# FOLATE BINDERS IN HEMATOPOIESIS & CELL REPLICATION

> **NIH NIH R01** · SUNY DOWNSTATE MEDICAL CENTER · 1992 · $159,226

## Abstract

A number of human diseases have been described which are not
due to a quantitative deficiency of folic acid but which may
respond to large doses of the vitamin.  These include
hematopoietic disorders, such as some forms of aplastic anemia, a
hereditary form of dyserythropoiesis, neurologic disorders such as
dementia, some forms of schizophrenia, the recently recognized
fragile X chromosome syndrome, and drug induced disorders of
folate metabosism.  The response to large doses of folate suggests
that a common defect may underlie these disorders.  The folate
binding proteins (FBPs) which have now been identified in the
membrane, in the soluble, and most recently in the nuclear
fraction of mammalian cells could be the common link.  Most of
the work on these proteins from mammalian cells have focused on
their structural properties rather than on their function and
turnover in the cell.  In addition, there have been no studies on
the molecular genetics of the FBP to characterize the structure,
organization and expression of the gene.

The primary aims of this project, therefore, are to establish the
precise function(s) of the folate binding proteins (FBPs) in the
cellular uptake and intracellular metabolism of folate and to
characterize fully the molecular genetics of this protein(s).  The
experiments will be designed to achieve the following objectives:
1) define the kinetics for the synthesis and degradation of the FBP
in human KB cells and study the factors that affect these
parameters using intrinsic labeling with (35S)methionine 2) map
the cellular and topographic distribution of the FBP in the KB cell
using electron microscopy immunocytology and study the factors
that modify this distribution using monoclonal antibodies 3) clone
the FBP gene from KB cells and then characterize its
organization and nucleotide sequence, determine its chromosomal
location, and examine different human cell lines and tissues for
expression and restriction fragment length polymorphism of the
gene 4) determine if transfection of the functional FBP gene into
cells which express little or no FBP improves the viability of
these cells in folate deficient medium.  The study could provide
definitive evidence that the FBP provides a critical function in
cellular metabolism.

## Key facts

- **NIH application ID:** 3170326
- **Project number:** 5R01CA032369-10
- **Recipient organization:** SUNY DOWNSTATE MEDICAL CENTER
- **SAM.gov UEI:** NJ14V2NZYM68
- **Principal Investigator:** SHELDON P ROTHENBERG
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1992
- **Award amount:** $159,226
- **Award type:** 5
- **Project period:** 1982-05-01 → 1993-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3170326

## Citation

> US National Institutes of Health, RePORTER application 3170326, FOLATE BINDERS IN HEMATOPOIESIS & CELL REPLICATION (5R01CA032369-10). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3170326. Licensed CC0.

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