human P53 (TP53) shRNA Adenovirus
This is an pre-made gene silencing adenovirus that expresses a shRNA to knockdown human P53 (TP53) gene. The shRNA expression is driven by an U6 promoter.
The knockdown of this human gene was validated by western blot in A549 cells.
1854
Ad-h-P53 (TP53)-shRNA
Ready-to-use human P53 (TP53) shRNA Adenovirus. human P53 (TP53) shRNA adenovirus gene knockdown1854
Gene Reference Data
Alternate Names
antigen NY-CO-13; BCC7; cellular tumor antigen p53; LFS1; mutant tumor protein 53; P53; p53 tumor suppressor; phosphoprotein p53; transformation-related protein 53; TRP53; tumor protein 53; Tumor suppressor p53; tumor supressor p53
Description (eCommerce)
p53 is a tumor suppressor protein that is mutated or inactivated in over 50% of human cancers. Loss of function defects in p53 are the cause of the autosomal dominant familial cancer syndrome, Li-Fraumeni syndrome (LFS) that is characterized by the development of a diverse set of malignancies at very early ages. At the cellular level p53 is involved in the negative regulation of cell the cycle via its transactivational control of genes required for cell cycle progression. Depending on the physiological circumstance, p53 can promote growth arrest or apoptosis.
Description (Vector)
TP53 encodes tumor protein p53, which responds to diverse cellular stresses to regulate target genes that induce cell cycle arrest, apoptosis, senescence, DNA repair, or changes in metabolism. 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 is a DNA-binding protein containing transcription activation, DNA-binding, and oligomerization domains. 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. Alterations of this gene occur not only as somatic mutations in human malignancies, but also as germline mutations in some cancer-prone families with Li-Fraumeni syndrome. Multiple p53 variants due to alternative promoters and multiple alternative splicing have been found. These variants encode distinct isoforms, which can regulate p53 transcriptional activity.
Gene ID
7157
Gene Name (eCommerce)
tumor protein p53
Gene Name (Vector)
tumor protein p53
Gene Symbol
TP53
HGNC ID
HGNC:11998
NCBI Taxonomy ID (eCommerce)
9606.0
ORF Size (aa)
1182
Protein Name (eCommerce)
Cellular tumor antigen p53
RefSeq ID
NM_000546
RefSeq Synonyms
NM_001276761, NM_001276760, NM_001276699, NM_001276698, NM_001276697, NM_001276696, NM_001276695, NM_001126118, NM_001126117, NM_001126116, NM_001126115, NM_001126114, NM_001126113, NM_001126112, NM_000546, BC003596,
Research Areas
Aging,Alzheimer's Disease,Amyotrophic Lateral Sclerosis (ALS),Apoptosis,Autophagy,Bladder Cancer,Breast Cancer,Cancer,Cardiology,Cardiovascular,Cell Cycle,Chromatin Remodeling,Colorectal Cancer,DNA Damage/Repair,DNA Replication,EGFR Signaling,Gene Expression,Glioma,Helicase Activity,Histone Modification,Host-Virus Interactions,Huntington's Disease,Hypoxia,IFN Signaling,Immunology,Leukemia,LKB1 Signaling,Lung Cancer,MAPK Signaling,MicroRNAs in Cancer,Mitochondrion,Neurobiology,Neurodegeneration,Neurodevelopment,p53 Signaling,Parkinson's Disease,PI3K/Akt Signaling,Prostate Cancer,Replication,RNA Binding,Signal Transduction,TGF-beta Signaling,Transcription Factor/Regulator,Transcriptional Misregulation in Cancer,Tumor Suppressors/Oncoproteins,Viral Carcinogenesis,Wnt Signaling
Research Areas (Faceted)
cancer,cardiovascular,cell_biology,cell_cycle,developmental_biology,genetics,immunology,infectious_disease,neurobiology,signal_transduction,transcription_translation
Species
human
Target Sentence
p53 is a tumor suppressor protein that is mutated or inactivated in over 50% of human cancers. Loss of function defects in p53 are the cause of the autosomal dominant familial cancer syndrome, Li-Fraumeni syndrome (LFS) that is characterized by the development of a diverse set of malignancies at very early ages. At the cellular level p53 is involved in the negative regulation of cell the cycle via its transactivational control of genes required for cell cycle progression. Depending on the physiological circumstance, p53 can promote growth arrest or apoptosis.
UniGene ID
Hs.654481
UniProt ID (eCommerce)
P04637
Related Citations
- Notch signaling enhances stemness by regulating metabolic pathways through modifying p53, NF-kB, and HIF-1a. H Moriyama, etc, (2018), Stem Cells and Development
- Use of p53-Silenced Endothelial Progenitor Cells to Treat Ischemia in Diabetic Peripheral Vascular Disease. Kundu N, etc, (2017), Journal of the American Heart Association
- The p53 tumor suppressor protein protects against chemotherapeutic stress and apoptosis in human medulloblastoma cells. Waye S, etc, (2015), AGING
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About Storage Conditions
All our viral products should be kept at -80°C. At this temperature, the virus will remain stable for 6-12 months (and in some cases, up to 2 years). Once thawed, the product can be stored at 4°C for 2-3 weeks without significant loss of biological activity.
We recommend aliquoting your vectors into low protein binding tubes upon receipt. This helps avoid repeated freeze-thaw cycles, as well as prevent loss of virus. To maintain accurate titer, aliquot in at least 20ul per tube.