELISA, 0.3-1.5 µg/mL of this antibody will block 50% of the binding of 50 ng/mL of Recombinant Chicken Netrin-2 (Catalog # 127-N2) to immobilized Recombinant Mouse DCC Fc Chimera (Catalog # 844-DC) coated at 2 µg/mL (100 µL/well). At 10 μg/mL, this antibody will block >90% of the binding.
来源Polyclonal Goat IgG
产品组分
性能
供应商R&D Systems
Entrez Gene IDs1630 (Human); 13176 (Mouse)
应用文献
R&D Systems personnel manually curate a database that contains references using R&D Systems products. The data collected includes not only links to publications in PubMed, but also provides information about sample types, species, and experimental conditions.

Neural RNA-binding protein Musashi1 controls midline crossing of precerebellar neurons through posttranscriptional regulation of Robo3/Rig-1 expression.
Authors: Kuwako K, Kakumoto K, Imai T
Neuron, 2010;67(3):407-21.
Species: Mouse
Sample Type: Tissue Homogenates
Application: WB
Netrin-4 enhances angiogenesis and neurologic outcome after cerebral ischemia.
Authors: Hoang S, Liauw J, Choi M
J. Cereb. Blood Flow Metab., 2009;29(2):385-97.
Species: Mouse
Sample Type: Whole Tissue
Application: IHC Frozen
Sonic hedgehog promotes the migration and proliferation of optic nerve oligodendrocyte precursors.
Authors: Merchan P, Bribian A, Sanchez-Camacho C, Lezameta M, Bovolenta P, De Castro F
Mol. Cell. Neurosci., 2007;36(3):355-68.
Species: Mouse
Sample Type: Whole Cells
Application: Neut
Netrin 1 mediates spinal cord oligodendrocyte precursor dispersal.
Authors: Tsai HH, Tessier-Lavigne M, Miller RH
Development, 2003;130(10):2095-105.
Species: Chicken
Sample Type: Whole Cells
Application: ICC

纯化方式Antigen Affinity-purified
免疫原S. frugiperda insect ovarian cell line Sf 21-derived recombinant mouse DCC
Phe32-Asn1097
Accession # P70211
内毒素水平<0.10 EU per 1 μg of the antibody by the LAL method.
生物活性Mouse
标记Unconjugated
溶解方法Reconstitute at 0.2 mg/mL in sterile PBS.
背景

Deleted in colorectal cancer (DCC) was originally identified as a putative tumor suppressor gene that is lost in more than 70% of colorectal cancers. This gene has also been found to be deleted in several different kinds of cancers. DCC encodes a type I transmembrane glycoprotein that belongs to the immunoglobulin (Ig) superfamily. The extracellular domain is composed of four Ig-like domains and six fibronectin type III repeats. Two forms of the protein (the long and the short isoforms) are produced from the same gene by the use of alternative initiation sites. A third isoform that is produced by alternative splicing is expressed only in the embryo. The extracellular domain of mouse DCC shares 97% and 99% amino acid sequence identity with the human and rat DCC extracellular domains, respectively. In adults, DCC is highly expressed in the brain but is also expressed at very low levels in multiple tissues. In the embryo, high levels of expression are detected in the brain and neural tube. DCC has been shown to be a receptor for the netrins that are important for axon guidance. DCC has also been shown to induce apoptosis in the absence of ligand binding and to block apoptosis when engaged by netrin-1. DCC has been shown to be a caspase substrate. The pro-apoptotic effects of DCC were found to be dependent on the proteolytic cleavage of the unoccupied receptor by caspase. It is likely that DCC functions as a tumor-suppressor gene by inducing apoptosis in cells that are not exposed to netrins.

运输条件Blue Ice
存放说明4℃
参考文献
  1. Fearon, E.R.et al. (1990) Science 247:49.
  2. Keino-Masu, K.et al. (1996) Cell 87:175.
  3. Mehlen, P.et al. (1998) Nature 395:801.
  4. Culotti, J.G. and D.C. Merz (1998) Current Opinion in Cell Biology 10:609.