Chemokine CXCL12
Chemokine CXCL13
Chemokine CXCL10
Chemokine CXCL6
Chemokine CXCL11
Chemokine CXCL1
Chemokines, CXC
Receptors, Chemokine
Chemokine CXCL5
Receptors, CXCR4
Receptors, CXCR3
Chemokines
Chemokine CCL5
Receptors, CXCR5
Receptors, Interleukin-8B
Chemokine CCL2
Chemokine CXCL2
Chemokine CCL21
Chemotaxis, Leukocyte
Chemokine CCL4
Cell Movement
Chemokine CCL22
Chemokine CCL3
Chemokine CCL17
Receptors, Scavenger
Chemokine CCL19
Chemokine CX3CL1
Chemokines, CC
Interleukin-8
Heterocyclic Compounds
Chemotaxis
Platelet Factor 4
Chemokine CCL7
Chemokine CCL20
Cells, Cultured
Chemokine CCL11
Chemokine CCL1
Neutrophil Infiltration
Signal Transduction
Chemokine CCL27
Mice, Knockout
Up-Regulation
Flow Cytometry
Receptors, CCR2
Receptors, CCR1
RNA, Messenger
Receptors, CCR5
Chemokine CCL8
Cytokines
Inflammation
Gene Expression Regulation
Macrophage Inflammatory Proteins
Reverse Transcriptase Polymerase Chain Reaction
Enzyme-Linked Immunosorbent Assay
Receptors, CCR4
Receptors, Interleukin-8A
T-Lymphocytes
Receptors, CCR3
Immunohistochemistry
Macrophages
Endothelial Cells
Receptors, CCR7
Disease Models, Animal
Receptors, CCR10
Mice, Transgenic
Receptors, CCR8
Interferon-gamma
Chemokine CCL24
CD4-Positive T-Lymphocytes
Receptors, Cytokine
Monocyte Chemoattractant Proteins
Blotting, Western
Gene Expression
Protein Binding
Bone Marrow Cells
Gene Expression Profiling
Chemokines, CX3C
Chemotactic Factors
Receptors, CCR6
Cell Differentiation
Transfection
Monokines
Monocytes
Neutrophils
Ligands
Receptors, HIV
Duffy Blood-Group System
Dendritic Cells
Cell Migration Inhibition
Intercellular Signaling Peptides and Proteins
Inflammation Mediators
Tumor Necrosis Factor-alpha
NF-kappa B
Lung
Chemotactic Factors, Eosinophil
Leukocytes
Molecular Sequence Data
HIV-1
Stromal Cells
Down-Regulation
Lipopolysaccharides
Th2 Cells
Epithelial Cells
Amino Acid Sequence
Lymph Nodes
Leukocytes, Mononuclear
Th1 Cells
Angiostatic Proteins
Lymphocyte Activation
Eosinophils
Immunity, Innate
Lymphoid Tissue
T-Lymphocyte Subsets
CD8-Positive T-Lymphocytes
Coculture Techniques
Chemokine and chemokine receptor gene variants and risk of non-Hodgkin's lymphoma in human immunodeficiency virus-1-infected individuals. (1/2152)
Normal B-lymphocyte maturation and proliferation are regulated by chemotactic cytokines (chemokines), and genetic polymorphisms in chemokines and chemokine receptors modify progression of human immunodeficiency virus-1 (HIV-1) infection. Therefore, 746 HIV-1-infected persons were examined for associations of previously described stromal cell-derived factor 1 (SDF-1) chemokine and CCR5 and CCR2 chemokine receptor gene variants with the risk of B-cell non-Hodgkin's lymphoma (NHL). The SDF1-3'A chemokine variant, which is carried by 37% of whites and 11% of blacks, was associated with approximate doubling of the NHL risk in heterozygotes and roughly a fourfold increase in homozygotes. After a median follow-up of 11.7 years, NHL developed in 6 (19%) of 30 SDF1-3'A/3'A homozygotes and 22 (10%) of 202 SDF1-+/3'A heterozygotes, compared with 24 (5%) of 514 wild-type subjects. The acquired immunodeficiency syndrome (AIDS)-protective chemokine receptor variant CCR5-triangle up32 was highly protective against NHL, whereas the AIDS-protective variant CCR2-64I had no significant effect. Racial differences in SDF1-3'A frequency may contribute to the lower risk of HIV-1-associated NHL in blacks compared with whites. SDF-1 genotyping of HIV-1-infected patients may identify subgroups warranting enhanced monitoring and targeted interventions to reduce the risk of NHL. (+info)Identification of CXCR4 domains that support coreceptor and chemokine receptor functions. (2/2152)
The interaction of the chemokine stromal cell-derived factor 1 (SDF-1) with its receptor CXCR4 is vital for cell trafficking during development, is capable of inhibiting human immunodeficiency virus type 1 (HIV-1) utilization of CXCR4 as a coreceptor, and has been implicated in delaying disease progression to AIDS in vivo. Because of the importance of this chemokine-chemokine receptor pair to both development and disease, we investigated the molecular basis of the interaction between CXCR4 and its ligands SDF-1 and HIV-1 envelope. Using CXCR4 chimeras and mutants, we determined that SDF-1 requires the CXCR4 amino terminus for binding and activates downstream signaling pathways by interacting with the second extracellular loop of CXCR4. SDF-1-mediated activation of CXCR4 required the Asp-Arg-Tyr motif in the second intracellular loop of CXCR4, was pertussis toxin sensitive, and did not require the distal C-terminal tail of CXCR4. Several CXCR4 mutants that were not capable of binding SDF-1 or signaling still supported HIV-1 infection, indicating that the ability of CXCR4 to function as a coreceptor is independent of its ability to signal. Direct binding studies using the X4 gp120s HXB, BH8, and MN demonstrated the ability of HIV-1 gp120 to bind directly and specifically to the chemokine receptor CXCR4 in a CD4-dependent manner, using a conformationally complex structure on CXCR4. Several CXCR4 variants that did not support binding of soluble gp120 could still function as viral coreceptors, indicating that detectable binding of monomeric gp120 is not always predictive of coreceptor function. (+info)Distinct biological effects of macrophage inflammatory protein-1alpha and stroma-derived factor-1alpha on CD34+ hemopoietic cells. (3/2152)
