|Vector Type||Mammalian Expression Vector|
|Expression Method||Constiutive, Stable / Transient|
|Selection In Mammalian Cells||Hygromycin|
Human influenza hemagglutinin (HA) is a surface glycoprotein required for the infectivity of the human virus. The HA tag is derived from the HA-molecule corresponding to amino acids 98-106 has been extensively used as a general epitope tag in expression vectors. Many recombinant proteins have been engineered to express the HA tag, which does not appear to interfere with the bioactivity or the biodistribution of the recombinant protein. This tag facilitates the detection, isolation, and purification of the proteins.
The actual HA tag is as follows: 5' TAC CCA TAC GAT GTT CCA GAT TAC GCT 3' or 5' TAT CCA TAT GAT GTT CCA GAT TAT GCT 3' The amino acid sequence is: YPYDVPDYA.
|小鼠 p53 基因ORF全长cDNA克隆(表达载体), C-GFPSpark 标签||MG50534-ACG|
|小鼠 p53 基因ORF全长cDNA克隆(表达载体), C-OFPSpark 标签||MG50534-ACR|
|小鼠 p53 基因ORF全长cDNA克隆(表达载体), N-GFPSpark 标签||MG50534-ANG|
|小鼠 p53 基因ORF全长cDNA克隆(表达载体), N-OFPSpark 标签||MG50534-ANR|
|小鼠 p53 基因ORF全长cDNA克隆(表达载体), C-Flag 标签||MG50534-CF|
|小鼠 p53 基因ORF全长cDNA克隆(表达载体), C-His 标签||MG50534-CH|
|小鼠 p53 基因ORF全长cDNA克隆(表达载体), C-Myc 标签||MG50534-CM|
|小鼠 p53 基因ORF全长cDNA克隆(表达载体), C-HA 标签||MG50534-CY|
|小鼠 p53 基因ORF全长cDNA(克隆载体)||MG50534-M|
|小鼠 p53 基因ORF全长cDNA克隆(表达载体), N-Flag 标签||MG50534-NF|
|小鼠 p53 基因ORF全长cDNA克隆(表达载体), N-His 标签||MG50534-NH|
|小鼠 p53 基因ORF全长cDNA克隆(表达载体), N-Myc 标签||MG50534-NM|
|小鼠 p53 基因ORF全长cDNA克隆(表达载体), N-HA 标签||MG50534-NY|
|小鼠 p53 基因ORF全长cDNA克隆(表达载体)||MG50534-UT|
p53, also known as Tp53, is a DNA-binding protein which belongs to the p53 family. It contains transcription activation, DNA-binding, and oligomerization domains. p53 protein is expressed at low level in normal cells and at a high level in a variety of transformed cell lines, where it's believed to contribute to transformation and malignancy. p53 (TP53) is a transcription factor whose protein levels and post-translational modification state alter in response to cellular stress (such as DNA damage, hypoxia, spindle damage). Activation of p53 begins through a number of mechanisms including phosphorylation by ATM, ATR, Chk1 and MAPKs. MDM2 is a ubiquitn ligase that binds p53 and targets p53 for proteasomal degradation. Phosphorylation, p14ARF and USP7 prevent MDM2-p53 interactions, leading to an increase in stable p53 tetramers in the cytoplasm. Further modifications such as methylation and acetylation lead to an increase in Tp53 binding to gene specific response elements. Tp53 regulates a large number of genes (>100 genes) that control a number of key tumor suppressing functions such as cell cycle arrest, DNA repair, senescence and apoptosis. Whilst the activation of p53 often leads to apoptosis, p53 inactivation facilitates tumor progression. It is postulated to bind to a p53-binding site and activate expression of downstream genes that inhibit growth and/or invasion, and thus function as a tumor suppressor. Mutants of p53 that frequently occur in a number of different human cancers fail to bind the consensus DNA binding site, and hence cause the loss of tumor suppressor activity. Defects in TP53 are a cause of esophageal cancer, Li-Fraumeni syndrome, lung cancer and adrenocortical carcinoma.