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Chemokine CXCL12

Chemokine CXCL12: A key player in cell migration and tissue homeostasis.
This small cytokine is involved in a variety of biological processes, including immune cell trafficking, stem cell mobilization, and tissue repair.
CXCL12 binds to its receptor CXCR4, triggering signaling cascades that guide cell movement and promote cell survival.
Reserach into CXCL12 function and regulation holds promise for developing novel therapies for cancer, inflamation, and other disorders.

Most cited protocols related to «Chemokine CXCL12»

We conducted a genetic association study with three stages as displayed in Figure 1. Stage 1 consisted of the Myocardial Infarction Genetics Consortium (MIGen), a collection of 2,967 cases of early-onset MI (in men ≤50 years old or women ≤60 years old) and 3,075 age- and sex-matched controls free of MI from six international sites: Boston and Seattle in the United States as well as Sweden, Finland, Spain, and Italy (Table 1). At each site, MI was diagnosed on the basis of autopsy evidence of fatal MI or a combination of chest pain, electrocardiographic evidence of MI, or elevation of one or more cardiac biomarkers (creatine kinase or cardiac troponin). The mean age at the time of MI was 41 years among male cases and 47 years among female cases.
We took forward SNPs into two stages of replication (Stages 2 and 3, Figure 1). 1441 SNPs were tested in Stage 2 based on two criteria: i) strength of statistical evidence in Stage 1 (1433 SNPs from loci with P < 10-3 in Stage 1) or ii) belonging to one of eight reported loci from recent genome-wide association studies for coronary artery disease (a common SNP from each of 9p21.3, near CXCL12, SMAD3, MTHFD1L, MIA3, near CELSR2/PSRC1/SORT1, 2q36, and PCSK9)3 (link),7 (link).
Stage 2 consisted of in silico comparisons with four recently completed GWAS for MI consisting of a symmetric effective sample size of up to 3,942 cases of MI and 3,942 controls. These studies included the Wellcome Trust Case Control Consortium Coronary Heart Disease study3 (link), German MI Family Study I3 (link), PennCATH, and MedStar (Supplementary Table 1). In each Stage 2 study, the analysis was restricted to the phenotype of MI with an age of onset threshold of <66 years for men or women. Although this age cutoff is slightly less restrictive than that used in Stage 1, this cutoff is at or below the mean age of first MI in the US (65 years for men and 70 years for women).
Thirty-three SNPs were taken forward to Stage 3, which consisted of genotyping an additional 6 studies with a symmetric effective sample size of up to 5,469 cases of MI and 5,469 controls. These six studies included Acute MI Gene Study/Dortmund Health Study, Verona Heart Study29 (link), Mid-America Heart Institute Study30 (link), Irish Family Study31 (link), German MI Family Study II, and INTERHEART32 (link) (European ancestry and South Asian ancestry each analyzed separately) (Supplementary Table 2). Stage 3 was comprised of 25 SNPs with the best combined statistical evidence for MI from Stages 1 and 2 (P < 10-5) and the eight previously-reported SNPs discussed above. In each Stage 3 study, the analysis was restricted to the phenotype of MI and in four of the six studies, an age of onset threshold was established at <66 years for men or women.
Publication 2009
Asian Persons Autopsy Biological Markers CELSR2 protein, human Chemokine CXCL12 Chest Pain Coronary Artery Disease Creatine Kinase DNA Replication Electrocardiography Europeans Genes Genetic Association Studies Genome-Wide Association Study Heart Heart Disease, Coronary Males migen Myocardial Infarction PCSK9 protein, human Phenotype Single Nucleotide Polymorphism SMAD3 protein, human SORT1 protein, human Troponin Woman

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Publication 2014
Animals Biological Assay Bones Cell Cycle Chemokine CXCL12 Cytosine Diphtheria Toxin Flow Cytometry fluorexon Human Body Inosine Institutional Animal Care and Use Committees leptin receptor, human Males Mus Poly A Protein, Nestin Radiotherapy Tamoxifen tdTomato WNT1 protein, human X-Ray Microtomography