Chemokines are important regulators of both hemopoietic progenitor cell (HPC) proliferation and adhesion to extracellular matrix molecules. Here, we compared the biological effects of the CC chemokine macrophage inflammatory protein-1alpha (MIP-1alpha) with those of the CXC chemokine stroma-derived factor-1alpha (SDF-1alpha) on immunomagnetically purified CD34+ cells from leukapheresis products (LP CD34+). In particular, studies on chemokine-induced alterations of LP CD34+ cell attachment to fibronectin-coated plastic surfaces, proliferation of these cells in colony-forming cell (CFC) assays and intracellular calcium mobilization were performed. MIP-1alpha but not SDF-1alpha was found to increase the adhesion of LP CD34+ cells to fibronectin in a dose-dependent manner. Both chemokines elicited growth-suppressive effects on LP CD34+ cells in CFC assays. While MIP-1alpha reduced the number of granulomonocytic (CFC-GM) and erythroid (BFU-E) colonies to the same extent, SDF-1alpha showed a significantly greater inhibitory effect on CFC-GM than BFU-E. Finally, we demonstrated that SDF-1alpha but not MIP-1alpha triggers increases in intracellular calcium in LP CD34+ cells. The SDF-1alpha-induced calcium response was rapid and concentration-dependent, with a maximal stimulation observed at > or = 15 ng/ml. In conclusion, our data suggest distinct biological properties of SDF-1alpha and MIP-1alpha in terms of modulation of LP CD34+ cell adhesion to fibronectin and intracellular calcium levels. However, comparable growth-suppressive effects on HPC proliferation were observed, indicating that this feature may be independent of chemokine-induced calcium responses. (+info)Opposite effects of SDF-1 on human immunodeficiency virus type 1 replication. (4/2152)
The alpha-chemokine SDF-1 binds CXCR4, a coreceptor for human immunodeficiency virus type 1 (HIV-1), and inhibits viral entry mediated by this receptor. Since chemokines are potent chemoattractants and activators of leukocytes, we examined whether the stimulation of HIV target cells by SDF-1 affects the replication of virus with different tropisms. We observed that SDF-1 inhibited the entry of X4 strains and increased the infectivity of particles bearing either a CCR5-tropic HIV-1 envelope or a vesicular stomatitis virus G envelope. In contrast to the inhibitory effect of SDF-1 on X4 strains, which is at the level of entry, the stimulatory effect does not involve envelope-receptor interactions or proviral DNA synthesis. Rather, we observed an increased ability of Tat to transactivate the HIV-1 long terminal repeat in the presence of the chemokine. Therefore, the effects of SDF-1 on the HIV-1 life cycle can be multiple and opposite, including both an inhibition of viral entry and a stimulation of proviral gene expression. (+info)Shared usage of the chemokine receptor CXCR4 by primary and laboratory-adapted strains of feline immunodeficiency virus. (5/2152)
Strains of the feline immunodeficiency virus (FIV) presently under investigation exhibit distinct patterns of in vitro tropism. In particular, the adaptation of FIV for propagation in Crandell feline kidney (CrFK) cells results in the selection of strains capable of forming syncytia with cell lines of diverse species origin. The infection of CrFK cells by CrFK-adapted strains appears to require the chemokine receptor CXCR4 and is inhibited by its natural ligand, stromal cell-derived factor 1alpha (SDF-1alpha). Here we found that inhibitors of CXCR4-mediated infection by human immunodeficiency virus type I (HIV-1), such as the bicyclam AMD3100 and short peptides derived from the amino-terminal region of SDF-1alpha, also blocked infection of CrFK by FIV. Nevertheless, we observed differences in the ranking order of the peptides as inhibitors of FIV and HIV-1 and showed that such differences are related to the species origin of CXCR4 and not that of the viral envelope. These results suggest that, although the envelope glycoproteins of FIV and HIV-1 are substantially divergent, FIV and HIV-1 interact with CXCR4 in a highly similar manner. We have also addressed the role of CXCR4 in the life cycle of primary isolates of FIV. Various CXCR4 ligands inhibited infection of feline peripheral blood mononuclear cells (PBMC) by primary FIV isolates in a concentration-dependent manner. These ligands also blocked the viral transduction of feline PBMC by pseudotyped viral particles when infection was mediated by the envelope glycoprotein of a primary FIV isolate but not by the G protein of vesicular stomatitis virus, indicating that they act at an envelope-mediated step and presumably at viral entry. These findings strongly suggest that primary and CrFK-adapted strains of FIV, despite disparate in vitro tropisms, share usage of CXCR4. (+info)The CC chemokine receptor-7 ligands 6Ckine and macrophage inflammatory protein-3 beta are potent chemoattractants for in vitro- and in vivo-derived dendritic cells. (6/2152)
