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Last update 08 May 2025

TP53BP2

Last update 08 May 2025

Basic Info

Synonyms

53BP2, Apoptosis-stimulating of p53 protein 2, ASPP2

+ [9]

Introduction

Regulator that plays a central role in regulation of apoptosis and cell growth via its interactions with proteins such as TP53 (PubMed:12524540). Regulates TP53 by enhancing the DNA binding and transactivation function of TP53 on the promoters of proapoptotic genes in vivo. Inhibits the ability of NAE1 to conjugate NEDD8 to CUL1, and thereby decreases NAE1 ability to induce apoptosis. Impedes cell cycle progression at G2/M. Its apoptosis-stimulating activity is inhibited by its interaction with DDX42.

Drugs associated with TP53BP2

ASPP2k-specific siRNA(Kantonsspital St. Gallen)

Target

TP53BP2

Mechanism

TP53BP2 inhibitors

Active Org.

Kantonsspital St. Gallen

Originator Org.

Kantonsspital St. Gallen

Active Indication

Triple Negative Breast Cancer

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with TP53BP2

100 Translational Medicine associated with TP53BP2

0 Patents (Medical) associated with TP53BP2

260

Literatures (Medical) associated with TP53BP2

02 Jan 2025·Current Eye Research

ASPP2 Upregulation as a Novel Approach to TGF-β2-Induced Proliferative Vitreoretinopathy In Vivo and In Vitro

Article

Author: Chen, Xiaoli ; Wang, Haiwei ; Liu, Lu ; Yue, Yankun

PURPOSEProliferative vitreoretinopathy (PVR) can cause blindness and the pathogenesis is unclear. Transforming growth factor (TGF)-β-induced epithelial-mesenchymal transition (EMT) of RPE cells is vital. P53 protein 2 (ASPP2) was previously reported to inhibit EMT in PVR rats, but the specific mechanism is unveiled.METHODSTGF-β was used to induce EMT in ARPE-19 cells, and evaluated by immunofluorescence and western blot. ARPE-19 cells were transfected with scrambled/ASPP2-lentivirus, followed by TGF-β treatment. After that, alterations of EMT and autophagy were measured by western blot and transmission electron microscopy. Moreover, TGF-β and ARPE-19 cells treated with scrambled/ASPP2-lentivirus were employed to establish the PVR model via intravitreal injection to SD rats, and retinal changes as well as EMT and autophagy activity were evaluated accordingly.RESULTSASPP2 expression was decreased during TGF-β-induced EMT in ARPE-19 cells. In vitro, EMT and autophagy was activated by TGF-β, which could be partly reversed by ASPP2 upregulation. In vivo, ASPP2 upregulation protected against structural and functional changes in PVR retinas. Additionally, expressions of EMT and autophagy markers in retinas were inhibited by ASPP2 upregulation.CONCLUSIONSASPP2 upregulation inhibited the EMT and autophagy process caused by TGF-β in ARPE-19 cells. Correspondingly, upregulation of ASPP2 alleviated intraocular fibrosis and protected visual function in PVR rats.

01 Nov 2024·The Journal of Nutritional Biochemistry

The protective effect of dulcitol on lipopolysaccharide-induced intestinal injury in piglets: mechanistic insights

Article

Author: Liang, Shiyue ; Li, Ning ; Mu, Shuqin ; Zhong, Ruqing ; Zheng, Zi ; Wang, Han ; Chen, Liang ; Han, Hui ; Yan, Jun ; Liu, Zhengqun

This study investigated the protective effect of dulcitol on LPS-induced intestinal injury in piglets and explored the underlying molecular mechanisms. A total of 108 piglets were divided into three groups: CON, LPS, and DUL. The CON and LPS groups were fed a basal diet, the DUL group was fed a diet supplementation with 500 mg/kg dulcitol. On day 29, 6 piglets in the LPS and DUL groups were injected with 100 μg/kg BW of LPS. At 4 h postchallenge, all pigs were slaughtered, and colonic samples were collected. Results showed that dulcitol supplementation boosted intestinal barrier function in LPS-challenged piglets by enhancing intestinal morphology and integrity, and increasing the gene expression of zonula occludens-1, claudin-1, and occludin in the colonic mucosa (P <0.05). Metabolomics showed DUL supplementation mainly increased (P <0.05) the metabolites related to steroid and vitamin metabolism (Cholesterol and Vitamin C). Proteomics showed that dulcitol supplementation altered the protein expression involved in maintaining barrier integrity (FN1, CADM1, and PARD3), inhibiting inflammatory response (SLP1, SFN, and IRF3), and apoptosis (including FAS, ING1, BTK, MTHFR, NOX, and P53BP2) in LPS-challenged piglets (P <0.05). Additionally, dulcitol addition also suppressed the TLR4/NF-κB signaling pathway and apoptosis in mRNA and protein levels. Dulcitol increased the abundance of short-chain fatty acid-producing bacteria (Lactobacillus, Blautia, and Faecalibacterium) at the genus level, but decreased the relative abundance of Proteobacteria at the phylum level and Pseudomonas and Delftia at the genus level in piglets (P<.05). In conclusion, these results suggested that the addition of dulcitol alleviated LPS-induced intestinal barrier injury in piglets, probably by maintaining its integrity, inhibiting the TLR4/NF-κB signaling pathways and apoptosis, and modulating the gut microbiota. Therefore, dulcitol can be considered a potential dietary additive for improving intestinal health in pig models.

01 Jun 2024·Molecular Therapy - Nucleic Acids

LNA-i-miR-221 activity in colorectal cancer: A reverse translational investigation

Article

Author: Grillone, Katia ; Tagliaferri, Pierosandro ; Tassone, Pierfrancesco ; Caridà, Giulio ; Staropoli, Nicoletta ; Ciliberto, Domenico ; Fiorillo, Lucia ; Di Martino, Maria Teresa ; Ali, Asad ; Ascrizzi, Serena

Colorectal cancer (CRC) is one of the most common malignancies and a relevant cause of cancer-related deaths worldwide. Dysregulation of microRNA (miRNA) expression has been associated with the development and progression of various cancers, including CRC. Among them, miR-221 emerged as an oncogenic driver, whose high expression is associated with poor patient prognosis. The present study was conceived to investigate the anti-CRC activity of miR-221 silencing based on early clinical data achieved from a first-in-human study by our group. Going back from bedside to bench, we demonstrated that LNA-i-miR-221 reduces cell viability, induces apoptosis in vitro, and impairs tumor growth in preclinical in vivo models of CRC. Importantly, we disclosed that miR-221 directly targets TP53BP2, which, together with TP53INP1, is known as a positive regulator of the TP53 apoptotic pathway. We found that (1) both these genes are overexpressed following miR-221 inhibition, (2) the strong anti-tumor activity of LNA-i-miR-221 was selectively observed on TP53 wild-type cells, and (3) this activity was reduced in the presence of the TP53-inhibitor Pifitrin-α. Our data pave the way to further investigations on TP53 functionality as a marker predictive of response to miR-221 silencing, which might be relevant for clinical applications.

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TP53BP2

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