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Publication 2011
Anti-Antibodies Biological Assay BLOOD Cell Migration Assays Cells Chemokine CXCL12 Culture Media Cytokine Edetic Acid Endothelial Cells Endothelium Fibronectins Hematopoietic System Humidity Hyperostosis, Diffuse Idiopathic Skeletal Mesenchyma Mesenchymal Stem Cells Microspheres Migration, Cell Phlebotomy Serum Stem, Plant Stem Cells Trypan Blue
PTENflox/flox mice (Dr. Tak Mak, Ontario Cancer Institute, University of Toronto, Toronto, Ontario)27 (link), SMMHC-CreERT2 transgenic mice (Dr. Stephen Offermanns, U. Heidelberg, Heidelberg, Ger)28 (link), and ROSA26 reporter (R26R) mice (Jackson Laboratory) were bred to generate tamoxifen-inducible SMC-specific PTEN knockout mice carrying the R26R allele (PTEN iKO). Controls expressed SMMHC-CreERT2 and R26R, but were wild type for PTEN (WT). Mice received bone marrow transplants using transgenic UBI-EGFP donor mice. Mice received 1 mg I.P. tamoxifen injections for 5 consecutive days one week prior to femoral artery wire-induced injury29 (link). For SDF-1⟨ neutralization, mice received 100 μg I.P. control IgG or neutralizing SDF-1⟨ antibody (clone 79014; R&D Systems) 24 hours before and immediately following injury; mice received additional 50 μg I.P. injections twice weekly for the duration of the experiment. Mice were maintained in the Center for Comparative Medicine and procedures performed under a protocol approved by the Institutional Animal Care and Use Committee at the University of Colorado Denver. Morphometric analysis, Immunohistochemistry, SMC-macrophage co-culture, quantitative RT-PCR, Western analysis, and ELISA were performed as described previously18 (link),22 (link),30 (link). Full Materials and Methods are detailed in the Supplement (http://atvb.ahajournals.org).
Publication 2011
Alleles Antibodies, Neutralizing Bone Marrow Transplantation Chemokine CXCL12 Clone Cells Coculture Techniques Dietary Supplements Donors Enzyme-Linked Immunosorbent Assay Femoral Artery Immunohistochemistry Injuries Institutional Animal Care and Use Committees Macrophage Malignant Neoplasms Mice, Knockout Mice, Laboratory Mice, Transgenic MYH11 protein, human Pharmaceutical Preparations PTEN protein, human Reverse Transcriptase Polymerase Chain Reaction Tamoxifen
DNA and gene expression analysis were performed on 54 tumor specimens from Leiden, in which the BAP1 status was known. The QIAmp DNA Mini kit was used to isolate DNA for single-nucleotide polymorphism (SNP) analysis (Qiagen, Venlo, The Netherlands). SNP analysis was then performed with the Affymetrix 250K_NSP microarray and Affymetrix Cytoscan HD chip (Affymetrix, Santa Clara, California, United States of America) to detect aberrations of chromosome 3 as described previously [20 (link)]. Information on chromosome 8q was obtained by digital polymerase chain reaction (dPCR) [20 (link)]. A threshold of >2.1 was defined as having extra copies of chromosome 8q. The RNeasy mini kit was used to isolate RNA for gene expression analyses (Qiagen, Venlo, The Netherlands). Gene expression levels of CD3 and CD8 (T cells), CD68 (macrophages), and pro-inflammatory cytokines, specifically macrophage inflammatory protein 1α (CCL3), vascular endothelial growth factor A (VEGFA), stromal cell-derived factor 1 (CXCL12), CCL7, CSF-1, monocyte chemoattractant protein-1 (CCL2), RANTES (CCL5), interferon gamma-induced protein 10 (CXCL10), CCR7, and CXCR4 were obtained using the Illumina HT-12 v4 chip (Illumina, San Diego, California, United States of America). The pro-inflammatory cytokines were selected based on our previous papers [31 (link)–33 (link)]. We could validate the probes for CD3,CD8 and CD68 in 24 tumors in which gene expression levels had been determined with an Illumina HT12 v4 array and in which the number of infiltrating cells was analyzed by IF. In addition, data on RNA sequencing and Affymetrix SNP 6.0 array from 80 samples of UM were obtained from the TCGA Research Network: http://cancergenome.nih.gov/. Copy numbers for 8q were determined by Affymetrix SNP 6.0 array and analyzed with the GISTIC 2.0 algorithm [34 (link), 35 (link)]. Copy numbers >2 were categorized as extra copies of chromosome 8q. BAP1, CD68, CD3, and CD8 expression were obtained by RNA sequencing and quantified as log2(RSEM+1). BAP1 expression was dichotomized into BAP1-positive and BAP1-negative expression at the median.
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Publication 2017
CCL2 protein, human CCL3 protein, human CCL5 protein, human CCL7 protein, human CD8-Positive T-Lymphocytes Chemokine CXCL12 Chromosome Aberrations Chromosomes CSF1 protein, human CXCR4 protein, human Cytokine DNA Chips Fingers Gene Expression Gene Expression Profiling Inflammation Interferon Type II Macrophage Microarray Analysis Monocyte Chemoattractant Protein-1 Neoplasms Polymerase Chain Reaction Proteins RANTES Single Nucleotide Polymorphism Small Inducible Cytokine A3 Vascular Endothelial Growth Factor A

