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Facts about Delta-like protein 1.
Is necessary for embryonic development and maintenance of adult stem cells in many different tissues and immune systeme; the DLL1-induced Notch signaling is mediated via an intercellular communication that modulates cell lineage, cell specification, cell patterning and morphogenesis through effects on differentiation and proliferation (PubMed:17194759, PubMed:19562077, PubMed:18997111, PubMed:23695674, PubMed:16495313, PubMed:21238454, PubMed:22282195, PubMed:7671806, PubMed:17960184, PubMed:22529374, PubMed:19389377, PubMed:23699523, PubMed:19144989, PubMed:23688253, PubMed:23806616, PubMed:26114479, PubMed:22940113, PubMed:25220152, PubMed:20081190, PubMed:21572390, PubMed:22096075). Plays a role in brain development at different level, namely by regulating neuronal differentiation of neural precursor cells through cell-cell interaction, most likely through the lateral inhibitory system in an endogenous level dependent-manner (PubMed:7671806, PubMed:18997111).
Mouse | |
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Gene Name: | Dll1 |
Uniprot: | Q61483 |
Entrez: | 13388 |
Belongs to: |
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No superfamily |
delta (Drosophila)-like 1; Delta 1; Delta; Delta1; delta-like 1 (Drosophila); delta-like protein 1; DL1; DLL1; Drosophila Delta homolog 1; H-Delta-1
Mass (kDA):
78.449 kDA
Mouse | |
---|---|
Location: | 17 A2|17 8.95 cM |
Sequence: | 17; |
In the embryo, expressed in the paraxial mesoderm and nervous system. Expressed at high levels in adult heart and at lower levels, in adult lung. Highly expressed in satellite cells from masseter and tongue than in satellite cells from leg and extraocular muscle.? (PubMed:25220152).
The stem cell adhesion molecule DLL1 is the DLL1 marker. It is highly expressed by extra-ocular muscle satellite cells. It is a potential target for cancer treatment due to its high expression in these cells. Here are a few of the most efficient uses of DLL1 markers. This includes: Cancer therapy: It can target stem cells
Further examination of the mechanisms behind the HIV-1 in vitro and OP9 DL1 cell coculture models allowed for further exploration. The decline in CD34+CD7+CXCR4+ cell counts could be preceded by the diminution of CD4+ T-cell production in HIV+ cocultures. CD4+ T-cell depletion might also result from direct the effects of cytopathic apoptosis, apopto and antigen-specific immune mechanisms.
OP9-DL1 expression has been shown in a variety of tissues, including cancer. The system also facilitates the development of functional T cells from several stem cell sources, including human HSCs. Despite its limitations, the system can induce functional T cell formation from multiple stem cells sources. One study revealed that co-culture of OP9 and DL1 cells created T cell precursors in lethally-irradiated allogeneic recipients. Adoptive transfer of T cells could result in enhanced T-cell-dependent immune responses and significantly improved graft-versus host disease.
The cocultures OP9-DL1 make it possible to study the T-cell differentiation process in the laboratory. This method allows for the study of early T cell differentiation processes, including the maturation and generation of lymphoid progenitor cells. The study will give more information about the way that cells express OP9-DL1 in the process of differentiation.
T-cell development is dependent on Notch signaling. Retroviral transduction enables OP9 cells to expand in 2-D monolayers and supports T-cell differentiation from HSCs. In addition, OP9-DL1-overexpressed cells could generate both CD8+ SP and DP cells. These findings changed the paradigm regarding in-vitro T lymphopoiesis.
Persistent HIV replication was observed in the coculture of OP9–DL1 cells and CD34+ cell cultures. Flow cytometry was used to evaluate HIV infection in 12 cells. HIV p24+ percentage was determined through intracellular staining and CD34+ cell concentrations were measured by ELISA. These data were correlatively analysed between weeks two through five. Spearman's correlation coefficients and Wilcoxon signed rank test were employed for statistical comparisons.
The DLL1 gene is vital for embryonic development and adult stem maintenance of stem cells. Dll1 is crucial for cell-cell interaction in patterning and specification differentiation and proliferation, cell-cell interaction, and cell-cell interaction. Dll1 is also essential for neuronal differentiation in neural precursor cells.
This study used miR-34a mimics of GenePharma and CD133 antibody from Miltenyi Biotec. BOSTER purchased the vWF antibody. The medium used to grow cells was enriched in boster bio DLL1-expressing cells. The CD133+ U251 cells resulting from the experiment were transfected using miR-34a mimics and NC oligos. The cells transfected displayed stem cell-like characteristics when co-transfected with miR-34a and NC plasmid.
DLL1 was discovered to be a novel molecular target for neuroblastoma in children. Researchers found that DLL1 was the most expressed Notch pathway component in cells with MYCN amplifying. They also discovered that DLL1 reduction can hinder cell proliferation and trigger the development of cells, suggesting a pro-oncogenic role. This suggests that miRNA-34b may be a therapeutic target for cancers that have DLL1 as a marker.
The DLL1 gene is a direct target for miRNA-34b. This small RNA is involved in downregulating cell differentiation and is a direct target of the Notch signaling pathway. Moreover, miRNA-34b is toxic to cells in high concentrations and further research is necessary to determine the precise role of this gene in tumor development. Furthermore, DLL1 has been shown to be linked to the expression of other genes controlled by N-Myc. These genes have been associated with cerebral ischemia and lung Adenocarcinoma.
DLL1 is associated with the Notch pathway, in addition to the DLL1 gene. This pathway activates Notch-1 which is a transcription factor for Notch signaling pathway. DLL1 is known to enhance the levels of the NICD Protein as a transmembrane-bound ligand for the Notch signaling pathway. Researchers compared the levels of DLL1 protein between two neuroblastoma line varieties -- SH-SY5Y and IMR-32. They discovered that IMR32 cells had higher levels of Notch activation compared to SH–SY5Y cells. Western blot and densitometric analysis of the two cell lines demonstrated that DLL1 protein was significantly increased in IMR-32 cells.
The MiRNA-34 family has been identified in a number of cancers as possible therapeutic targets. They regulate a variety of cell processes, including cell cycles and the process of apoptosis. In-silico analysis revealed that DLL1-ligands target miRNA 34, which is well-known for its role as a tumor suppressor in a variety of cancers. A study of the DLL1 ligand has revealed that it inhibits neuroblastoma cells growth and slows the progression of tumors in orthotopic mouse models.
PMID: 7671806 by Bettenhausen B., et al. Transient and restricted expression during mouse embryogenesis of Dll1, a murine gene closely related to Drosophila Delta.
PMID: 21572390 by Jin G., et al. MT1-MMP cleaves Dll1 to negatively regulate Notch signalling to maintain normal B-cell development.