TGFB induced factor homeobox 1
Last updated 18 Aug 2020
Meets Patient’s editorial guidelines
- DownloadDownload
- Share
- Language
- Discussion
- Audio Version
- Add to preferred sources on Google
The TGIF1 gene provides instructions for making a protein called TG-interacting factor. This protein is important for normal development of the front part of the brain (forebrain). TG-interacting factor is a transcription factor, which means that it regulates the activity of certain genes. This protein turns off genes by attaching (binding) to specific regions of DNA or by interacting with other DNA-binding proteins.
Normal function
The TGIF1 gene provides instructions for making a protein called TG-interacting factor. This protein is important for normal development of the front part of the brain (forebrain). TG-interacting factor is a transcription factor, which means that it regulates the activity of certain genes. This protein turns off genes by attaching (binding) to specific regions of DNA or by interacting with other DNA-binding proteins.
TG-interacting factor regulates signaling pathways that are important for embryonic development. This protein blocks the signals of the transforming growth factor beta (TGF-β) pathway. This signaling pathway transmits chemical signals from the cell surface to the nucleus, which allows the environment outside the cell to affect how the cell produces other proteins. TG-interacting factor also blocks a molecule called retinoic acid from regulating gene activity. Retinoic acid, a form of vitamin A, binds to a group of transcription factors that regulate a number of genes important for early development. By blocking these signaling pathways, TG-interacting factor ensures that certain genes are turned off at the proper time.
Conditions referring to this gene or chromosome
Other names
5'-TG-3' interacting factor
5'-TG-3'-interacting factor 1
homeobox protein TGIF
homeobox protein TGIF1
HPE4
MGC39747
MGC5066
TALE homeobox TG-interacting factor
TGFB-induced factor homeobox 1
TGIF
TGIF1_HUMAN
transforming growth factor-beta-induced factor
Related patient information and medicines

Patient information leaflet
Pulmonary fibrosis
Pulmonary fibrosis is a serious lung disease where the tiny air sacs of the lungs (the alveoli) and the lung tissue next to the alveoli become damaged and scarred, resulting in lung fibrosis. The main symptom is shortness of breath that gradually gets worse. The cause is often not known but pulmonary fibrosis can be caused by a variety of.

Patient information leaflet
Chorionic villus sampling
A note about DNA, genes and chromosomes In most cells of your body you have 46 chromosomes arranged in 23 pairs. 22 of the pairs are matching pairs. The 23rd pair is the sex chromosomes, which match exactly in women (who have two X chromosomes) but not in men (who have one X and one Y). One chromosome from each pair comes from your mother and one.

Patient information leaflet
Thrombophilia
The body has a natural clotting process in the blood, which is altered in thrombophilia. The normal clotting process is called haemostasis. Thrombophilia refers to a group of conditions where the blood clots more easily than normal. This can lead to unwanted blood clots (called thromboses) forming within blood vessels. These blood clots can cause.

Patient information leaflet
Type 1 diabetes
Type 1 diabetes is the type of diabetes that typically develops in children and in young adults. In type 1 diabetes the body stops making insulin and the blood sugar (glucose) level goes very high. Treatment to control the blood glucose level is with insulin injections and a healthy diet. They include reducing blood pressure if it is high and.

Patient information leaflet
Ankylosing spondylitis
The type of inflammation in AS causes the affected joints to join together, therefore reducing mobility. Ankylosing spondylitis is an auto-immune disease. It is not known exactly why ankylosing spondylitis occurs but there is a genetic predisposition. 6 out of 100 people who have a particular gene variant called HLA-B27 have ankylosing spondylitis.

Patient information leaflet
Antiphospholipid syndrome
Antiphospholipid syndrome (APS) - also called Hughes' syndrome - makes blood more likely than normal to clot (a thrombophilia ). This increases the risk of developing blood clots (called thromboses) within blood vessels. APS can cause disability, serious illness and even death in a pregnant woman or her unborn baby if untreated. Unfortunately, it.
Further reading and references
- TGFB induced factor homeobox 1; MedlinePlus, National Library of Medicine.
- Aguilella C, Dubourg C, Attia-Sobol J, Vigneron J, Blayau M, Pasquier L, Lazaro L, Odent S, David V. Molecular screening of the TGIF gene in holoprosencephaly: identification of two novel mutations. Hum Genet. 2003 Feb;112(2):131-4. doi: 10.1007/s00439-002-0862-8. Epub 2002 Nov 21.
- Dubourg C, Bendavid C, Pasquier L, Henry C, Odent S, David V. Holoprosencephaly. Orphanet J Rare Dis. 2007 Feb 2;2:8. doi: 10.1186/1750-1172-2-8.
- El-Jaick KB, Powers SE, Bartholin L, Myers KR, Hahn J, Orioli IM, Ouspenskaia M, Lacbawan F, Roessler E, Wotton D, Muenke M. Functional analysis of mutations in TGIF associated with holoprosencephaly. Mol Genet Metab. 2007 Jan;90(1):97-111. doi: 10.1016/j.ymgme.2006.07.011. Epub 2006 Sep 7.
- Gripp KW, Wotton D, Edwards MC, Roessler E, Ades L, Meinecke P, Richieri-Costa A, Zackai EH, Massague J, Muenke M, Elledge SJ. Mutations in TGIF cause holoprosencephaly and link NODAL signalling to human neural axis determination. Nat Genet. 2000 Jun;25(2):205-8. doi: 10.1038/76074.
- Roessler E, Muenke M. The molecular genetics of holoprosencephaly. Am J Med Genet C Semin Med Genet. 2010 Feb 15;154C(1):52-61. doi: 10.1002/ajmg.c.30236.
- Solomon BD, Mercier S, Velez JI, Pineda-Alvarez DE, Wyllie A, Zhou N, Dubourg C, David V, Odent S, Roessler E, Muenke M. Analysis of genotype-phenotype correlations in human holoprosencephaly. Am J Med Genet C Semin Med Genet. 2010 Feb 15;154C(1):133-41. doi: 10.1002/ajmg.c.30240.
- Tekendo-Ngongang C, Muenke M, Kruszka P. Holoprosencephaly Overview. 2000 Dec 27 [updated 2026 Jun 9]. In: Adam MP, Bick S, Mirzaa GM, Wallace SE, Amemiya A, editors. GeneReviews(R) [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2026. Available from http://www.ncbi.nlm.nih.gov/books/NBK1530/
Join the conversation
Share your thoughts or experiences with others in our patient communities.

Ask, share, connect.
Browse discussions, ask questions, and share experiences across hundreds of health topics.
Sign up to the Patient newsletter
Your weekly dose of clear, trustworthy health advice - written to help you feel informed, confident and in control.
By subscribing you accept our Privacy Policy. You can unsubscribe at any time. We never sell your data.