RANKL Lentiviral cDNA ORF Clone, Mouse, C-GFPSpark® tag

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RANKL Lentiviral cDNA ORF Clone, Mouse, C-GFPSpark® tag: 製品情報

遺伝子
Mouse
NCBI 参考シーケンス番号
遺伝子の長さ
951 bp
シーケンスの特徴
Identical with the Gene Bank Ref. ID sequence (Nucleotide may contain silent mutation without changing amino acid sequence)
製品の特徴
Full length Clone DNA of Mus musculus tumor necrosis factor (ligand) superfamily, member 11.
プラスミド
プロモーター
Enhanced CMV mammalian cell promoter
ベクター
タグシーケンス
GFPSpark Tag Sequence: GTGAGCAAGGGC……GAGCTGTACAAG
シークエンシングプライマー
pLen-F(CTCGTTTAGTGAACCGTCAGAATT), pLen-R(GAACCGGAACCCTTAAACATGT)
品質管理
The plasmid is confirmed by full-length sequencing.
スクリーニング
細菌スクリーニング抵抗力
Ampicillin
保存 & 配送
配送方法
Each tube contains 10μg lyophilized plasmid
保存条件
The lyophilized plasmid can be stored at room temperature for three months

RANKL Lentiviral cDNA ORF Clone, Mouse, C-GFPSpark® tag: 別名

Ly109l cDNA ORF Clone, Mouse; ODF cDNA ORF Clone, Mouse; OPG cDNA ORF Clone, Mouse; OPGL cDNA ORF Clone, Mouse; RANKL cDNA ORF Clone, Mouse; Trance cDNA ORF Clone, Mouse

RANKL 背景情報

Tumor necrosis factor ligand superfamily member 11, also known as Receptor activator of nuclear factor kappa-B ligand, Osteoprotegerin ligand, TNFSF11, RANKL, TRANCE, OPGL and CD254, is a single-pass type II membrane protein which belongs to the tumor necrosis factor family. The receptor activator of nuclear factor-kappaB ligand (RANKL), its cognate receptor RANK, and its natural decoy receptor osteoprotegerin have been identified as the final effector molecules of osteoclastic bone resorption. RANK and RANKL are key regulators of bone remodeling and regulate T cell/dendritic cell communications, and lymph node formation. Moreover, RANKL and RANK are expressed in mammary gland epithelial cells and control the development of a lactating mammary gland during pregnancy. Genetically, RANKL and RANK are essential for the development and activation of osteoclasts and bone loss in response to virtually all triggers tested. Inhibition of RANKL function via the natural decoy receptor osteoprotegerin (OPG, TNFRSF11B) prevents bone loss in postmenopausal osteoporosis and cancer metastases. Importantly, RANKL appears to be the pathogenetic principle that causes bone and cartilage destruction in arthritis. RANK-RANKL signaling not only activates a variety of downstream signaling pathways required for osteoclast development, but crosstalk with other signaling pathways also fine-tunes bone homeostasis both in normal physiology and disease. In addition, RANKL and RANK have essential roles in lymph node formation, establishment of the thymic microenvironment, and development of a lactating mammary gland during pregnancy.
完全な名称
tumor necrosis factor (ligand) superfamily, member 11
参考文献
  • Takayanagi H, et al. (2002) Signaling crosstalk between RANKL and interferons in osteoclast differentiation. Arthritis Res. 4 Suppl 3: S227-32.
  • Nakashima T, et al. (2003) RANKL and RANK as novel therapeutic targets for arthritis. Curr Opin Rheumatol. 15(3): 280-7.
  • Schwarz EM, et al. (2007) Clinical development of anti-RANKL therapy. Arthritis Res Ther. 9 Suppl 1: S7.
  • Leibbrandt A, et al. (2008) RANK/RANKL: regulators of immune responses and bone physiology. Ann N Y Acad Sci. 1143: 123-50.
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