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Last update 23 Jan 2025

CFC1

Last update 23 Jan 2025

Basic Info

Synonyms

CFC1, cripto, FRL-1, cryptic family 1, CRYPTIC

+ [3]

Introduction

NODAL coreceptor involved in the correct establishment of the left-right axis. May play a role in mesoderm and/or neural patterning during gastrulation.

Drugs associated with CFC1

HG-1265

Target

CFC1

Mechanism

CFC1 modulators

Active Org.-

Originator Org.

Human Genome Sciences, Inc.

Active Indication-

Inactive Indication-

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with CFC1

100 Translational Medicine associated with CFC1

0 Patents (Medical) associated with CFC1

Literatures (Medical) associated with CFC1

01 Jan 2024·Advances in Experimental Medicine and Biology

Human Genetics of Ventricular Septal Defect

Article

Author: Perrot, Andreas ; Rickert-Sperling, Silke

Ventricular septal defects (VSDs) are recognized as one of the commonest congenital heart diseases (CHD), accounting for up to 40% of all cardiac malformations, and occur as isolated CHDs as well as together with other cardiac and extracardiac congenital malformations in individual patients and families. The genetic etiology of VSD is complex and extraordinarily heterogeneous. Chromosomal abnormalities such as aneuploidy and structural variations as well as rare point mutations in various genes have been reported to be associated with this cardiac defect. This includes both well-defined syndromes with known genetic cause (e.g., DiGeorge syndrome and Holt-Oram syndrome) and so far undefined syndromic forms characterized by unspecific symptoms. Mutations in genes encoding cardiac transcription factors (e.g., NKX2-5 and GATA4) and signaling molecules (e.g., CFC1) have been most frequently found in VSD cases. Moreover, new high-resolution methods such as comparative genomic hybridization enabled the discovery of a high number of different copy number variations, leading to gain or loss of chromosomal regions often containing multiple genes, in patients with VSD. In this chapter, we will describe the broad genetic heterogeneity observed in VSD patients considering recent advances in this field.

01 Jul 2022·Journal of Cellular BiochemistryQ3 · BIOLOGY

Optimization of production and characterization of a recombinant soluble human Cripto‐1 protein inhibiting self‐renewal of cancer stem cells

Q3 · BIOLOGY

Article

Author: Nawara, Hend M. ; Alam, Md Jahangir ; Saitoh, Koichi ; Salomon, David S. ; H Zahra, Maram ; Afify, Said M. ; Seno, Akimasa ; Seno, Masaharu ; Sheta, Mona ; Hassan, Ghmkin ; Mansour, Hager ; Du, Juan ; Oh, Sue Young ; Xu, Yanning ; Abu Quora, Hagar A. ; Monzur, Sadia

AbstractHuman Cripto‐1 is a member of the epidermal growth factor (EGF)‐Cripto‐FRL‐1‐Cryptic (CFC) family family and performs critical roles in cancer and various pathological and developmental processes. Recently we demonstrated that a soluble form of Cripto‐1 suppresses the self‐renewal and enhances the differentiation of cancer stem cells (CSCs). A functional form of soluble Cripto‐1 was found to be difficult to obtain because of the 12 cysteine residues in the protein which impairs the folding process. Here, we optimized the protocol for a T7 expression system, purification from inclusion bodies under denatured conditions refolding of a His‐tagged Cripto‐1 protein. A concentrations of 0.2−0.4 mM isopropyl β‐D‐1‐thiogalactopyranoside (IPTG) at 37°C was found to be the optimal concentration for Cripto‐1 expression while imidazole at 0.5 M was the optimum concentration to elute the Cripto‐1 protein from a Ni‐column in the smallest volume. Cation exchange column chromatography of the Cripto‐1 protein in the presence of 8 M urea exhibited sufficient elution profile at pH 5, which was more efficient at recovery. The recovery of the protein reached to more than 26.6% after refolding with arginine. The purified Cripto‐1 exhibited high affinity to the anti‐ALK‐4 antibody and suppressed sphere forming ability of CSCs at high dose and induced cell differentiation.

02 Nov 2021·Systems Biology in Reproductive MedicineQ4 · MEDICINE

Investigating the role ofEGF-CFCgene family in recurrent pregnancy loss through bioinformatics and molecular approaches

Q4 · MEDICINE

Article

Author: Fraga, Lucas Rosa ; Bremm, João Matheus ; Vianna, Fernanda Sales Luiz ; Boquett, Juliano André ; Silva Michels, Marcus ; Kowalski, Thayne Woycinck ; Vieira Sanseverino, Maria Teresa ; Gomes, Flávia Gobetti

Recurrent pregnancy loss (RPL) is the most common reproductive failure, reaching 1-5% of women throughout their lives, and having unknown etiology in 50% of the cases. In humans, EGF-CFC1 (Epidermal Growth Factors & Cripto/FRL-1/Cryptic) gene family is composed by TDGF1 and CFC1, two developmental genes. The aim of this study was to investigate the role of EGF-CFC on RPL. To this, multiple approaches were performed; we conducted an expression analysis of TDGF1 and CFC1 using publicly available data from Gene Omnibus Expression (GEO), systems biology analyses and functional prediction; and a molecular analysis carried out in a case-control study. Our GEO analysis showed a decrease in TDGF1 expression in the endometrium (p=0.049) and CFC1 expression in placenta (p=0.015) of women with RPL. Network analysis, gene ontology and literature pointed to a strong connection between EGF-CFC1 gene family to pathways that play key roles during pregnancy, including TGF-β, c-Src/MAPK/AKT, Notch, TNFα, IFNγ and IL-6. A pathogenicity score developed for this gene family showed that the c.-14+1429T>C (rs3806702) variant in the TDGF1 and the p.Arg47Gln (rs201431919) variant in CFC1 gene would be the ones with the highest deleterious effect for RPL. In the case-control study, which involved 149 women with RPL and 159 controls, no statistical difference was observed in the allele and genotype distributions of the variants studied in the two groups. In this study, we performed extensive bioinformatics analysis for biomarker prioritization followed by experimental validation of proposed selected markers. Although there is no statistical difference in the frequencies of these variants between RPL and controls, the expression analysis results suggest that TDGF1 and CFC1 genes might play a role in RPL. In addition, systems biology analyzes raise the hypothesis that genes in other signaling pathways that may be related to RPL as good candidates for future studies.Abbreviations RPL: recurrent pregnancy loss; EGF-CFC1: Epidermal Growth Factors - Cripto/FRL-1; GEO: Gene Omnibus Expression; KEGG: Kyoto Encyclopedia of Genes and Genomes.

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