NOD1

Official Full Name

nucleotide binding oligomerization domain containing 1

Organism

Homo sapiens

GeneID

10392

Background

This gene encodes a member of the nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) family of proteins. The encoded protein plays a role in innate immunity by acting as a pattern-recognition receptor (PRR) that binds bacterial peptidoglycans and initiates inflammation. This protein has also been implicated in the immune response to viral and parasitic infection. Major structural features of this protein include an N-terminal caspase recruitment domain (CARD), a centrally located nucleotide-binding domain (NBD), and 10 tandem leucine-rich repeats (LRRs) in its C terminus. The CARD is involved in apoptotic signaling, LRRs participate in protein-protein interactions, and mutations in the NBD may affect the process of oligomerization and subsequent function of the LRR domain. Mutations in this gene are associated with asthma, inflammatory bowel disease, Behcet disease and sarcoidosis in human patients. [provided by RefSeq, Aug 2017]

Synonyms

CARD4; NLRC1; hNod1; CLR7.1;

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Detailed Information

NOD1 (also known as CARD4) and NOD2 (also known as CARD15) are the earliest intracellular pattern recognition receptors found in the NOD-like receptor family, which recognize specific molecules in peptidylglycan (PGN), which are cell wall components of bacteria. NOD1 has important physiological significance in the immunological response.

In addition to being activated by bacteria, NOD1 can also be activated by other microorganisms. Studies have shown that NOD1 can be widely expressed in respiratory epithelial cells and lung tissues of the respiratory system, and that the expression of NOD1 in the lungs is significantly up-regulated when Aspergillus fumigatus is infected, suggesting that NOD1 plays a certain role in infection with true bacteria. The hepatitis C virus (HCV) RNA-dependent RNA polymerase, NS5B, has replication activity. NS5B stimulates primary and passage liver cells to activate the NOD1 pathway, indicating that NOD1 of liver cells can recognize double-stranded RNA produced during viral replication, and mediate the production of innate immunity. Studies have shown that the NOD1/RIP2 signaling pathway in macrophages can be activated by oxidized low-density lipoprotein in a dose-dependent manner. Activation of the NOD1/RIP2 signaling pathway promotes inflammatory activation of macrophages and their phenotypic changes. This may be the main mechanism involved in the formation and development of arterial atherosclerosis. These results suggest that NOD1 can regulate the host's natural immune process and play an important role in the occurrence and development of various diseases.

NOD1

Figure 1. Model of NOD1 and NOD2 signaling cascades. (Saxena, M. , et al. 2014)

NOD1 and Diabetes

Diabetes is a systemic chronic metabolic disease with chronic hyperglycemia as the main clinical feature caused by various pathogenic factors acting on the body. Among them, insulin resistance (IR) is an important mechanism of type 2 diabetes (T2DM), which runs through the entire occurrence and development of T2DM. Wild-type mice were knocked out with the NOD1/NOD2 receptor double gene knockout, fed a high-fat diet for 16 weeks, and then evaluated for metabolic and inflammatory properties. It was discovered that diet-induced inflammation and insulin intolerance ultimately determined that NOD protein is involved in natural immunity. Acute activation of NOD protein through PGN leads to systemic IR, supporting unique bacteria that can directly cause IR through innate immunity. Therefore, NOD1 receptors can directly cause inflammation and IR. Studies on the relationship between T2DM and the intestinal flora have found that the onset of T2DM is related to intestinal flora imbalance, and its pathogenesis includes the metabolism of high fat diets caused by NOD1 receptors and subsequent metabolic diseases.

NOD1 and Tumor

Studies have confirmed that NOD1 is associated with tumors and found that NOD1 can act as a sensitizer to the TNF pathway and promote cell apoptosis. SK-BR-3 breast cancer cell line and estrogen-sensitive MCF-7 breast cancer cell line were used to construct NOD1 knockout and NOD1 overexpressing cells in vitro. It was found that NOD1 can regulate the apoptotic pathway in both cell lines. Subsequently, they confirmed that NOD1 can inhibit the production of estrogen-sensitive tumors and significantly reduce the expression of estrogen receptors in tumors. Studies in head and neck squamous cell carcinoma have found that IL-8 can promote tumor progression through the CXCR1/ 2-mediated NOD1/RIP2 signaling pathway, and similarly no significant change in NOD2.

References:

Saxena, M. , & Yeretssian, G. . (2014). Nod-like receptors: master regulators of inflammation and cancer. Frontiers in Immunology, 5.
Byndloss, Mariana X., Keestra-Gounder, Arina Marijke, B?umler, Andreas J., & Tsolis, Renée M. . Nod1 and nod2: new functions linking endoplasmic reticulum stress and inflammation. Dna & Cell Biology, dna.2016.3396.
Roberta Caruso, Neil Warner, Naohiro Inohara, & Gabriel Núñez. (2014). Nod1 and nod2: signaling, host defense, and inflammatory disease. Immunity, 41(6), 898-908.

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