Most recents protocols related to «Chemokine CXCL12»

Fig. S1 shows the expression of Aldh1a1 gene among tissues, cellular characterization of ALDH-producing cells in omentum, and localization of ALDH1A2+ cells in the omentum. Fig. S2 shows gene expression analysis of Aldh1a2+ FRCs. Fig. S3 shows targeting construct of Postn-DTR allele and population analysis of omental stromal fractions. Fig. S4 includes Desmin+ FRC network, scRNA-seq analysis, and lymphoid organization of WT and Postn-DTR mice. Fig. S5 shows HEV populations in WT and Postn-DTR omenta and quantification of CXCL12 signal in the lumen of HEVs.
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Publication 2023
ALDH1A1 protein, human ALDH1A2 protein, human Alleles Cells Chemokine CXCL12 Desmin Gene Expression Gene Expression Profiling Hepatitis E virus Lymph Mus Omentum Population Group Single-Cell RNA-Seq Tissues
CRC cells were seeded in 24-well plates and grown in culture medium. At 90% confluence, the medium was replaced with medium without FBS, containing or not containing (control) PMPs, and the cells were incubated for 4 h at 37 °C in a humidified atmosphere with 5% CO2. To determine whether migration was CXCR4-dependent, cells were incubated with the CXCR4 antagonist AMD3100 (at a final concentration of 10 μM) or with anti-CXCR4 antibodies (at a final concentration of 100 μg/ml). SDF-1 (at a final concentration of 400 ng/ml) was added after incubation of CRC cells with PMPS to stimulate CXCR4-dependent cell migration. Cell migration was evaluated by measuring the cell-free surface at the beginning of the experiment (immediately after the scratch was made) and every 2 h until a 24-h period (Additional file 2: Supplementary Methods). The migration and invasion properties of tumour cells labelled with CellTracker after incorporation of PMPs were evaluated in uncoated or Matrigel-coated (10 mg/ml, Thermo Fisher Scientific) Boyden chambers, respectively (Additional file 2: Supplementary Methods).
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Publication 2023
AMD 3100 Anti-Antibodies Atmosphere Cells Chemokine CXCL12 CXCR4 protein, human matrigel Migration, Cell Neoplasm Invasiveness
Tumours were fixed in 10% neutral buffered formalin, dehydrated, and embedded in paraffin. For H&E staining, 5-μm-thick sections were cut and were examined by light microscopy (10 × and 40 × magnification).
Using a microtome, 4-µm-thin tissue slices were cut from tumours and transferred to gelatine-coated slides. The paraffin‐embedded tumour tissue sections were incubated overnight at 4°C with anti‐STAT3 (Santa Cruz Biotechnology, USA), anti‐CD163 (Proteintech, USA), anti‐TGF‐β (Santa Cruz Biotechnology, USA), anti‐vimentin (Invitrogen, USA), anti‐IL‐10 (Invitrogen, USA), and anti-CXCL12 (Novusbio, USA) (all in a dilution to 1:300). Slices were rinsed in PBS and treated with a secondary antibody conjugated to streptavidin/Haptoglobin-Related Protein (HRP) (Biocare Medical, Concord, CA, USA). Immunoreactivity to various proteins was visualized using a colorimetric-based detection kit (TrekAvidin-HRP Label + Kit from Biocare Medical, Pacheco, USA) according to