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- Table of Contents
4 Citations 8 Q&As
12 Citations 7 Q&As
6 Citations 8 Q&As
1 Citations
Facts about C-C motif chemokine 3.
One of the Significant HIV-suppressive factors produced by CD8+ T-cells. Recombinant MIP-1-alpha induces a dose-dependent inhibition of different strains of HIV-1, HIV-2, and simian immunodeficiency virus (SIV).
Human | |
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Gene Name: | CCL3 |
Uniprot: | P10147 |
Entrez: | 6348 |
Belongs to: |
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intercrine beta (chemokine CC) family |
C-C motif chemokine 3; MIP1-(a); AI323804; CCL3; chemokine (C-C motif) ligand 3; G0S19-1; LD78a; LD78alpha; MIP1 alpha; MIP-1 alpha; MIP1A; MIP-1alpha; MIP1-alpha; PAT 464.1; SCYA3; SIS-beta
Mass (kDA):
10.085 kDA
Human | |
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Location: | 17q12 |
Sequence: | 17; NC_000017.11 (36088256..36090143, complement) |
Secreted.
CCL3 is a good choice to consider if you're in search of an immunotherapy product. This chemical ligand for chemokines is a crucial regulator of monocyte chemotaxis. Multiple myeloma is one of its many well-known uses. This article will look at the benefits of CCL3 and its many potential applications. You'll also learn about CCL3 and its role in multiple myeloma.
CCL3 (macrophage-inflammatory protein 1a) is a cell surface molecule that plays a crucial role in the regulation and growth of leukocytes. CCL3 is produced by numerous cells, including resident monocytes and macrophages recruited. These molecules regulate the production of leukocytes and secretion of IFN-g as well as inhibiting immature T cell growth. This study suggests that CCL3 is an important mediator of leukocyte aggregation as well as function.
In animal models, CCL3 inhibits hematopoiesis and is thought to be a possible chemical therapy agent to protect bone marrow against cancer-related toxicants. CCL3 also decreases T cells' activity, thereby increasing their ability to produce cytokines and chemokines. CCL3 inhibition is currently being studied in animals as models for autoinflammatory disease however, no human trials have been done.
The results showed that mice lacking CCL3 were significantly less likely than controls to survive a K. pneumoniae outbreak. CCR5 mice performed similarly to wild-type mice, minus their higher lethality. Additionally, mice lacking CCR1 were found to have decreased survival rates following an infection with intracellular Aspergillus fuigatus.
Mice lacking CCL3 demonstrated increased neutrophil recruitment as a result of intraracheal K. pneumoniae but did not show higher levels of monocytes. Conversely, mice deficient of CCL3 showed significantly diminished polymorphonuclear lukocyte recruitment and phagocytic activity. Additionally, the macrophages of the alveolar region is an important part of the early phase of the immune response did not display CCL3 expression in mice with impaired CCL3 secretion.
The function of CCL3 in the immune system is established. This chemokine can be secreted by neutrophils and monocytes in response to inflammatory stimuli. This chemokine activates macrophages and monocytes as well as other immune cells. However, when monocytes consume these chemokines they exhibit the proinflammatory character. M1 macrophages, for instance exhibit a proinflammatory phenotype , and promote the accumulation and spread of viruses and bacteria throughout the body. Because of their hyperactivated, bactericidal function The proinflammatory phenotypes exhibited by M1 macrophages could be responsible for the destruction of tissues.
Although CCL3 inhibits the process of hematopoiesis in vitro but it has not been found to be a beneficial treatment to stop cancer chemotherapeutics from causing damage to the bone marrow. Its inhibitory properties are being studied in the animal models of autoinflammatory diseases. CCL3 inhibitors are being developed however they have not yet been tested in humans.
The anti-MIP-la/CCL3 antibodies reduce total lung collagen by 49 percent. This reduction in MIP-la/CCL3 does however not completely eliminate fibrogenic and inflammatory responses. It is possible that other mediators are involved. CCL4 and MIP-1a are both CC chemokines that are similar in their functions. Additionally, they could function as a signaling molecules for leukocyte recruitment.
Inflammatory processes require leukocyte-derived CCL3 to enhance neutrophil migration. Leukocyte-derived CCL3 is believed to be a factor in the pathogenesis and progression of atherosclerosis. It is an essential element in the progression development of the lesion. Leukocytes move across a gradient of CCL3 when the body is in an inflammatory state.
A cell lysate has been prepared in RIPA buffer by adding tablets of protease inhibitor cocktail. After centrifugation, the insoluble matter was removed. The cell lysate was subjected to SDS-PAGE in 12% denaturing SDS polyacrylamide gel. The membrane was then blocked using 0.05 percent Tween-20, 5% nonfat milk. Cell Signaling Technologies purchased the anti-human antibodies and anti-FLIP from them. Anti-human p65 was also purchased (D14E12/D7H5M).
CCL3 and other inflammation proteins are frequently linked to multiple myeloma. The role it plays in multiple myeloma remains unclear, however it has been linked to a large number of bone-related complications. CCL3 serum levels are elevated in myeloma patients with severe bone disease. Researchers also discovered that CCL3 expression is very high on tumor plasma cells and is associated with osteolytic burden. CCL3 negatively correlates to osteoblast (OCN), activity in multiple myeloma patients. These results suggest that CCL3 negatively regulates OCN through direct and indirect signaling mechanisms.
Researchers have discovered that CCL3 plays a role in the development and infiltrates of lymph nodes. In addition to its function in multiple myeloma, CCL3 also plays a role in regulating the expression of HIF-2a in the disease. For more information, refer to the table below. If you are diagnosed with multiple myeloma CCL3 is an essential candidate for treatment.
As previously mentioned the presence of plasmacytoma, an etiological sign of MM is an important indicator of the development of MM. The International Myeloma Working Group also modified the International Staging System in order to include chromosomal anomalies. The revised International Staging System has a better prognostic significance. Serum LDH has a higher prognostic value in MM.
CCL3 hinders osteoblast differentiation and stimulates osteoblast activity that is deregulated in MM patients. However, the inhibition effect is not fully understood. Researchers have discovered that CCL3 may influence osteogenesis. However CCL3's inflammatory response could also affect the formation of bone. They are currently examining whether CCL3 blocks osteoblast growth in this case.
PMID: 3086300 by Obaru K., et al. A cDNA clone used to study mRNA inducible in human tonsillar lymphocytes by a tumor promoter.
PMID: 2521882 by Zipfel P.F., et al. Mitogenic activation of human T cells induces two closely related genes which share structural similarities with a new family of secreted factors.
*Showing only the more recent 20. More publications can be found for each product on its corresponding product page