DLX4: Difference between revisions
CSV import |
CSV import Tags: mobile edit mobile web edit |
||
| Line 28: | Line 28: | ||
[[Category:Homeobox genes]] | [[Category:Homeobox genes]] | ||
{{medicine-stub}} | {{medicine-stub}} | ||
{{No image}} | |||
{{No image}} | {{No image}} | ||
Revision as of 13:04, 10 February 2025
DLX4 is a gene that encodes a member of the Distal-less (Dlx) gene family. The Dlx gene family is involved in embryonic development and primarily regulates the formation of craniofacial structures. The DLX4 gene is located on chromosome 17 in humans and is expressed in a variety of tissues, including the placenta and bone marrow.
Function
The DLX4 gene is a homeobox gene, which means it encodes a protein that binds to specific DNA sequences and regulates the activity of other genes. The protein encoded by the DLX4 gene is a transcription factor, which means it helps control the process of converting, or transcribing, DNA into RNA.
In particular, the DLX4 protein is thought to play a role in the development of the placenta during pregnancy. It may also be involved in the regulation of hematopoiesis, the process by which the body produces new blood cells.
Clinical Significance
Alterations in the DLX4 gene have been associated with a variety of health conditions. For example, overexpression of DLX4 has been observed in several types of cancer, including breast cancer and ovarian cancer. This overexpression may contribute to the growth and spread of cancer cells.
In addition, mutations in the DLX4 gene have been linked to pre-eclampsia, a potentially serious condition that can occur during pregnancy. Pre-eclampsia is characterized by high blood pressure and damage to organs such as the liver and kidneys.
Research
Research into the DLX4 gene and its associated protein is ongoing. Scientists are particularly interested in understanding how alterations in the DLX4 gene contribute to the development of cancer and other diseases. This research could potentially lead to new treatments for these conditions.
See Also
References
<references />
