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GeneQ18056674· pop 6· linked from 4 articles

Also known as FEZ, ZNF312B, HH22, FEZ family zinc finger 1

FEZ family zinc finger 1 is a protein that in humans is encoded by the FEZF1 gene.

In the Vinony graph

Vinony's link graph records 4 inbound references to FEZF1, and connects out to PubMed, human chromosome 7 and Ensembl genome database project.

It is catalogued under the topic Genes on human chromosome 7.

Vinony links it to 6 Wikipedia language editions.

Gene data

FEZF1
Name
FEZ family zinc finger 1
Type
protein-coding
Position
122,301,303–122,310,735 (−)
Aliases
FEZ, HH22, ZNF312B
RefSeq RNA
NM_001024613.4, NM_001160264.3, NM_001445549.1, NM_001445550.1, NM_001445551.1
RefSeq protein
NP_001019784.2, NP_001153736.1, NP_001432478.1, NP_001432479.1, NP_001432480.1

This gene encodes a transcriptional repressor that belongs to the zinc finger double domain protein family. The encoded protein is thought to play a role in the embryonic migration of gonadotropin-releasing hormone neurons into the brain. Mutations in this gene are associated with hypogonadotropic hypogonadism-22 with anosmia. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Oct 2014].

via MyGene.info

Gene · Ensembl

FEZ family zinc finger 1

Symbol
FEZF1
Biotype
Protein coding
Organism
Homo sapiens
Location
7:122,301,303-122,310,735
Strand
Reverse (−)
Assembly
GRCh38
View on Ensembl →

via Ensembl · EMBL-EBI

Wikidata facts

Instance of
gene
Show 7 more facts
HomoloGene ID
19252
found in taxon
Homo sapiens
genomic start
122301303
genomic end
121950745
cytogenetic location
7q31.32
Sources (4)

via Wikidata · CC0

~1 min read

Encyclopedic overview

3 sections
Contents
  • Clinical significance
  • References
  • Further reading

FEZ family zinc finger 1 is a protein that in humans is encoded by the FEZF1 gene.

== Clinical significance == FEZF1 is a gene that encodes for transcriptional repressors, and it has been shown to repress the transcription factor HES5. In the mouse, FEZF1 is expressed in the forebrain in early development of the embryo. This suppression of HES5 helps to control the differentiation of neural stem cells. FEZF1 also helps to divide the caudal forebrain into three distinct parts during development: the prethalamus, the thalamus, and the pretectum. Mice lacking FEZF1 had no prethalamus and had a smaller thalamus. A loss of function mutation in FEZF1 causes Kallmann Syndrome. As axons are developing and migrating in the early embryo, FEZF1 allows the axons of olfactory neurons to attach to the central nervous system in the mice model. During neural development, GnRH neurons migrate through one of these olfactory axon pathways, and the loss of function of FEZF1 therefore results in the loss of GnRH neurons in the brain, the hallmark of Kallmann Syndrome.

Excerpted from Wikipedia’s “FEZF1” article, available under the CC BY-SA 4.0 licence.

Available in 6 languages

via Wikidata sitelinks · CC0

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