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CXCL5 (chemokine (C-X-C motif) ligand 5)

Written2013-05Anna A Bulysheva, W Andrew Yeudall
VCU Philips Institute of Oral, Craniofacial Molecular Biology, Virginia Commonwealth University, Richmond, VA 23298, USA

(Note : for Links provided by Atlas : click)


Alias (NCBI)ENA-78
HGNC Alias symbENA-78
HGNC Previous nameSCYB5
HGNC Previous namesmall inducible cytokine subfamily B (Cys-X-Cys), member 5 (epithelial-derived neutrophil-activating peptide 78)
 chemokine (C-X-C motif) ligand 5
LocusID (NCBI) 6374
Atlas_Id 40223
Location 4q13.3  [Link to chromosome band 4q13]
Location_base_pair Starts at 73995642 and ends at 73998677 bp from pter ( according to GRCh38/hg38-Dec_2013)  [Mapping CXCL5.png]
Local_order On the reverse strand.
Fusion genes
(updated 2017)
Data from Atlas, Mitelman, Cosmic Fusion, Fusion Cancer, TCGA fusion databases with official HUGO symbols (see references in chromosomal bands)


  Solid blue boxes - coding regions; patterned boxes - non-coding regions; single lines - intervening (intronic) sequences; start / stop codons and direction of transcription are indicated.
Description The CXCL5 gene is located on human chromosome 4 at 4q13.3, starting at position 74861359 and ending at position 74864496 on the reverse strand. It consists of 4 exons.
Transcription The transcript consists of 2538bp. The coding sequence begins at residue 119 and ends at residue 463. The mRNA is polyadenylated and is translated to produce a 114 residue polypeptide.


  Schematic representation of human CXCL5. C-X-C motif is indicated in red, together with predicted intrachain disulphide bridges; E-L-R motif is indicated in blue.
Description The full length polypeptide consists of 114 amino acids. The N-terminal 36 amino acids are removed to generate the mature molecule 78 amino acids in length. An E-L-R (Glu-Leu-Arg) motif, important for receptor binding, is found immediately N-terminal to the C-X-C motif (Cys-Val-Cys). The E-L-R motif is found in pro-angiogenic chemokines (Belperio et al., 2000), while the presence of the C-X-C motif places this protein into the CXC-chemokine family. CXCL5 has homology to (Walz et al., 1991).
Expression Ubiquitous in adult.
Localisation Secreted.
Function Chemotaxis, neutrophil activation, angiogenesis. Human CXCL5 is a substrate for several proteases (Van den Steen et al., 2003; Dean et al., 2008; Starr et al., 2012). These include matrix metalloprotease MMP-1, MMP-9, MMP-12, and MMP-25 (MT6-MMP), which cleave the N-terminal region of the mature (78aa) polypeptide. MMP-12 has been reported to inactivate CXCL5, as it results in cleavage within the ELR motif, as well as between residues 5 and 6. MMP-25 is also thought to activate CXCL5 by removing the N-terminal 7 amino acids from the mature polypeptide, resulting in a 71 amino acid product (8-78). MMP-9 digests CXCL5 at multiple sites: early proteolysis involves the N-terminal region and is thought to potentiate CXCL5 activity, whereas later proteolysis (upon extended incubation with the protease) results in CXCL5 inactivation.
Homology IL-8. Conservation of this gene is observed in chimpanzee, dog and cow.