the manufacturer's procedure. The digital images were captured using a high-power objective (40 ×) and a light microscope (Nikon Eclipse 2000 equipped with Nikon DS-Fi2; Nikon Corporation, Tokyo, Japan). The following scale was used to as-sess the intensity of cell immunostaining: Absence of positive cells (#1), small number of positive cells (#2), moderate number of positive cells (#3), and substantial number of positive cells (#4). Two previously trained examiners performed a double-blind evaluation of labelling intensity [18] (link).
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Publication 2023
CD163 protein, human Cells Chemokine CXCL12 Colorimetry Formalin Gelatins Haptoglobins IL10 protein, human Immunoglobulins Light Microscopy Microtomy Neoplasms Paraffin Paraffin Embedding Proteins Staphylococcal Protein A STAT3 Protein Streptavidin Technique, Dilution Tissues Transforming Growth Factor beta Vimentin
Cells were plated on coverslips coated with poly-L-lysine (Sigma) in a 6-well plate, and transfected with 2.5ug of respective plasmids with lipofectamine. Cells were serum starved overnight; treated with either 2uM GSK-F1 or 4ug/ml AMD-3100 for 2 hours and then ligand-induced with CXCL12 (200mg/ml, Peprotech). After treatment, cells were fixed with 4% PFA with 0.2% glutaraldehyde at room temperature for 15 minutes. After aspiration, cells were further incubated with 50mM NH4Cl in PBS and washed for 10 minutes, 3 times. Then cells were thoroughly washed with water, and mounted on slides using Vectashield with DAPI. Cells were imaged using a Leica DMi3000 B fluorescence microscope.
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Publication Preprint 2023
AMD 3100 Cells Chemokine CXCL12 DAPI Glutaral Ligands Lipofectamine Lysine Microscopy, Fluorescence Plasmids Poly A Serum
The chemokine CXCL12 was expressed and purified as previously described52 (link). Briefly, mature chemokine sequence, preceded by an 8His tag and an enterokinase cleavage site, was cloned into a pET21-based vector and expressed in BL21(DE3)pLysS cells by IPTG induction. Cells were lysed by sonication and chemokine containing inclusion bodies were dissolved in 50 mM Tris, 6 M guanidine-HCl, 50 mM NaCl, pH 8.0. The chemokines were bound to a Ni-NTA column, washed with 50 mM MES, 6 M guanidine-HCl, 50 mM NaCl, pH 6, and eluted with 50 mM acetate, 6 M guanidine-HCl, 50 mM NaCl, pH 4. CXCL12 was refolded in 50 mM Tris, 500 mM arginine-HCl, 1 mM EDTA, 1 mM glutathione disulfide, pH 7.5 before removal of the tag by enterokinase. The cleaved material was then bound to a C18 HPLC column (Vydac) (buffer A: 0.1% trifluoroacetic acid; buffer B: 0.1% trifluoroacetic acid, 90% acetonitrile) and eluted by a linear gradient of buffer B from 33–45%. The peak was collected, lyophilized, and stored at −80°C until use.
Publication Preprint 2023
Acetate acetonitrile Arginine Hydrochloride Buffers Cells Chemokine Chemokine CXCL12 Cloning Vectors Cytokinesis Edetic Acid Enteropeptidase Glutathione Disulfide Guanidine High-Performance Liquid Chromatographies Inclusion Bodies Isopropyl Thiogalactoside Sodium Chloride Trifluoroacetic Acid Tromethamine

