CDH5

Official Full Name

cadherin 5

Organism

Homo sapiens

GeneID

1003

Background

This gene encodes a classical cadherin of the cadherin superfamily. The encoded preproprotein is proteolytically processed to generate the mature glycoprotein. This calcium-dependent cell-cell adhesion molecule is comprised of five extracellular cadherin repeats, a transmembrane region and a highly conserved cytoplasmic tail. Functioning as a classical cadherin by imparting to cells the ability to adhere in a homophilic manner, this protein plays a role in endothelial adherens junction assembly and maintenance. This gene is located in a gene cluster in a region on the long arm of chromosome 16 that is involved in loss of heterozygosity events in breast and prostate cancer. [provided by RefSeq, Nov 2015]

Synonyms

7B4; CD144;

Bio Chemical Class

Cadherin protein

Protein Sequence

MQRLMMLLATSGACLGLLAVAAVAAAGANPAQRDTHSLLPTHRRQKRDWIWNQMHIDEEKNTSLPHHVGKIKSSVSRKNAKYLLKGEYVGKVFRVDAETGDVFAIERLDRENISEYHLTAVIVDKDTGENLETPSSFTIKVHDVNDNWPVFTHRLFNASVPESSAVGTSVISVTAVDADDPTVGDHASVMYQILKGKEYFAIDNSGRIITITKSLDREKQARYEIVVEARDAQGLRGDSGTATVLVTLQDINDNFPFFTQTKYTFVVPEDTRVGTSVGSLFVEDPDEPQNRMTKYSILRGDYQDAFTIETNPAHNEGIIKPMKPLDYEYIQQYSFIVEATDPTIDLRYMSPPAGNRAQVIINITDVDEPPIFQQPFYHFQLKENQKKPLIGTVLAMDPDAARHSIGYSIRRTSDKGQFFRVTKKGDIYNEKELDREVYPWYNLTVEAKELDSTGTPTGKESIVQVHIEVLDENDNAPEFAKPYQPKVCENAVHGQLVLQISAIDKDITPRNVKFKFILNTENNFTLTDNHDNTANITVKYGQFDREHTKVHFLPVVISDNGMPSRTGTSTLTVAVCKCNEQGEFTFCEDMAAQVGVSIQAVVAILLCILTITVITLLIFLRRRLRKQARAHGKSVPEIHEQLVTYDEEGGGEMDTTSYDVSVLNSVRRGGAKPPRPALDARPSLYAQVQKPPRHAPGAHGGPGEMAAMIEVKKDEADHDGDGPPYDTLHIYGYEGSESIAESLSSLGTDSSDSDVDYDFLNDWGPRFKMLAELYGSDPREELLY

Open

Cat.No.	Product Name	Price

Cat.No.	Product Name	Price

Cat.No.	Product Name	Price

Cat.No.	Product Name	Price

Detailed Information

The CDH5 gene is located on the long arm of human chromosome 16 (16q22.1) and belongs to the cadherin superfamily. Comprising many exons and encoding a precursor protein (preproprotein) that undergoes proteolytic cleavage to generate a mature glycoprotein, the gene spans over 78 kb. Comprising five conventional extracellular cadherin repeats, a transmembrane domain, and a highly conserved cytoplasmic tail, the CDH5 protein is Its special biological activities depend on these structural elements.

By binding calcium ions, the extracellular cadherin repeats facilitate homophilic adhesion, therefore allowing selective intercellular adhesion. CDH5 interacts with proteins like α-catenin in the cytoplasm to attach to the cytoskeleton and control cell polarity by means of signal transduction.

Biological Functions

CDH5 is a core component of endothelial cell-cell adhesion. Stable junctions vital for vascular permeability and homeostasis are formed via homophilic adhesion with nearby cells. Studies have shown that CDH5 malfunction disturbs vascular barriers, hence increasing vascular leakage and aggravating inflammation and associated vascular disorders.

