DLK1 Antibodies

Structure of DLK1

The molecular weight of the DLK1 protein is approximately 38 kDa. However, due to glycosylation modifications, specific bands are often observed at 50-60 kDa during actual detection. This protein exhibits high sequence conservation across different species.

DLK1 is a single transmembrane protein consisting of 383 amino acids. Its extracellular region contains 6 epidermal growth factor-like repeat domains, which mediate protein-protein interactions. This characteristic structure can be cleaved by proteases after synthesis to release a soluble form, which exerts paracrine regulatory effects. DLK1 belongs to the non-classical Notch ligand family. Its intracellular region lacks the classic signal transduction domains and mainly regulates cell differentiation direction by competing with Notch receptors. This protein is highly expressed in undifferentiated cells and its expression level gradually decreases as the cell differentiation process progresses. This expression pattern change is closely related to the temporal sequence of embryonic development.

Fig. 1 Crystal structure of DLK1 EGF5-6 bound to ACVR2B.¹

Key structural properties of DLK1:

• Extracellular domain containing six EGF-like repeating domains
• Protease cleavage site at juxtamembrane
• Single transmembrane domain
• Short intracellular tails lacking signal transduction activity

Functions of DLK1

The core function of DLK1 is to regulate cell differentiation and proliferation. Additionally, this gene is involved in various physiological processes, including fat formation, neural development, and skeletal muscle regeneration.

The expression pattern of DLK1 shows stage-dependent downregulation during development, which is closely related to the process of cells transitioning from proliferation to differentiation. Its extracellular domain is structurally similar to that of the Notch receptor, but lacks the intracellular signaling domain. It exerts negative regulatory effects by competitively binding.

Applications of DLK1 and DLK1 Antibody in Literature

1. Antfolk, Daniel, et al. "Molecular mechanism of Activin receptor inhibition by DLK1." Nature Communications 16.1 (2025): 5976. https://doi.org/10.1038/s41467-025-60634-3

This study found that DLK1 does not bind to the Notch receptor, but instead mimics the TGF-β ligand to competitively bind to ACVR2B, antagonizing the myostatin signaling and thereby promoting myogenic differentiation. Its effect on Notch stems from interfering with the formation of the NICD-SMAD complex, revealing a new mechanism for muscle development.

2. Grassi, Elisa Stellaria, and Alexander Pietras. "Emerging roles of DLK1 in the stem cell niche and cancer stemness." Journal of Histochemistry & Cytochemistry 70.1 (2022): 17-28. https://doi.org/10.1369/00221554211048951

This study reveals that DLK1, as a maternal imprinted gene, regulates stem cell differentiation through spatiotemporal-specific expression and splicing, in a NOTCH-dependent or -independent manner. It also maintains the characteristics of cancer stem cells in various tumors and has potential as a therapeutic target.

3. Lu, Hsin-Pin, et al. "TRIM28 regulates Dlk1 expression in adipogenesis." International journal of molecular sciences 21.19 (2020): 7245. https://doi.org/10.3390/ijms21197245

The study found that TRIM28 regulates Dlk1 expression by recruiting E2f1. The absence of TRIM28 alters the histone methylation at the Dlk1 promoter (increased H3K4/H3K27 decreased), upregulates its expression, and thereby inhibits adipogenic differentiation. Knockdown of Dlk1 can rescue differentiation, demonstrating that the TRIM28-DLK1 axis is crucial for adipogenesis.

4. Huang, Deyu, et al. "Dlk1 maintains adult mice long-term HSCs by activating Notch signaling to restrict mitochondrial metabolism." Experimental Hematology & Oncology 12.1 (2023): 11. https://doi.org/10.1186/s40164-022-00369-9

The study found that adult mouse hematopoietic stem cells highly express Dlk1. Although knocking out Dlk1 increased the number of LT-HSCs, it caused these cells to enter the cell cycle and enhance metabolic activity (increasing ROS), thereby damaging the long-term reconstitution ability. Mechanistically, it is regulated by the Notch signaling pathway, revealing the crucial role of Dlk1 in maintaining the quiescent state of hematopoietic stem cells.

5. Dai, Rujuan, Zhuang Wang, and S. Ansar Ahmed. "Epigenetic contribution and genomic imprinting Dlk1-Dio3 miRNAs in systemic lupus erythematosus." Genes 12.5 (2021): 680. https://doi.org/10.3390/genes12050680

This review explores the mutual regulation between DNA methylation and miRNAs in SLE: Abnormal methylation affects miRNA expression, while miRNAs target methylation enzymes. The focus is on the dysregulation of the imprinted Dlk1-Dio3 miRNA cluster, which is regulated by methylation, in autoimmune diseases such as SLE.

Creative Biolabs: DLK1 Antibodies for Research

Creative Biolabs specializes in the production of high-quality DLK1 antibodies for research and industrial applications. Our portfolio includes monoclonal and polyclonal antibodies tailored for ELISA, Flow Cytometry, Western blot, immunohistochemistry, and other diagnostic methodologies.

• Custom DLK1 Antibody Development: Tailor-made solutions to meet specific research requirements.
• Bulk Production: Large-scale antibody manufacturing for industry partners.
• Technical Support: Expert consultation for protocol optimization and troubleshooting.
• Aliquoting Services: Conveniently sized aliquots for long-term storage and consistent experimental outcomes.

For more details on our DLK1 antibodies, custom preparations, or technical support, contact us at email.