Rabbit Anti-Acetyl-p53 (Lys317) Polyclonal Antibody#abs130619

Rabbit Anti-Acetyl-p53 (Lys317) Polyclonal Antibody#abs130619

Please note that the price mentioned above is only for your reference. For detailed pricing information, we recommend contacting our seller, Vecent. Data Examples Western blot analysis of extracts from HeLa cells, treated with TSA 400nM 24h, using Acetyl-p53 (Lys317) Antibody. The lane on the...

Description

Catalog-specification

Delivery time

USD price

abs130619-50ug

1-2 Weeks

201

abs130619-100ug

1-2 Weeks

301

Please note that the price mentioned above is only for your reference. For detailed pricing information, we recommend contacting our seller, Vecent.


Overview

Description

The nuclear protein tumor protein p53 plays a crucial role in regulating the cell cycle, with a specific focus on the transition from G0 to G1. Its presence is usually low within normal cells, but in various transformed cell lines, it is highly expressed, which contributes to the development of malignant cells.

Other names

p53, also known as Tumor Protein 53, TRP53, or Transformation-related Protein 53, is an important cellular tumor antigen. It plays a crucial role as a tumor suppressor and is encoded by the gene TP53. Mutations in the TP53 gene are associated with various types of cancer.
Another name for p53 is Cellular Tumor Antigen p53 or CTAG p53. This phosphoprotein is involved in regulating cell cycle progression, DNA repair, and apoptosis. Its function is vital for maintaining genetic stability and preventing the development of cancer.
p53 is also referred to as FLJ92943 or LFS1. This mutant tumor protein 53 is often found in mutated forms in cancer cells, leading to the loss of its tumor-suppressing abilities. However, the normal, non-mutated p53 acts as a guardian of the genome and prevents the proliferation of cells with damaged DNA.
Identified as BCC7 or Antigen NY-CO-13, p53 has gained significant attention in cancer research due to its pivotal role in controlling cell division and suppressing tumor formation. Its activity is regulated by post-translational modifications, such as phosphorylation, acetylation, and ubiquitination.
In summary, p53 is a multifunctional protein that serves as a critical tumor suppressor. Its disruption through mutations can contribute to the development and progression of various types of cancer. Understanding the mechanisms and functions of p53 is crucial for developing targeted therapies against cancer.

Source

Rabbit

Specificity

The acetyl-p53 (Lys317) Antibody specifically recognizes the presence of total p53 protein in its acetylated form at lysine317. This antibody is capable of detecting endogenous levels of p53 protein only when acetylated at lysine317. We can ensure accurate detection and analysis of p53 protein acetylation using this highly effective antibody.

ReactivityHuman;Mouse;Rat
AntigenAcetyl-p53

Application

::1:500~1:1000, (IHC):1:50~1:500, (IF):1:200, (ELISA) ():1:20000-1:40000。

Immunogen

The antibody was created targeting a chemically synthesized peptide that originates from the acetylated region of Lys317 in the human p53 protein. This closely mimics the original peptide sequence and was used to generate the antiserum.


Properties

MW53KD

Concentration

1mg/ml


Purification

affinity purification.

Clonality

Polyclonal Antibody

Stability & Storage

It is recommended to store the product for one year at a temperature of -20 °C. To maintain its quality, avoid subjecting it to repeated freeze/thaw cycles.


Storage buffer

Phosphate buffered saline with Rabbit IgG, pH 7.4, containing 150mM NaCl, 0.02% sodium azide, and 50% glycerol can be stored at -20 °C. It remains stable for 12 months starting from the date of receipt.

Target

Background

TP53, also known as p53, acts as a crucial tumor suppressor in various types of tumors. It plays a pivotal role in regulating cell growth and can either induce growth arrest or trigger apoptosis, depending on the specific circumstances and cell type. Its primary function involves controlling a subset of genes that are essential for cell division, thus negatively regulating this process. One of the genes activated by TP53 is an inhibitor of cyclin-dependent kinases, which are critical for cell cycle progression. Furthermore, TP53 can stimulate the expression of BAX and FAS antigens to promote apoptosis or suppress the expression of Bcl-2 to initiate programmed cell death.
Additionally, TP53 collaborates with mitochondrial PPIF to activate oxidative stress-induced necrosis, independent of transcriptional regulation. It also plays a role in transcriptional regulation by inducing the expression of long intergenic non-coding RNA p21 (lincRNA-p21) and lincRNA-Mkln1. LincRNA-p21 contributes to TP53-dependent transcriptional repression, leading to apoptosis and having no effect on cell cycle regulation. TP53 is also involved in Notch signaling crossover.
In response to DNA damage, TP53 prevents cell cycle progression by inhibiting the activity of CDK7 kinase when associated with the CAK complex. Different isoforms of TP53 exert varying effects on its transactivation activity and growth suppression capabilities. For example, isoform 2 enhances the transactivation activity of isoform 1 from certain TP53-inducible promoters, while isoform 4 inhibits transactivation activity and impairs growth suppression mediated by isoform 1. Furthermore, isoform 7 inhibits isoform 1-mediated apoptosis.
Moreover, TP53 regulates the circadian clock by repressing the transcriptional activation of PER2 mediated by CLOCK-ARNTL/BMAL1.
Overall, TP53 plays a multifaceted role in tumor suppression, cell cycle regulation, apoptosis induction, and circadian rhythm modulation. Its activity is tightly regulated, and its dysregulation can have significant implications in various disease processes, particularly in cancer.