Dendritic cell migration to secondary lymphoid tissues is critical for Ag presentation to T cells necessary to elicit an immune response. Despite the importance of dendritic cell trafficking in immunity, at present little is understood about the mechanisms that underlie this phenomenon. Using a novel transwell chemotaxis assay system, we demonstrate that the CC chemokine receptor-7 (CCR7) ligands 6Ckine and macrophage inflammatory protein (MIP)-3 beta are selective chemoattractants for MHC class IIhigh B7-2high bone marrow-derived dendritic cells at a potency 1000-fold higher than their known activity on naive T cells. Furthermore, these chemokines stimulate the chemotaxis of freshly isolated lymph node dendritic cells, as well as the egress of skin dendritic cells ex vivo. Because these chemokines are expressed in lymphoid organs and 6Ckine has been localized to high endothelial venules and lymphatic endothelium, we propose that they may play an important role in the homing of dendritic cells to lymphoid tissues. (+info)B cell antigen receptor engagement inhibits stromal cell-derived factor (SDF)-1alpha chemotaxis and promotes protein kinase C (PKC)-induced internalization of CXCR4. (7/2152)
The entry of B lymphocytes into secondary lymphoid organs is a critical step in the development of an immune response, providing a site for repertoire shaping, antigen-induced activation and selection. These events are controlled by signals generated through the B cell antigen receptor (BCR) and are associated with changes in the migration properties of B cells in response to chemokine gradients. The chemokine stromal cell-derived factor (SDF)-1alpha is thought to be one of the driving forces during those processes, as it is produced inside secondary lymphoid organs and induces B lymphocyte migration that arrests upon BCR engagement. The signaling pathway that mediates this arrest was genetically dissected using B cells deficient in specific BCR-coupled signaling components. BCR-induced inhibition of SDF-1alpha chemotaxis was dependent on Syk, BLNK, Btk, and phospholipase C (Plc)gamma2 but independent of Ca2+ mobilization, suggesting that the target of BCR stimulation was a protein kinase C (PKC)-dependent substrate. This target was identified as the SDF-1alpha receptor, CXCR4, which undergoes PKC- dependent internalization upon BCR stimulation. Mutation of the internalization motif SSXXIL in the COOH terminus of CXCR4 resulted in B cells that constitutively expressed this receptor upon BCR engagement. These studies suggest that one pathway by which BCR stimulation results in inhibition of SDF-1alpha migration is through PKC-dependent downregulation of CXCR4. (+info)Down-regulation of CXCR4 by human herpesvirus 6 (HHV-6) and HHV-7. (8/2152)
Recent studies have demonstrated that human herpesvirus 6 (HHV-6) and HHV-7 interact with HIV-1 and alter the expression of various surface molecules and functions of T lymphocytes. The present study was undertaken to clarify whether coreceptors for HIV-1, CXCR4 and CCR5, are necessary for HHV-6 and HHV-7 infection. Although CXCR4 and CCR5 appeared not to be the coreceptors for these viruses, marked down-regulation of CXCR4, but not CCR5, was detected in HHV-6 variant A (HHV-6A)-, HHV-6 variant B (HHV-6B)-, and HHV-7-infected cells. Down-regulation of CXCR4 resulted in impairment of chemotaxis and a decreased level of elevation of the intracellular Ca2+ concentration in response to stromal cell-derived factor-1. Northern blot analysis of mRNAs extracted from HHV-6A-, HHV-6B-, and HHV-7-infected CD4+ T lymphocytes demonstrated a markedly decreased level of CXCR4 gene transcription, but the posttranscriptional stability of CXCR4 mRNA was not significantly altered. These data demonstrate that unlike HIV-1, HHV-6 and HHV-7 infections do not require expression of CXCR4 or CCR5, whereas marked down-regulation of CXCR4 is induced by these viruses, suggesting that HHV-6 and HHV-7 infections may render CD4+ T lymphocytes resistant to T lymphocyte-tropic HIV-1 infection. (+info)There are several key features of inflammation:
1. Increased blood flow: Blood vessels in the affected area dilate, allowing more blood to flow into the tissue and bringing with it immune cells, nutrients, and other signaling molecules.
