CDKN2AIP

Last update 23 Jan 2025

Basic Info

Synonyms

CARF, CDKN2A interacting protein, CDKN2A-interacting protein

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Introduction

Regulates DNA damage response in a dose-dependent manner through a number of signaling pathways involved in cell proliferation, apoptosis and senescence.

100 Clinical Results associated with CDKN2AIP

100 Translational Medicine associated with CDKN2AIP

0 Patents (Medical) associated with CDKN2AIP

Literatures (Medical) associated with CDKN2AIP

01 Dec 2024·Acta Biochimica et Biophysica Sinica

CARF regulates the alternative splicing and piwi/piRNA complexes during mouse spermatogenesis through PABPC1

Article

Author: Ao, Fei ; Liu, Jie ; Wang, Shengnan ; Wang, Li ; Wei, Zexiao ; Liang, Yan ; Cao, Yuming ; Xu, Jinfeng

ADP-ribosylation factor collaborator (CARF), which is also known as CDKN2AIP, was first recognized as an ADP-ribosylation factor-interacting protein that participates in the activation of the ARF-p53-p21 (WAF1) signaling pathway under different conditions, such as oxidative and oncogenic stresses. The activation of this pathway often leads to cell growth arrest and apoptosis as well as senescence. Previous studies revealed that CARF, an RNA-binding protein, is critical for maintaining stem cell pluripotency and somatic differentiation. Nevertheless, its involvement in spermatogenesis has not been well examined. In this study, we show that male mice deficient in Carf expression present impaired spermatogenesis and fertility. IP-MS and RNA-seq analyses reveal that CARF/ Carf interacts with multiple key splicing factors, such as PABPC1, and directly targets 356 different types of mRNAs in spermatocytes. Carf-associated mRNAs display aberrant splicing patterns when Carf expression is deficient. In addition, our results demonstrate that PIWIL1 expression and localization are altered in the Carf ^{-/ -} mouse model through the downregulation of PABPC1, which further affects the ratio of pachytene-piRNA. Our study suggests that CARF is critical for regulating alternative splicing in mammalian spermatogenesis and determining infertility in male mice.

28 Oct 2024·International Journal of Biological Sciences

NR4A3 inhibits the tumor progression of hepatocellular carcinoma by inducing cell cycle G0/G1 phase arrest and upregulation of CDKN2AIP expression

Article

Author: Li, Jinjun ; Min, Xuejie ; Wang, Zhenyu ; Zhao, Fangyu ; Chen, Xiaoxia ; Chen, Taoyang ; Zhao, Xinge ; Ge, Chao ; Tian, Hua

Nuclear receptor subfamily 4 group A member 3 (NR4A3) is a member of the orphan nuclear receptor superfamily, and exhibits transcription factor activity by binding to sequence-specific DNA. Considering that the specific mechanism by which NR4A3 regulates gene transcription in HCC (hepatocellular carcinoma) has not yet been elucidated, our study aimed to explore the transcriptional role of NR4A3 in regulating the target gene CDKN2AIP (CDKN2A interacting protein), which will suppress the development of HCC. Our data show that NR4A3 is downregulated in human HCC tissues, and that low expression of NR4A3 is correlated with poor prognosis, indicating that NR4A3 could act as a tumor suppressor gene in HCC. NR4A3 overexpression suppresses cell proliferation, clone formation, cell cycle arrest at G0/G1 phase and tumor growth in vitro and in vivo and promote DNA damage. NR4A3 could directly regulate the expression of CDKN2AIP at the transcriptional level, suggesting that NR4A3 may play a role as a transcription factor in HCC and may serve as a potential biomarker for predicting prognosis for HCC patients.

01 Aug 2023·Experimental Cell Research

Stress-induced changes in CARF expression serve as a quantitative predictive measure of cell proliferation fate

Article

Author: Wadhwa, Renu ; Khurana, Mallika ; Li, Xiaoshuai ; Kalra, Rajkumar Singh ; Kaul, Sunil C ; Omar, Amr ; Chaudhary, Anupama

Discovery of CARF (Collaborator of ARF)/CDKN2AIP as an ARF-interacting protein that promotes ARF-p53-p21^WAF1 signaling and cellular senescence, initially established its role in genomic stress. Multiple reports further unraveled its role in regulation of senescence, growth arrest, apoptosis, or malignant transformation of cells in response to a variety of stress conditions in cultured human cells. It has been established as an essential protein. Whereas CARF-compromised cells undergo apoptosis, its enrichment has been recorded in a variety of cancer cells and has been associated with malignant transformation. We earlier demonstrated its role in stress-induced cell phenotypes that ranged from growth arrest, apoptosis, or malignant transformation. In the present study, we assessed the molecular mechanism of quantitative impact of change in CARF expression level on these cell fates. Stress-induced changes in CARF expression were assessed quantitatively with proteins involved in proteotoxicity, oxidative, genotoxic, and cytotoxic stress. These comparative quantitative analyses confirmed that (i) CARF responds to diverse stresses in a quantitative manner, (ii) its expression level serves as a reliable predictive measure of cell fates (iii) it correlates more with the DNA damage and MDA levels than the oxidative and proteotoxic signatures and (iv) CARF-expression based quantitative assay may be recruited for stress diagnostic applications.

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CDKN2AIP

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