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Updated: Feb 6, 2026

An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis

Published on: February 8, 2019

Nuclear Folate Metabolism.

Martha S Field¹, Elena Kamynina¹, James Chon²

¹Division of Nutritional Sciences, Cornell University, Ithaca, New York 14853, USA;

Annual Review of Nutrition

|August 22, 2018

Summary

This summary is machine-generated.

Folate deficiency increases disease risk, but the exact biochemical link is unclear. Nuclear thymidylate synthesis impacts genome stability and is crucial for understanding folate-related pathologies.

Keywords:

DNA synthesis folate neural tube defects replitase thymidylate

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Area of Science:

Biochemistry
Molecular Biology
Genetics

Background:

Folate deficiency is linked to human pathologies and birth defects.
The precise biochemical pathways connecting folate to disease etiology are not fully understood.
Nuclear thymidylate synthesis plays a role in DNA replication and repair.

Purpose of the Study:

To elucidate the causal biochemical pathway linking folate to disease and birth defect etiology.
To understand the roles and regulation of nuclear de novo thymidylate synthesis.
To explore the relationship between nuclear thymidylate synthesis, genome stability, and one-carbon metabolism.

Main Methods:

Investigating the translocation of de novo and salvage pathways for thymidylate synthesis to the nucleus.
Analyzing the association of these pathways with DNA replication and repair machinery.
Examining impairments in nuclear de novo thymidylate synthesis in pathologies related to one-carbon metabolism.

Main Results:

Nuclear translocation of thymidylate synthesis pathways limits uracil misincorporation into DNA.
Impairments in nuclear de novo thymidylate synthesis are observed in various pathologies.
These impairments are linked to disruptions in one-carbon metabolism.

Conclusions:

Understanding nuclear de novo thymidylate synthesis is key to understanding folate-related diseases.
The regulation of this pathway is critical for maintaining genome stability.
Further research will illuminate mechanisms underlying folate- and vitamin B12-associated pathologies.