Tissue specificity

Ubiquitous. Isoforms are expressed in a wide range of normal tissues but in a tissue-dependent manner. Isoform 2 is expressed in most normal tissues but is not detected in brain, lung, prostate, muscle, fetal brain, spinal cord and fetal liver. Isoform 3 is expressed in most normal tissues but is not detected in lung, spleen, testis, fetal brain, spinal cord and fetal liver. Isoform 7 is expressed in most normal tissues but is not detected in prostate, uterus, skeletal muscle and breast. Isoform 8 is detected only in colon, bone marrow, testis, fetal brain and intestine. Isoform 9 is expressed in most normal tissues but is not detected in brain, heart, lung, fetal liver, salivary gland, breast or intestine.

Posttranslational modificationAcetylated. Acetylation of Lys-382 by CREBBP enhances transcriptional activity. Deacetylation of Lys-382 by SIRT1 impairs its ability to induce proapoptotic program and modulate cell senescence. Deacetylation by SIRT2 impairs its ability to induce transcription activation in a AKT-dependent manner.Phosphorylation on Ser residues mediates transcriptional activation. Phosphorylated by HIPK1 (By similarity). Phosphorylation at Ser-9 by HIPK4 increases repression activity on BIRC5 promoter. Phosphorylated on Thr-18 by VRK1. Phosphorylated on Ser-20 by CHEK2 in response to DNA damage, which prevents ubiquitination by MDM2. Phosphorylated on Ser-20 by PLK3 in response to reactive oxygen species (ROS), promoting p53/TP53-mediated apoptosis. Phosphorylated on Thr-55 by TAF1, which promotes MDM2-mediated degradation. Phosphorylated on Ser-33 by CDK7 in a CAK complex in response to DNA damage. Phosphorylated on Ser-46 by HIPK2 upon UV irradiation. Phosphorylation on Ser-46 is required for acetylation by CREBBP. Phosphorylated on Ser-392 following UV but not gamma irradiation. Phosphorylated on Ser-15 upon ultraviolet irradiation; which is enhanced by interaction with BANP. Phosphorylated by NUAK1 at Ser-15 and Ser-392; was initially thought to be mediated by STK11/LKB1 but it was later shown that it is indirect and that STK11/LKB1-dependent phosphorylation is probably mediated by downstream NUAK1 (PubMed:21317932). It is unclear whether AMP directly mediates phosphorylation at Ser-15. Phosphorylated on Thr-18 by isoform 1 and isoform 2 of VRK2. Phosphorylation on Thr-18 by isoform 2 of VRK2 results in a reduction in ubiquitination by MDM2 and an increase in acetylation by EP300. Stabilized by CDK5-mediated phosphorylation in response to genotoxic and oxidative stresses at Ser-15, Ser-33 and Ser-46, leading to accumulation of p53/TP53, particularly in the nucleus, thus inducing the transactivation of p53/TP53 target genes. Phosphorylated by DYRK2 at Ser-46 in response to genotoxic stress. Phosphorylated at Ser-315 and Ser-392 by CDK2 in response to DNA-damage.Dephosphorylated by PP2A-PPP2R5C holoenzyme at Thr-55. SV40 small T antigen inhibits the dephosphorylation by the AC form of PP2A.May be O-glycosylated in the C-terminal basic region. Studied in EB-1 cell line.Ubiquitinated by MDM2 and SYVN1, which leads to proteasomal degradation (PubMed:10722742, PubMed:12810724, PubMed:15340061, PubMed:17170702, PubMed:19880522). Ubiquitinated by RFWD3, which works in cooperation with MDM2 and may catalyze the formation of short polyubiquitin chains on p53/TP53 that are not targeted to the proteasome (PubMed:10722742, PubMed:12810724, PubMed:20173098). Ubiquitinated by MKRN1 at Lys-291 and Lys-292, which leads to proteasomal degradation (PubMed:19536131). Deubiquitinated by USP10, leading to its stabilization (PubMed:20096447). Ubiquitinated by TRIM24, RFFL, RNF34 and RNF125, which leads to proteasomal degradation (PubMed:19556538). Ubiquitination by TOPORS induces degradation (PubMed:19473992). Deubiquitination by USP7, leading to stabilization (PubMed:15053880). Isoform 4 is monoubiquitinated in an MDM2-independent manner (PubMed:15340061). Ubiquitinated by RFWD2, which leads to proteasomal degradation (PubMed:19837670). Ubiquitination and subsequent proteasomal degradation is negatively regulated by CCAR2 (PubMed:25732823).Monomethylated at Lys-372 by SETD7, leading to stabilization and increased transcriptional activation. Monomethylated at Lys-370 by SMYD2, leading to decreased DNA-binding activity and subsequent transcriptional regulation activity. Lys-372 monomethylation prevents interaction with SMYD2 and subsequent monomethylation at Lys-370. Dimethylated at Lys-373 by EHMT1 and EHMT2. Monomethylated at Lys-382 by KMT5A, promoting interaction with L3MBTL1 and leading to repress transcriptional activity. Dimethylation at Lys-370 and Lys-382 diminishes p53 ubiquitination, through stabilizing association with the methyl reader PHF20. Demethylation of dimethylated Lys-370 by KDM1A prevents interaction with TP53BP1 and represses TP53-mediated transcriptional activation.Sumoylated with SUMO1. Sumoylated at Lys-386 by UBC9.

Celluar localization

Cytosol;Endoplasmic reticulum;Mitochondrion;Nucleus;

UniPort

P04637


Data Examples

Western blot analysis of extracts from HeLa cells, treated with TSA 400nM 24h, using Acetyl-p53 (Lys317) Antibody. The lane on the left is treated with the synthesized peptide.


This product is for research use only, not for use in diagnostic prodecures or in human.


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