2. Leukocyte migration: White blood cells, such as neutrophils and monocytes, migrate towards the site of inflammation in response to chemical signals.
3. Release of mediators: Inflammatory mediators, such as cytokines and chemokines, are released by immune cells and other cells in the affected tissue. These molecules help to coordinate the immune response and attract more immune cells to the site of inflammation.
4. Activation of immune cells: Immune cells, such as macrophages and T cells, become activated and start to phagocytose (engulf) pathogens or damaged tissue.
5. Increased heat production: Inflammation can cause an increase in metabolic activity in the affected tissue, leading to increased heat production.
6. Redness and swelling: Increased blood flow and leakiness of blood vessels can cause redness and swelling in the affected area.
7. Pain: Inflammation can cause pain through the activation of nociceptors (pain-sensing neurons) and the release of pro-inflammatory mediators.
Inflammation can be acute or chronic. Acute inflammation is a short-term response to injury or infection, which helps to resolve the issue quickly. Chronic inflammation is a long-term response that can cause ongoing damage and diseases such as arthritis, asthma, and cancer.
There are several types of inflammation, including:
1. Acute inflammation: A short-term response to injury or infection.
2. Chronic inflammation: A long-term response that can cause ongoing damage and diseases.
3. Autoimmune inflammation: An inappropriate immune response against the body's own tissues.
4. Allergic inflammation: An immune response to a harmless substance, such as pollen or dust mites.
5. Parasitic inflammation: An immune response to parasites, such as worms or fungi.
6. Bacterial inflammation: An immune response to bacteria.
7. Viral inflammation: An immune response to viruses.
8. Fungal inflammation: An immune response to fungi.
There are several ways to reduce inflammation, including:
1. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs).
2. Lifestyle changes, such as a healthy diet, regular exercise, stress management, and getting enough sleep.
3. Alternative therapies, such as acupuncture, herbal supplements, and mind-body practices.
4. Addressing underlying conditions, such as hormonal imbalances, gut health issues, and chronic infections.
5. Using anti-inflammatory compounds found in certain foods, such as omega-3 fatty acids, turmeric, and ginger.
It's important to note that chronic inflammation can lead to a range of health problems, including:
1. Arthritis
2. Diabetes
3. Heart disease
4. Cancer
5. Alzheimer's disease
6. Parkinson's disease
7. Autoimmune disorders, such as lupus and rheumatoid arthritis.
Therefore, it's important to manage inflammation effectively to prevent these complications and improve overall health and well-being.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
CXCR4
Mir-126
Chemokine
Julia Wilson (scientist)
Noxxon Pharma
Kate Scott (academic)
RNA therapeutics
Stromal cell-derived factor 1
ACKR3
CXC chemokine receptors
Transcription elongation regulator 1
Tumor microenvironment
Dendritic cell
L-Ribonucleic acid aptamer
Michael R. Gold
Cancer stem cell
Invasion (cancer)
Remyelination
Chromosome 10
Jaime Imitola
Intravascular lymphomas
Hematopoietic stem cell niche
CD20
NR58-3.14.3
Spermatogonial stem cell
Ibrutinib
Cortical thymic epithelial cells
Dock2
Monoclonal antibody therapy
CCL19
Robyn S. Klein
WHIM syndrome
Cancer-associated fibroblast
CXCR4 antagonist
Pathophysiology of multiple sclerosis
Pathological roles of the homeostatic chemokine CXCL12 - PubMed
The chemokine CXCL12 mediates the anti-amyloidogenic action of painless human nerve growth factor - PubMed
The chemokine CXCL12 mediates the anti-amyloidogenic action of painless human nerve growth factor
Cxcl12 evolution - subfunctionalization of a ligand through altered interaction with the chemokine receptor | SUSI
The bone marrow-expressed antimicrobial cationic peptide LL-37 enhances the responsiveness of hematopoietic stem progenitor...
