Target intelligence / Profile preview

Nucleolar protein 4-like (NOL4L)

Target
NOL4L
Molecular classification
Other
01

Overview

Nucleolar protein 4-like (NOL4L) is a nuclear, predominantly nucleolar protein encoded by the human gene NOL4L (also known as C20orf112, C20orf113, among other aliases), located on chromosome 20q11.21[1][4]. It is not a classical receptor, enzyme, transporter, or known drug target. Instead, NOL4L appears to function in the nucleus, potentially interacting with chromatin and other proteins involved in gene regulation[5]. NOL4L has been identified as part of protein complexes such as those with CHD4, implicating a possible role in chromatin remodeling and transcriptional repression, possibly through effects on pathways like Notch signaling or via PI3K/AKT signaling activation in cancers[2][5]. Biologically, NOL4L promotes cell proliferation, cell cycle progression, migration, and invasion—functions strongly linked to its oncogenic role in neuroblastoma and ovarian cancer, where its overexpression correlates with tumor growth, metastasis, and poor clinical prognosis[1][2]. NOL4L was first reported in acute myeloid leukemia, and gene fusions involving NOL4L have been detected in leukemias, although its normal physiological role remains poorly characterized[4][6]. No direct interactions with drugs or established drug mechanisms are currently known. However, its emerging role in cancer progression suggests potential as a biomarker for prognosis and possibly as a future therapeutic target after further research.

Other names
C20orf112C20orf113dJ1184F4.2dJ1184F4.4DKFZP566G1424hypothetical protein LOC140688NOL4L
02

Biological functions

Cell proliferationCell cycle progressionCell migrationCell invasionPotential transcriptional regulationChromatin interaction
03

Disease associations

Cancer, specifically neuroblastomaovarian canceracute myeloid leukemiaacute lymphoblastic leukemia
04

Biomarkers

Potential prognostic biomarker for ovarian cancer (associated with poor prognosis when overexpressed)

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