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Merck
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主要文件

SRP3026

Sigma-Aldrich

sDLL-4 human

recombinant, expressed in HEK 293 cells, ≥95% (SDS-PAGE), ≥95% (HPLC), suitable for cell culture

别名:

Delta-like protein 4, Drosophila Delta homolog 4

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About This Item

分類程式碼代碼:
12352200
NACRES:
NA.32

生物源

human

重組細胞

expressed in HEK 293 cells

化驗

≥95% (HPLC)
≥95% (SDS-PAGE)

形狀

lyophilized

效力

>1.5 μg/mL (
)

分子量

54.0 kDa

包裝

pkg of 25 μg

技術

cell culture | mammalian: suitable

雜質

<0.1 EU/μg endotoxin, tested

顏色

white

UniProt登錄號

運輸包裝

wet ice

儲存溫度

−20°C

基因資訊

human ... DLL4(54567)

一般說明

Human sDLL4 comprises the extracellular signaling domain of DLL, a member of a structurally-related family of single-pass type I trans-membrane proteins that serve as ligands for Notch receptors. DLL4 functions to specifically activate the Notch-1 and Notch-4 receptors. The Notch signaling pathway regulates endothelial-cell differentiation, proliferation and apoptosis, and is essential for the development, maintenance and remodeling of the vascular system. Targeted deletion of the DLL4 gene in mice resulted in severe vascular defects and death before birth. Up-regulation of DLL4 expression has been implicated in the vascular development of certain tumors. Recombinant human sDLL4 is a 54.0 kDa glycoprotein containing 498 amino-acid residues. DLL4 is a membrane-bound notch ligand that belongs to the d protein family. Apart from the membrane-bound region, it consists of extracellular growth factor (EGF)-like domains and a receptor-binding DSL domain. DLL4 is selectively expressed in the endothelial cells and may act as a regulator of blood vessel biology.

生化/生理作用

Human sDLL4 comprises the extracellular signaling domain of DLL, a member of a structurally-related family of single-pass type I trans-membrane proteins that serve as ligands for Notch receptors. Recombinant human sDLL4 is a 54.0 kDa glycoprotein containing 498 amino-acid residues.

序列

SGVFQLQLQE FINERGVLAS GRPCEPGCRT FFRVCLKHFQ AVVSPGPCTF GTVSTPVLGT NSFAVRDDSS GGGRNPLQLP FNFTWPGTFS LIIEAWHAPG DDLRPEALPP DALISKIAIQ GSLAVGQNWL LDEQTSTLTR LRYSYRVICS DNYYGDNCSR LCKKRNDHFG HYVCQPDGNL SCLPGWTGEY CQQPICLSGC HEQNGYCSKP AECLCRPGWQ GRLCNECIPH NGCRHGTCST PWQCTCDEGW GGLFCDQDLN YCTHHSPCKN GATCSNSGQR SYTCTCRPGY TGVDCELELS ECDSNPCRNG GSCKDQEDGY HCLCPPGYYG LHCEHSTLSC ADSPCFNGGS CRERNQGANY ACECPPNFTG SNCEKKVDRC TSNPCANGGQ CLNRGPSRMC RCRPGFTGTY CELHVSDCAR NPCAHGGTCH DLENGLMCTC PAGFSGRRCE VRTSIDACAS SPCFNRATCY TDLSTDTFVC NCPYGFVGSR CEFPVGLP

外觀

Lyophilized from 1x PBS, pH 7.5.

重構

Centrifuge the vial prior to opening. Reconstitute in water to a concentration of 0.1-1.0 mg/ml. Do not vortex. This solution can be stored at 2-8°C for up to 1 week. For extended storage, it is recommended to further dilute in a buffer containing a carrier protein (example 0.1% BSA) and store in working aliquots at -20°C to -80°C.

儲存類別代碼

11 - Combustible Solids

水污染物質分類(WGK)

WGK 3

閃點(°F)

Not applicable

閃點(°C)

Not applicable


历史批次信息供参考:

分析证书(COA)

Lot/Batch Number

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访问文档库

Molecular cloning of delta-4, a new mouse and human Notch ligand
T Yoneya
Biochemistry, 129 (2001)
G Thurston et al.
British journal of cancer, 99(8), 1204-1209 (2008-10-02)
Tumour angiogenesis has become an important target for antitumour therapy, with most current therapies aimed at blocking the VEGF pathway. However, not all tumours are responsive to VEGF blockers, and some tumours that are responsive initially may become resistant during
Minhong Yan et al.
Clinical cancer research : an official journal of the American Association for Cancer Research, 13(24), 7243-7246 (2007-12-21)
Intense research efforts have been focused toward the identification of regulators of angiogenesis and the development of antiangiogenesis-based cancer therapies. The approval of anti-vascular endothelial growth factor (VEGF) monoclonal antibody (bevacizumab) for use in colorectal and lung cancer provides clinical
Dll4, a novel Notch ligand expressed in arterial endothelium
J R Shutter
Genes & Development, 14 (2000)
Haploinsufficiency of delta-like 4 ligand results in embryonic lethality due to major defects in arterial and vascular development
Nicholas W
Proceedings of the National Academy of Sciences of the USA (2004)

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