Bone marrow-derived cells or C-X-C motif chemokine 12 (CXCL12) treatment improve thin endometrium in a mouse model<...
Development of plasmacytoid dendritic cells in bone marrow stromal cell niches requires CXCL12-CXCR4 chemokine signaling |...
Publication Detail
Biomarkers Search
Unique Clinical, Immune, and Genetic Signature in Patients with Borrelial Meningoradiculoneuritis - Volume 28, Number 4-April...
PA-11-064: Neuroimmune Mechanisms Of Alcohol Related Disorders (R01)
Biomarkers Search
PA-11-064: Neuroimmune Mechanisms Of Alcohol Related Disorders (R01)
Recombinant Murine SDF-1α (CXCL12)
Ackr3 atypical chemokine receptor 3 [Mus musculus (house mouse)] - Gene - NCBI
HIV-associated Neurocognitive Disorder (HAND): Overview, Pathophysiology, Epidemiology
Interobserver Agreement Rates on C-X-C Motif Chemokine Recep... : Clinical Nuclear Medicine
How Injured Nerves Stop Themselves From Healing - Neuroscience News
JCI -
Volume 127, Issue 9
Recombinant Human/Feline CXCL12/SDF-1 beta (aa 22-93) 351-FS-010: R&D Systems
MeSH Browser
Zohreh Ghorashi - Rafsanjan University of Medical Sciences, Rafsanjan, Iran - Training Course in Sexual and Reproductive Health...
High Levels of Expression of Human Stromal Cell-Derived Factor-1 Are Associated with Worse Prognosis in Patients with Stage II...
David H. McDermott, M.D. | NIH: National Institute of Allergy and Infectious Diseases
Research Festival | Intramural Research Program | National Institutes of Health
Chemokine Prostate Cancer Biomarkers
Antioxidants | Free Full-Text | Cigarette Smoke Extract Activates Hypoxia-Inducible Factors in a Reactive Oxygen Species...
NIH Clinical Center Search the Studies: Study Number, Study Title
Frontiers | Bone Marrow Fat and Hematopoiesis
Upregulation of chemokine receptor CCR10 is essential for glioma proliferation, invasion and patient survival | Oncotarget
Receptor21
- Was found that hNGFp acts on glial cells, modulating inflammatory proteins such as the soluble TNFa receptor II and the chemokine CXCL12. (nih.gov)
- We further established that the rescuing effect by hNGFp is mediated by CXCL12, as pharmacological inhibition of CXCL12 receptor CXCR4 occludes most of hNGFp effects. (nih.gov)
- Whereas all hPGCLCs strongly expressed the CXCR4 chemotaxis receptor, its ligand CXCL12/SDF1 was not significantly expressed in the whole EBs. (nih.gov)
- 25. The importance of the CXCL12-CXCR4 chemokine ligand-receptor interaction in prostate cancer metastasis. (nih.gov)
- The researchers worked out this effect when they specifically eliminated the receptor for CXCL12, called CXCR4, in the retinal nerve cells, rendering them blind to this protein. (neurosciencenews.com)
- It is still unknown why some of these nerve cells make CXCL12 and others make the receptor," says Fischer. (neurosciencenews.com)
- These new findings open the opportunity to develop pharmacological approaches aimed at disrupting the interaction of CXCL12 and its receptor on the nerve fibers, to free them from their captivity at the site of injury," concludes Fischer. (neurosciencenews.com)
- We focus on WHIMS (Warts, Hypogammaglobulinemia, Infections, and Myelokathexis Syndrome) which is due to autosomal dominant gain-of-function mutations in the CXCL12 chemokine receptor and HIV coreceptor known as CXCR4. (nih.gov)
- Here we report that the chemokine receptor CCR10 is highly expressed in human glioblastoma compared with control brain tissue. (oncotarget.com)
- The binding of chemokine receptor CXCR4 to stromal cell derived factor (SDF-1 or CXCL12) is an important interaction between a hematopoietic progenitor cell and its marrow environment. (nih.gov)
- Previous studies have shown that increased levels of chemokine receptor CXCR7 are associated with the increased invasiveness of prostate cancer cells. (elsevier.com)
- Rgs1 is an essential regulator of T-cell migration within lymphoid tissue, by modulating chemokine receptor activation. (guidetopharmacology.org)
- Activates the C-X-C chemokine receptor CXCR4 to induce a rapid and transient rise in the level of intracellular calcium ions and chemotaxis. (cusabio.com)
- Also binds to atypical chemokine receptor ACKR3, which activates the beta-arrestin pathway and acts as a scavenger receptor for SDF-1. (cusabio.com)
- Her thesis project focuses on the study of chemokine receptor conformations. (comfuturo.es)
- Chemokine receptors form oligomers on the cell surface, dynamic structures that are critical for the function of these mediators and are regulated by receptor levels and the presence of ligands. (comfuturo.es)
