Target intelligence / Profile preview

Protein LTV1 homolog (LTV1)

Target
LTV1
Molecular classification
Other (Ribosome biogenesis factor), Ribosome assembly factor
01

Overview

Protein LTV1 homolog (LTV1) is a conserved, non-ribosomal factor essential for the biogenesis of the eukaryotic 40S ribosomal subunit[1][2][3]. LTV1 functions as an assembly factor, facilitating the incorporation of ribosomal proteins Rps3 and Rps10 during the maturation of the 40S subunit, and includes a leucine-rich nuclear export signal at its C-terminus[1][3]. LTV1 shuttles between the nucleus and cytoplasm and interacts with both ribosomal protein S3 (RpS3) and the stress-responsive chaperone Yar1[2][3]. It is not directly a therapeutic target, enzyme, or receptor, but is crucial for fundamental processes such as ribosome assembly, cell proliferation, and organogenesis, especially during embryonic development[1][3]. Loss of LTV1 function leads to defects in ribosome biogenesis, resulting in developmental abnormalities, particularly affecting the digestive system and blood cell production (hematopoiesis), and is linked to ribosomopathies in humans and animal models[1]. LTV1 deficiency alters cellular sensitivity to stress and protein synthesis inhibitors, linking ribosome assembly to environmental stress response pathways[2]. No current drugs are known to directly target LTV1, and it is not used as a biomarker or therapeutic target in clinical practice.

Other names
Protein LTV1 homologLTV1C6orf93FLJ14909dJ468K18.4IPHAK
02

Biological functions

Ribosome biogenesis (specifically, 40S small ribosomal subunit assembly)Nuclear export (shuttle protein)Regulation of cell proliferation (via its role in ribosome biogenesis)Response to cellular stress (interaction with environmental stress pathways)
03

Disease associations

Ribosomopathies (a group of diseases due to ribosome biogenesis dysfunction, characterized by developmental defects in organs such as the digestive system and hematopoietic tissues)[1]Developmental abnormalities (e.g., digestive organ hypoplasia, hematopoietic failure as shown in knockout models)[1]Potential, but not directly established, involvement in cancer or other proliferative disorders due to the centrality of ribosome biogenesis
04

Safety considerations

Essential for proper ribosome biogenesis, loss of function results in impaired cell proliferation and organ development[1][2][3]Hypoplasia and hematopoiesis failure linked to gene knockout (i.e., developmental safety concerns in models)[1]

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