Top products related to «Chemokine CXCL12»

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CXCL12 is a recombinant protein that belongs to the CXC chemokine family. It functions as a chemoattractant for a variety of cell types, including lymphocytes, monocytes, and stem cells.
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CXCL12 is a recombinant human chemokine. Chemokines are a family of small cytokines or signaling proteins secreted by a variety of cell types. CXCL12 plays a key role in the trafficking and homing of cells expressing the CXCR4 receptor.
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AMD3100 is a small molecule that acts as a CXCR4 antagonist. It is used as a laboratory tool in research applications.
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SDF-1 is a recombinant human protein that functions as a chemoattractant for a variety of cell types, including hematopoietic stem and progenitor cells. It is a member of the CXC chemokine family and binds to the CXCR4 receptor.
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The SDF-1 is a laboratory instrument designed for the detection and measurement of specific proteins or molecules in a sample. It utilizes advanced spectroscopic techniques to provide accurate and reliable data. The core function of the SDF-1 is to facilitate quantitative analysis of target analytes in a wide range of research and diagnostic applications.
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Transwell chambers are a type of lab equipment used for cell culture and biological assays. They consist of a permeable membrane insert placed inside a well, allowing for the study of cell-cell interactions and the movement of molecules across a barrier. The core function of Transwell chambers is to provide a controlled environment for culturing cells and monitoring their behavior and permeability.
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TRIzol reagent is a monophasic solution of phenol, guanidine isothiocyanate, and other proprietary components designed for the isolation of total RNA, DNA, and proteins from a variety of biological samples. The reagent maintains the integrity of the RNA while disrupting cells and dissolving cell components.
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The Bio-Plex 200 system is a multiplex immunoassay platform that allows for the simultaneous detection and quantification of multiple analytes in a single sample. The system utilizes fluorescently-labeled magnetic beads and a dual-laser detection system to perform high-throughput, multiplexed analyses.
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Fetal Bovine Serum (FBS) is a cell culture supplement derived from the blood of bovine fetuses. FBS provides a source of proteins, growth factors, and other components that support the growth and maintenance of various cell types in in vitro cell culture applications.
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SDF-1 is a laboratory instrument manufactured by Merck Group. It is used for the detection and analysis of specific cellular markers or molecular targets. The core function of SDF-1 is to provide reliable and accurate data to support research and diagnostic applications.

More about "Chemokine CXCL12"

Chemokine CXCL12, also known as stromal cell-derived factor-1 (SDF-1), is a key player in cell migration and tissue homeostasis.
This small cytokine is involved in a variety of biological processes, including immune cell trafficking, stem cell mobilization, and tissue repair.
CXCL12 binds to its receptor CXCR4, triggering signaling cascades that guide cell movement and promote cell survival.
Research into CXCL12 function and regulation holds promise for developing novel therapies for cancer, inflammation, and other disorders.
Researchers often utilize tools like Transwell chambers, TRIzol reagent, and the Bio-Plex 200 system to study CXCL12 and its effects.
AMD3100, a CXCR4 antagonist, is also commonly used in CXCL12 research.
Exploring the latest insights into this important chemokine can help advance our understanding of cell migration, tissue homeostasis, and the potential therapeutic applications of CXCL12.
By leveraging the power of AI-assisted research platforms like PubCompare.ai, researchers can optimize their CXCL12 studies, ensure reliable and high-quality results, and accelerate the development of new treatments for a wide range of diseases.