- Atypical chemokine receptor that controls chemokine levels and localization via high-affinity chemokine binding that is uncoupled from classic ligand-driven signal transduction cascades, resulting instead in chemokine sequestration, degradation, or transcytosis. (nih.gov)
- Also known as interceptor (internalizing receptor) or chemokine-scavenging receptor or chemokine decoy receptor. (nih.gov)
- Acts as a receptor for chemokines CXCL11 and CXCL12/SDF1. (nih.gov)
- Plerixafor: A chemokine receptor-4 antagonist for mobilization of hematopoietic stem cells for transplantation after high-dose chemotherapy for non-Hodgkin's lymphoma or multiple myeloma. (nih.gov)
- BACKGROUND: Studies relating certain chemokine and chemokine receptor gene alleles with the outcome of HIV-1 infection have yielded inconsistent results. (nih.gov)
Receptors7
- The chemokine receptors Cxcr4a and Cxcr4b are expressed in lymphatic endothelium, whereas chemokine ligands Cxcl12a and Cxcl12b are expressed in adjacent tissues along which the developing lymphatics align. (nih.gov)
- 27. A prognostic model comprising pT stage, N status, and the chemokine receptors CXCR4 and CXCR7 powerfully predicts outcome in neoadjuvant resistant rectal cancer patients. (nih.gov)
- Tumor cell invasion share many similarities with leukocyte trafficking, which is critically regulated by chemokines and their receptors. (oncotarget.com)
- Chemokine receptors are cytokine receptors found on the surface of certain cells that interact with a type of cytokine called a chemokine. (oncotarget.com)
- There have been 19 distinct chemokine receptors in mammals. (oncotarget.com)
- Following interaction with their specific chemokine ligands, chemokine receptors trigger a flux in intracellular calcium (Ca2+) ions (calcium signaling). (oncotarget.com)
- Of these receptors, CXCR4 and its ligand CXCL12 play a determining role in the homeostasis of the organism and several inflammatory and autoimmune pathologies. (comfuturo.es)
Ligand3
- When stratified by specific clinical manifestation, patients with meningoradiculoneuritis had higher levels of B-cell chemoattractants CXC motif chemokine ligand (CXCL) 12 and CXCL13 and T-cell-associated mediators CXCL9, CXCL10, and interleukin 17, compared with those without radicular pain. (cdc.gov)
- 35. Epigenetic changes of CXCR4 and its ligand CXCL12 as prognostic factors for sporadic breast cancer. (nih.gov)
- Chemokine binding does not activate G-protein-mediated signal transduction but instead induces beta-arrestin recruitment, leading to ligand internalization and activation of MAPK signaling pathway. (nih.gov)
SDF11
- The present study was to assess the association of single nucleotide polymorphisms of MMP-2, MMP-9 and chemokine (CXCL-12/SDF1-3') in the north Indian population. (who.int)
Chemotactic4
- A CXC chemokine that is chemotactic for T-LYMPHOCYTES and MONOCYTES . (nih.gov)
- The focus of our program is currently on the identification, diagnosis, and treatment of various primary immunodeficiencies especially as related to the chemotactic cytokine (chemokine) system which directs the migration, adhesion, activation, and function of leukocytes. (nih.gov)
- Purinergic stimulation of human mesenchymal stem cells potentiates their chemotactic response to CXCL12 and increases the homing capacity and production of proinflammatory cytokines. (unibo.it)
- ATP potentiated the chemotactic response of hMSCs to the chemokine CXCL12, and increased their spontaneous migration. (unibo.it)
CCL23
- and notably high expression of a set of chemokines that would favour neutrophil and monocyte recruitment including CXCL2, CCL2, CXCL12, CXCL1, CXCL6, CCL28. (garvan.org.au)
- DNA damage) in the neuronal retina, which is accompanied by a low-grade chronic inflammation, para-inflammation, characterized by upregulated expression of chemokines (CCL2, CXCL12, and CX3CL1) and complement components (C4 and CFH), and microglial activation. (qub.ac.uk)
- The upregulation of chemokines CCL2 and CXCL12 and complement C4 lasted for more than 160 days, whereas the expression of CX3CL1 and CFH was upregulated for 2 weeks. (qub.ac.uk)
Lymphocytes1
- Stromal-Cell Derived Factor-1α (SDF-1α) (CXCL12) attracts lymphocytes and plays important roles in embryogenesis and angiogenesis with implications in tumor metastasis. (chemotactics.com)
Cytokines1
- In addition to their primary role in mediating neuroinflammation, neuroimmune factors, such as cytokines, chemokines, and MHC, are essential for a variety of normal brain functions. (nih.gov)
Attracts1
