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Anti-53BP2/ASPP2/BBP Rabbit Antibody [B12C16]

Catalog No.: F3853

Application: Reactivity: Mouse, Rat, Human

Usage Information

Dilution
WB1:10000 - 1:50000 IHC1:1000

Application
WB, IHC

Reactivity
Mouse, Rat, Human

Source
Rabbit

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
126 kDa 150 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight.

Positive Control	Rat liver; Mouse liver; Human spleen; Human kidney; Human testis; MCF7; Jurkat; Saos-2
Negative Control

Datasheet & SDS

Biological Description

Specificity
53BP2/ASPP2/BBP Rabbit mAb recognizes endogenous levels of total 53BP2/ASPP2/BBP protein.

Clone
B12C16

Synonym(s)
ASPP2, BBP, TP53BP2, Apoptosis-stimulating of p53 protein 2, Bcl2-binding protein, Renal carcinoma antigen NY-REN-51, Tumor suppressor p53-binding protein 2, Bbp, 53BP2, p53-binding protein 2, p53BP2

Background
Tumor suppressor p53-binding protein 2 (TP53BP2), also known as apoptosis-stimulating protein of p53-2 (ASPP2), plays a crucial role in tumor development by modulating cellular processes through both p53-dependent and p53-independent mechanisms. The expression level of TP53BP2 is closely linked to patient prognosis and survival in various malignancies. TP53BP2 interacts with a wide range of proteins, including p53, NF-κB p65, Bcl-2, HCV core protein, PP1, YAP, CagA, RAS, PAR3, and others, thereby influencing key cellular functions. It regulates several tumor-related processes, such as cell proliferation, apoptosis, autophagy, migration, epithelial-mesenchymal transition (EMT), and drug resistance through multiple signaling pathways, including NF-κB, RAS/MAPK, mevalonate, TGF-β1, PI3K/AKT, aPKC-ι/GLI1, and autophagy-related pathways. Altered expression of tumor suppressor genes is commonly associated with cancer development, and TP53BP2 is no exception. Its expression is frequently reduced in tumors due to hypermethylation of its promoter CpG islands. TP53BP2 is the most functionally distinct member of the ASPP protein family and is notably downregulated in several cancers, including lung, gastric, and breast cancers. TP53BP2 has numerous binding partners that coordinate to regulate cellular behavior. Most of these interactions occur at its C-terminal domain; however, the N-terminal domain also engages in significant interactions. For instance, the N-terminal region of TP53BP2 binds to RAS, influencing processes such as autophagy and cellular senescence, while also enhancing p53-mediated apoptotic responses.

Background

Tumor suppressor p53-binding protein 2 (TP53BP2), also known as apoptosis-stimulating protein of p53-2 (ASPP2), plays a crucial role in tumor development by modulating cellular processes through both p53-dependent and p53-independent mechanisms. The expression level of TP53BP2 is closely linked to patient prognosis and survival in various malignancies. TP53BP2 interacts with a wide range of proteins, including p53, NF-κB p65, Bcl-2, HCV core protein, PP1, YAP, CagA, RAS, PAR3, and others, thereby influencing key cellular functions. It regulates several tumor-related processes, such as cell proliferation, apoptosis, autophagy, migration, epithelial-mesenchymal transition (EMT), and drug resistance through multiple signaling pathways, including NF-κB, RAS/MAPK, mevalonate, TGF-β1, PI3K/AKT, aPKC-ι/GLI1, and autophagy-related pathways. Altered expression of tumor suppressor genes is commonly associated with cancer development, and TP53BP2 is no exception. Its expression is frequently reduced in tumors due to hypermethylation of its promoter CpG islands. TP53BP2 is the most functionally distinct member of the ASPP protein family and is notably downregulated in several cancers, including lung, gastric, and breast cancers. TP53BP2 has numerous binding partners that coordinate to regulate cellular behavior. Most of these interactions occur at its C-terminal domain; however, the N-terminal domain also engages in significant interactions. For instance, the N-terminal region of TP53BP2 binds to RAS, influencing processes such as autophagy and cellular senescence, while also enhancing p53-mediated apoptotic responses.

References
https://pubmed.ncbi.nlm.nih.gov/37492707/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

Tel: +1-832-582-8158 Ext:3
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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%