By means of recruiting and activating polarity protein complexes like the Par complex and signaling pathways like Rap1, CDH5 controls endothelial cell polarity and vascular lumen development. Both adult vascular homeostasis and embryonic vascular development depend on this capacity.

Moreover engaged in chromatin remodeling and gene control is CDH5. Target gene expression may be controlled and chromatin structure can be changed by CDH5 interacting with epigenetic regulators including the NuRD complex. Its functions in tumor suppression and regulation of gene expression are rooted in this mechanism.

Figure 1 illustrates how VE-cadherin regulates claudin-5 expression and endothelial barrier integrity, and how its destabilization by factors like VEGF or ROS leads to junction disruption and barrier breakdown. Figure 1. Cadherin 5 (VE-cadherin) maintains endothelial barrier integrity by regulating claudin-5 expression and junction organization, while its destabilization by factors like VEGF or ROS disrupts this balance, promoting barrier breakdown. (Gavard J, et al., 2008)

CDH5 and Disease

Breast, prostate, and lung cancers among other types of cancer have been linked to aberrant expression of the CDH5 gene. Often in tumors, the chromosomal region 16q22.1—where CDH5 resides—loses heterozygosity (LOH), therefore causing functional loss. Such gene loss is linked in breast and prostate malignancies to more tumor invasiveness and metastasis.

By weakening intercellular connections, downregulation of CDH5 protein lets cancer cells separate, infiltrate nearby tissues, and enter the lymphatic or circulatory systems, hence generating metastases. Fascinatingly, restoring CDH5 expression has been demonstrated to lower tumor cell invasiveness, hence underscoring its therapeutic target value.

Angiogenesis and vascular barrier integrity depend much on CDH5. Its malfunction has been connected to many diseases connected to blood vessels. Many times including damage to endothelium adhesion, inflammatory disorders also affect CDH5, therefore aggravating vascular leakage and inflammation. Moreover, several inherited disorders caused by CDH5 mutations cause endothelial dysfunction, therefore compromising homeostasis and vascular development.

Clinical Applications and Prospects

Strategies aiming at CDH5's expression or activity have great potential for cancer treatment as its importance in tumor development is clear. Small-molecule medicines or gene therapy methods restoring CDH5 expression, for example, might reduce cancer cell invasiveness. Moreover, creating medications aiming at CDH5-associated signaling pathways might provide fresh options for cancer therapy.

In vascular disorders, increasing CDH5 activity might help to restore vascular homeostasis and assist in the healing of vascular barriers. Correcting CDH5 mutations by gene-editing technology might help certain hereditary vascular diseases' symptoms go better. Furthermore, a fascinating future path of study is using CDH5-related molecular markers for early illness diagnosis and prognosis assessment.

Future Directions

A critical member of the traditional cadherin family, the CDH5 gene is essential for tumor suppression, vascular homeostasis, and intercellular adhesion. Diseases including cancer and vascular-related illnesses are intimately linked with its aberrant expression or malfunction. Future studies on CDH5 will provide important new perspectives on its processes in many tissues and disease environments.

Unresolved questions, including their particular functions in many physiological and pathological settings, need further research. Improved knowledge of CDH5 and its regulating systems would not only clarify the molecular foundations of disorders but also open the path for creative therapy approaches and precision medicine.

References:

Katoh M. Multi-layered prevention and treatment of chronic inflammation, organ fibrosis and cancer associated with canonical WNT/β-catenin signaling activation (Review). Int J Mol Med. 2018 Aug;42(2):713-725.
Barnhill MS, Real M, Lewis JH. Latest advances in diagnosing and predicting DILI: what was new in 2017? Expert Rev Gastroenterol Hepatol. 2018 Oct;12(10):1033-1043.
Gavard J, Gutkind JS. VE-cadherin and claudin-5: it takes two to tango. Nat Cell Biol. 2008 Aug;10(8):883-5.

Quick Inquiry

Interested in learning more?

Contact us today for a free consultation with the scientific team and discover how Creative Biogene can be a valuable resource and partner for your organization.

Request a quote today!

Inquiry