- At the site of injury, nerves release a protein called CXCL12 which attracts growing nerve fibers and keeps them trapped in place. (neurosciencenews.com)
CXCR75
- 22. The role of the CXCL12-CXCR4/CXCR7 axis in the progression and metastasis of bone sarcomas (Review). (nih.gov)
- 23. CXCL12 and CXCR4, but not CXCR7, are primarily expressed by the stroma in head and neck squamous cell carcinoma. (nih.gov)
- 31. Biological/pathological functions of the CXCL12/CXCR4/CXCR7 axes in the pathogenesis of bladder cancer. (nih.gov)
- 32. CXCR4/CXCL12/CXCR7 axis is functional in neuroendocrine tumors and signals on mTOR. (nih.gov)
- this study shows an essential role of CXCR7, together with CXCR4, in the control of normal and malignant hematopoietic cell migration and homing induced by CXCL12. (cusabio.com)
Inhibition1
- Additionally, claudin-low tumors express high levels of the chemokine CXCL12, and its inhibition may decrease Treg infiltration into the tumor. (unc.edu)
CXCL54
- Preliminary data from our laboratory demonstrates a potential utility for CXCL5 and CXCL12 as biomarkers to distinguish between patients at high-risk versus low-risk for harboring prostate malignancies. (nih.gov)
- Assess the robustness of serum, plasma, or urine measures of CXCL5 and CXCL12. (nih.gov)
- The results of these assays will determine whether statistically significant associations between disease status in the prostate (no disease, BPH, PCa with or without concomitant BPH) and serum, plasma, or urine protein levels for CXCL5 and/or CXCL12 are observed among patients with low but detectable serum PSA. (nih.gov)
- Conversely, if no statistically significant associations between disease status in the prostate and serum, plasma, or urine protein levels for CXCL5 and/or CXCL12 are observed, then we will conclude that these proteins do not comprise suitable biomarkers for disease status in the prostate, and that further studies are not warranted. (nih.gov)
Important Roles1
- 37. CXCL14-CXCR4 and CXCL12-CXCR4 Axes May Play Important Roles in the Unique Invasion Process of Endometrioid Carcinoma With MELF-Pattern Myoinvasion. (nih.gov)
Molecule1
- This molecule is a so-called chemokine known as CXCL12. (neurosciencenews.com)
Protein levels1
- Required for regulation of CXCR4 protein levels in migrating interneurons, thereby adapting their chemokine responsiveness. (nih.gov)
Tissue1
- The image on the left is immunohistochemistry of paraffin-embedded Human breast cancer tissue using CSB-PA185715(CXCL12 Antibody) at dilution 1/40, on the right is treated with synthetic peptide. (cusabio.com)
Levels1
- Serum, plasma, or urine chemokine levels are assessed using 50 ul frozen specimen per sandwich ELISA in duplicate using the appropriate commercially-available capture antibodies, detection antibodies, and standard ELISA reagents (R&D Systems), as we have described previously (15, 17, 18). (nih.gov)
Human1
- These NF- kappaB activated islets not only expressed the same chemokine profile observed in human islets, but also struggled to maintain normoglycemia post transplantation. (garvan.org.au)
Nerve3
- In further experiments, the Bochum-based researchers showed that knocking out CXCL12 in retinal nerve cells so that it could no longer be released at the injury site equally improved axonal regeneration into the optic nerve. (neurosciencenews.com)
- CXCR4/CXCL12-mediated entrapment of axons at the injury site compromises optic nerve regeneration " by Dietmar Fischer et al. (neurosciencenews.com)
- Here, we show that a chemoattractive CXCL12/CXCR4-dependent mechanism prevents the extension of growth-stimulated axons into the distal nerve. (neurosciencenews.com)
Outcome2
Gain-of-funct1
- Loss- and gain-of-function studies in zebrafish demonstrate that chemokine signaling orchestrates the stepwise assembly of the trunk lymphatic network. (nih.gov)
Cells1
- CXCL12 is abundantly expressed in the synovial tissues of patients with rheumatoid arthritis (RA), and the incidence of RA observed in murine models of the pathology is much lower in mice with CXCR4-deficient T cells. (comfuturo.es)
Patients1
- CXCL12 rs1801157 polymorphism in patients with breast cancer, Hodgkin's lymphoma, and non-Hodgkin's lymphoma. (cdc.gov)
Network1
- Here, we show that chemokine signaling provides critical guidance cues directing early trunk lymphatic network assembly and patterning. (nih.gov)
CXCR417
- In addition to this increased or differential transcription of CXCL12, also upregulation of its receptors CXC chemokine receptor 4 (CXCR4) and atypical chemokine receptor 3 (ACKR3) contributes to the onset or progression of diseases. (nih.gov)
