Target Name: CDKN2A
NCBI ID: G1029
Other Name(s): INK4A, p19, ARF
Drug Target Analysis Report Drug Target Analysis Report Content

About the Target

Based on the provided context information, here is a comprehensive summary of key viewpoints related to CDKN2A:

CDKN2A plays a crucial role in preventing senescence entry. Targeting CDKN2A with a specific mutation prevents senescence and increases the proliferative capacity of cells [1].

The transcriptional factors Smads, DMP1alpha, E2Fs, MYC, and FoxO activate ARF transcription, while E2F3b, Ezh2/Twist-1, CBX7, TBX2, BMI-1, and EGFR suppress ARF transcription. TGFbeta1 negatively regulates ARF transcription [2].

ARF function, stability, and localization are regulated by phosphorylation, ubiquitination, protein-protein interactions (PPIs), and chaperone-mediated autophagy (CMA). Various proteins, including PKCalpha, MKRN1, Siva1, ULF1, USP10, PANO, NPM, TBP-1, REG-gamma, and MDM2, regulate ARF through these mechanisms [3].

The CD47/NF-kB pathway plays a role in regulating UHRF1 and p16INK4A expression. CD47 activation induces the translocation of the active NF-kB complex, leading to UHRF1 gene activation and p16INK4A repression, promoting cell proliferation. Blocking CD47 function inhibits NF-kB transactivation, resulting in decreased cell proliferation via p16INK4A reactivation [4].

In carcinoids, CDK4/6 complex and CCND1 drive cell cycle progression, while in carcinomas, CDKN2A is upregulated, resulting in downregulation of these cell cycle mediators. Carcinomas instead rely on CDK2 and CCNE1 for cell cycle progression. Carcinomas also exhibit elevated expression of the anti-apoptotic protein BCL2, leading to apoptosis insensitivity [5].

Please note that the viewpoints have been summarized and merged from the provided context information without using any prior knowledge.
Based on the provided context, we can summarize some key viewpoints regarding the effect of p19 on the level of DCL1 and AGO2 during Cymbidium ringspot virus (CymRSV) infection:

Effect of p19 on the level of DCL1:
- In the presence of p19, the expression of DCL1 is increased during CymRSV infection through the high-affinity binding of NbmiR162 [6].
- This increased expression of DCL1 leads to an elevation in the expression of miRNAs, including miR168, which may act provirally [6].
- High levels of DCL1 suggestedly downregulate DCL4 expression, while the levels of DCL2 remain unaffected [6].
- The p19 protein not only enhances miR168-mediated restriction of AGO1 expression by inducing miR168 accumulation but also reduces the association of miR168 with its target [6].
- In the absence of p19, miR162 downregulates the expression of DCL1, resulting in low levels of miRNA expression and higher levels of DCL4 [6].

Effect of p19 on the level of AGO2:
- p19 increases the expression of AGO2 by binding to NbmiR403 during CymRSV infection [6].
- However, in the absence of p19, the level of AGO2 remains unaffected [6].

In summary, p19 plays a significant role in modulating the levels of DCL1 and AGO2 during CymRSV infection. It enhances the expression of DCL1, leading to increased miRNA expression, while also promoting miR168-mediated restriction of AGO1 expression. Additionally, p19 increases the expression of AGO2. These findings provide insights into the intricate interactions between viral proteins and host factors during CymRSV infection [6].

Figure [1]

Figure [2]

Figure [3]

Figure [4]

Figure [5]

Figure [6]

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