1: Int J Oncol. 2004 Nov;25(5):1495-500. 

Human FOX gene family (Review).

Katoh M, Katoh M.

M&M Medical BioInformatics, Hongo 113-0033, Japan. mkatoh@ncc.go.jp

Human Forkhead-box (FOX) gene family consists of at least 43 members, including
FOXA1, FOXA2, FOXA3, FOXB1, FOXC1, FOXC2, FOXD1, FOXD2, FOXD3, FOXD4, FOXD5
(FOXD4L1), FOXD6 (FOXD4L3), FOXE1, FOXE2, FOXE3, FOXF1, FOXF2, FOXG1 (FOXG1B),
FOXH1, FOXI1, FOXJ1, FOXJ2, FOXJ3, FOXK1, FOXK2, FOXL1, FOXL2, FOXM1, FOXN1,
FOXN2 (HTLF), FOXN3 (CHES1), FOXN4, FOXN5 (FOXR1), FOXN6 (FOXR2), FOXO1
(FOXO1A), FOXO2 (FOXO6), FOXO3 (FOXO3A), FOXO4 (MLLT7), FOXP1, FOXP2, FOXP3,
FOXP4, and FOXQ1. FOXE3-FOXD2 (1p33), FOXQ1-FOXF2-FOXC1 (6p25.3), and
FOXF1-FOXC2-FOXL1 (16q24.1) loci are FOX gene clusters within the human genome.
Members of FOX subfamilies A-G, I-L and Q were grouped into class 1 FOX
proteins, while members of FOX subfamilies H and M-P were grouped into class 2
FOX proteins. C-terminal basic region within the FOX domain was the common
feature of class 1 FOX proteins. FOXH1 and FOXO1 mRNAs are expressed in human
embryonic stem (ES) cells. FOXC1, FOXC2, FOXE1, FOXE3, FOXL2, FOXN1, FOXP2 and
FOXP3 genes are mutated in human congenital disorders. FOXA1 gene is amplified
and over-expressed in esophageal and lung cancer. FOXM1 gene is up-regulated in
pancreatic cancer and basal cell carcinoma due to the transcriptional regulation
by Sonic Hedgehog (SHH) pathway. FOXO1 gene is fused to PAX3 or PAX7 genes in
rhabdomyosarcoma. FOXO3 and FOXO4 genes are fused to MLL gene in hematological
malignancies. Deregulation of FOX family genes leads to congenital disorders,
diabetes mellitus, or carcinogenesis. Expression profiles, genetic alterations
and epigenetic changes of FOX family genes as well as binding proteins and
target genes of FOX family transcription factors should be comprehensively
investigated to develop novel therapeutics and preventives for human diseases.

Publication Types:
    Review

PMID: 15492844 [PubMed - indexed for MEDLINE]


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2: Anat Rec A Discov Mol Cell Evol Biol. 2004 Jan;276(1):22-33. 

Smooth muscle stem cells.

Hirschi KK, Majesky MW.

Center for Cell and Gene Therapy, Baylor College of Medicine, Houston, Texas,
USA.

Vascular smooth muscle cells (SMCs) originate from multiple types of progenitor
cells. In the embryo, the most well studied SMC progenitor is the cardiac neural
crest stem cell. Smooth muscle differentiation in the neural crest lineage is
controlled by a combination of cell intrinsic factors, including Pax3, Tbx1,
FoxC1, and serum response factor, interacting with various extrinsic factors in
the local environment such as bone morphogenetic proteins (BMPs), Wnts,
endothelin (ET)-1, and FGF8. Additional sources of multipotential cells that
give rise to vascular SMCs in the embryo include proepicardial cells and
possibly endothelial progenitor cells. In the adult, vascular SMCs must
continually repair arterial injuries and maintain functional mass in response to
changing demands upon the vessel wall. Recent evidence suggests that this is
accomplished, in part, by recruiting multipotential vascular progenitors from
bone marrow-derived stem cells as well as from less well defined sources within
adult tissues themselves. This article will review our current understanding of
the origins of vascular SMCs from multipotential stem and progenitor cells in
developing as well as adult vasculature. Copyright 2004 Wiley-Liss, Inc.

Publication Types:
    Review
    Review, Tutorial

PMID: 14699631 [PubMed - indexed for MEDLINE]


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