- We previously reported the discovery of a CXCL12-mimetic cyclic peptide (2) as a selective CXCR4 antagonist showing promising in vitro and in vivo anticancer activity. (nih.gov)
- We further established that the rescuing effect by hNGFp is mediated by CXCL12, as pharmacological inhibition of CXCL12 receptor CXCR4 occludes most of hNGFp effects. (nih.gov)
- Whereas all hPGCLCs strongly expressed the CXCR4 chemotaxis receptor, its ligand CXCL12/SDF1 was not significantly expressed in the whole EBs. (nih.gov)
- 22. The role of the CXCL12-CXCR4/CXCR7 axis in the progression and metastasis of bone sarcomas (Review). (nih.gov)
- 23. CXCL12 and CXCR4, but not CXCR7, are primarily expressed by the stroma in head and neck squamous cell carcinoma. (nih.gov)
- 25. The importance of the CXCL12-CXCR4 chemokine ligand-receptor interaction in prostate cancer metastasis. (nih.gov)
- 27. A prognostic model comprising pT stage, N status, and the chemokine receptors CXCR4 and CXCR7 powerfully predicts outcome in neoadjuvant resistant rectal cancer patients. (nih.gov)
- 31. Biological/pathological functions of the CXCL12/CXCR4/CXCR7 axes in the pathogenesis of bladder cancer. (nih.gov)
- 32. CXCR4/CXCL12/CXCR7 axis is functional in neuroendocrine tumors and signals on mTOR. (nih.gov)
- 35. Epigenetic changes of CXCR4 and its ligand CXCL12 as prognostic factors for sporadic breast cancer. (nih.gov)
- 37. CXCL14-CXCR4 and CXCL12-CXCR4 Axes May Play Important Roles in the Unique Invasion Process of Endometrioid Carcinoma With MELF-Pattern Myoinvasion. (nih.gov)
- CXCL12 binds to a receptor called CXCR4 on the surface of these stem cells. (nih.gov)
- Using computational methods, the researchers optimized the part of CXCL12 that initially binds CXCR4. (nih.gov)
- We focus on WHIMS (Warts, Hypogammaglobulinemia, Infections, and Myelokathexis Syndrome) which is due to autosomal dominant gain-of-function mutations in the CXCL12 chemokine receptor and HIV coreceptor known as CXCR4. (nih.gov)
- The binding of chemokine receptor CXCR4 to stromal cell derived factor (SDF-1 or CXCL12) is an important interaction between a hematopoietic progenitor cell and its marrow environment. (nih.gov)
- CXCR4-CXCL12-CXCR7, TLR2-TLR4, and PD-1/PD-L1 in colorectal cancer liver metastases from neoadjuvant-treated patients. (cdc.gov)
Receptor2
Prognostic1
- [ 59 ] With such multidimensional properties, understanding the prognostic significance of chemokines is complex. (medscape.com)
CCL41
- For instance, a high pretreatment expression of chemokines CCL3 and CCL4 in DLBCL is associated with shorter PFS and OS in comparison with low CCL4/CCL3 expression. (medscape.com)
Inflammation3
- Chemokines are proteins that help leucocyte migration to sites of tissue damage, inflammation and proliferation. (medscape.com)
- But chemokines also cause inflammation, and long-term inflammation in the brain and body can cause more harm than good. (nih.gov)
- A research team led by Dr. Evan Snyder from the Sanford Burnham Prebys Medical Discovery Institute tested whether they could engineer a natural chemokine to attract stem cells without causing inflammation. (nih.gov)
Interaction1
- Moreover, posttranslational modification of CXCL12 during disease progression, through interaction with locally produced molecules or enzymes, also affects CXCL12 activity, adding further complexity. (nih.gov)
Urine1
- Serum, plasma, or urine chemokine levels are assessed using 50 ul frozen specimen per sandwich ELISA in duplicate using the appropriate commercially-available capture antibodies, detection antibodies, and standard ELISA reagents (R&D Systems), as we have described previously (15, 17, 18). (nih.gov)
Role2
- Results from this Phase III study and many other ongoing Phase II studies could offer more information about the role of chemokine inhibitors as a class of drugs in treating T-cell lymphomas. (medscape.com)
- In addition to their primary role in mediating neuroinflammation, neuroimmune factors, such as cytokines, chemokines, and MHC, are essential for a variety of normal brain functions. (nih.gov)
Activity1
- Based on preclinical data, histone decetylase inhibitors and BTK inhibitors have been identified as potential agents that can suppress chemokine activity. (medscape.com)
Expression1
- In contrast to these homeostatic functions, increased expression of CXCL12 in general, or of a specific CXCL12 splicing variant has been demonstrated in various pathologies. (nih.gov)
Disease1
- They altered a chemokine called CXCL12, which can draw neural stem cells to sites of injury or disease in the brain and central nervous system. (nih.gov)