DCBLD1

Official Full Name

discoidin, CUB and LCCL domain containing 1

Organism

Homo sapiens

GeneID

285761

Background

Predicted to enable signaling receptor activity. Predicted to be located in membrane. Predicted to be active in plasma membrane. [provided by Alliance of Genome Resources, Feb 2025]

Synonyms

dJ94G16.1;

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Detailed Information

The DCBLD1 (Discoidin, CUB and LCCL domain-containing 1) gene is an emerging player in the field of molecular biology and cell signaling.

Structure And Domain Organization of DCBLD1

The DCBLD1 gene encodes a protein of approximately 600-700 amino acids in length, with a molecular weight of around 70-80 kDa. The primary sequence of DCBLD1 shares significant similarities with other proteins containing discoidin, CUB, and LCCL domains. The discoidin domain is characterized by a beta-sandwich structure, while the CUB domain exhibits a cysteine-rich structure. The LCCL domain, on the other hand, is an alpha/beta-hybrid structure. The discoidin domain is responsible for the protein's receptor-like activity, while the CUB domain facilitates cell adhesion and plays a role in signal transduction. The LCCL domain is involved in protein-protein interactions and cell-cell contacts.

DCBLD1 And Immunoregulation

DCBLD1 is a gene that plays a crucial role in immune regulation. The function of DCBLD1 in immune regulation becomes apparent in its role as a regulator of T cell activation. It has been demonstrated that DCBLD1 interacts with the T cell receptor (TCR) and modulates the signaling pathways leading to T cell activation. By doing so, DCBLD1 helps to control the immune response, ensuring that it remains balanced and targeted against actual pathogens. Furthermore, DCBLD1 is involved in the regulation of dendritic cells (DCs), which are key players in the immune system. It has been shown that DCBLD1 influences the maturation and function of DCs, thereby shaping the immune response. DCBLD1-deficient mice, for example, exhibit defects in DC maturation and function, leading to impaired immune responses. DCBLD1 is a gene that participate in immune regulation by controlling T cell activation and DC function. Its importance in maintaining a balanced and effective immune response makes it a target of interest for research on immune-mediated diseases, where dysregulated immune responses can lead to inflammation and tissue damage.

DCBLD1 And Cancer

DCBLD1 is a gene that has recently gained attention for its potential role in the development of cancer. This gene encodes a protein with diverse functional domains, including Discoidin, CUB and LCCL domains, which are involved in various cellular processes, such as cell signaling, differentiation, and proliferation. DCBLD1 gene is associated with various types of cancers, including breast cancer, colon cancer, and leukemia. In these tumors, the expression of DCBLD1 is often correlated with advanced disease stages and poor patient outcomes. This suggests that DCBLD1 may play a role in the progression of cancer and could be a valuable therapeutic target. The precise mechanism by which DCBLD1 contributes to cancer development is still under investigation. However, it is believed that the encoded protein interacts with other cellular molecules to promote tumorigenesis. For example, DCBLD1 has been shown to regulate cell signaling pathways that control cell growth and differentiation, and its abnormal activation can lead to uncontrolled cell proliferation, a hallmark of cancer.

Furthermore, DCBLD1 has been implicated in promoting the invasion and metastasis of cancer cells. Its interaction with extracellular matrix proteins and cell adhesion molecules plays a crucial role in facilitating the migration and invasion of cancer cells into surrounding tissues and distant organs.

Reference:

Kikuta, Kazutaka et al. "Discoidin, CUB and LCCL domain-containing protein 2 (DCBLD2) is a novel biomarker of myxofibrosarcoma invasion identified by global protein expression profiling." Biochimica et biophysica acta. Proteins and proteomics vol. 1865,9 (2017): 1160-1166. doi:10.1016/j.bbapap.2017.06.023

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