Implicated in

Entity Cancer, pulmonary fibrosis, inflammatory diseases and endometriosis.
Note CXCL5 is reportedly overexpressed in a number of human tumors such as head and neck squamous cell carcinoma, gastric, pancreatic, colorectal, prostate and lung cancer as well as in lung tissue of patients with pulmonary fibrosis. CXCL5 was found to be upregulated in many types of inflammatory conditions. It plays a significant role in inflammation that occurs in diseases such as acute coronary syndrome, allergy, rheumatoid arthritis, inflammatory bowel disease, pulmonary sarcoidosis, pancreatitis and endometriosis.
Oncogenesis Abnormal expression of CXCL5 has been correlated with increased tumor cell motility and proliferation in vitro and increased tumorigenicity in vivo. It is also associated with worse clinical prognosis in several cancer types.
Entity Head and neck squamous cell carcinoma
Oncogenesis It has been reported that metastatic head and neck cancer cells express comparatively high levels of CXCL5 relative to primary tumor cells, as measured by microarray and confirmed by quantitative real-time PCR and analysis of conditioned medium (Miyazaki et al., 2006). Biological consequences of CXCL5 overexpression have been investigated in terms of tumor cell proliferation and motility, both of which are reduced if CXCL5 expression is inhibited. In vivo growth of xenografted tumor cells was abrogated when CXCL5 expression was repressed by small hairpin RNA.
Entity Gastric cancer
Oncogenesis Overexpression of CXCL5 has been found to correlate with late stage gastric cancer and high N stage, suggesting a role for CXCL5 in progression of gastric cancer and nodal metastasis (Park et al., 2007). This was revealed by immunostaining of gastric tumors for CXCL5, as well as enzyme-linked immunosorbent assay (ELISA) measurement of serum CXCL5 levels.
Entity Colorectal cancer
Oncogenesis Low expression of CXCL5 in a rat model of colorectal cancer has been reported to increase the tumorigenic potential of cells that would otherwise form a less aggressive type of colon cancer (Speetjens et al., 2008). It has also been observed that human patients with low CXCL5 levels in their colorectal tumors had a poorer prognosis than those with higher expression of CXCL5.
Entity Pancreatic cancer
Oncogenesis CXCL5 is secreted by pancreatic cancer cell lines, and antibody-mediated blockade of the CXCR2 receptor inhibits neovascularization in corneal angiogenesis assays (Wente et al., 2006). CXCL5 is also overexpressed in pancreatic cancer specimens, and is linked to poor patient survival (Frick et al., 2008). Blocking CXCR2 with an antibody, or inhibiting CXCL5 expression with siRNA, inhibits tumor xenograft formation. CXCL5 activates signaling through AKT-, ERK- and STAT-dependent pathways in pancreatic cancer cells (Li et al., 2011).
Entity Prostate cancer
Oncogenesis Androgen-independent prostate cancers tend to overexpress CXCL5. It has been reported that CXCL5 overexpression leads to increased cell migration and epithelial-to-mesenchymal transition (Kuo et al., 2011).
Entity Non-small cell lung cancer
Oncogenesis CXCL5 was found to play a role in development of non-small cell lung cancer by enhancing tumor angiogenesis (Arenberg et al., 1998). High expression of CXCL5 was correlated with vascularity of tumors. Passive immunity against CXCL5 resulted in a reduction of tumor growth, vascularity and metastases in vivo, although there was no effect of passive immunity on tumor cell proliferation.
Entity Pulmonary fibrosis
Note Analysis of bronchoalveolar lavage (BAL) fluid and lung tissue from patients with idiopathic pulmonary fibrosis revealed elevated levels of the angiogenic chemokines CXCL5 and CXCL8, together with a relative decrease of angiostatic factors, correlating with increased fibrosis of lung tissue (Streiter et al., 2007).
Entity Acute coronary syndrome (ACS)
Note Examination of CXCL5 in inflammation associated with acute coronary syndrome indicated that a polymorphism in CXCL5 (156G>C; rs352046) was linked to a 2.7-fold rise in 3-year mortality (all causes; C/C genotype only). Mortality was reduced in G/G genotype individuals by the use of statins. Treatment of human umbilical vein endothelial cells (HUVECs) with atorvastatin in vitro reduced the levels of IL-1β-induced CXCL5 in a dose-dependent manner (Zineh et al., 2008).
Entity Allergy
Note Activated mast cells have been shown to increase CXCL5 production significantly compared to the level of CXCL5 in resting cells. Supernatants from sonicated MC-9 mast cells elicited a significant influx of neutrophils when injected intratracheally in mice. When the same supernatants were preincubated with CXCL5-specific antibodies, neutrophil influx was dramatically reduced, implicating CXCL5 produced by activated mast cells as a critical chemoattractant for neutrophils (Lukacs et al., 1998).
Entity Rheumatoid arthritis (RA)
Note CXCL5 is reported to be significantly elevated in synovial fluid of patients with rheumatoid arthritis compared to patients with other forms of arthritis (Koch et al., 1994). Studies of rat adjuvant-induced arthritis (AIA), as a model for RA, showed elevated CXCL5 levels in serum with progressive development of arthritis compared to control animals. Joint homogenates also had increased levels of CXCL5 and this correlated with disease progression. Anti-CXCL5 antibody treatments prior to the onset of AIA decreased the severity of the disease (Halloran et al., 1999). The results indicate that CXCL5 plays an important role in the onset and progression of RA.
Entity Inflammatory bowel disease
Note Immunohistochemical studies of colonic epithelial cells in normal subjects and patients with inflammatory bowel disease showed that CXCL5 is expressed predominantly by crypt epithelial cells (Keates et al., 1997). CXCL5 production is significantly higher in patients with ulcerative colitis, with less intense expression in Crohn's disease patients.
Entity Pulmonary sarcoidosis
Note Increased levels of CXCL5 were found in the serum and BAL fluid of patients with pulmonary sarcoidosis compared to normal subjects, as judged by ELISA. BAL levels of CXCL5 were elevated in stage III sarcoidosis (Sujiyama et al., 2006).
Entity Pancreatitis
Note Patients with severe acute pancreatitis had significantly higher serum levels of CXCL5 compared to individuals with mild acute pancreatitis (Shokuhi et al., 2002). Samples from patients with chronic pancreatitis also showed higher expression of CXCL5 than normal pancreatic tissues, predominantly in centroacinar ducts of pancreatic lobuli (Saurer et al., 2000). These findings suggest a role for CXCL5 in development and maintenance of both acute and chronic pancreatitis.
Entity Endometriosis
Note CXCL5 has also been implicated in the pathogenesis of endometriosis, with elevated levels of CXCL5 found in peritoneal fluid of patients with endometriosis compared to control subjects (Mueller et al., 2003). Further studies showed that glandular cells, stromal fibroblasts and peritoneal macrophages were primarily responsible for CXCL5 production in patients with endometriosis. Elevated levels of CXCL5 have also been found in the follicular fluid of patients with endometriosis compared to controls (Wunder et al., 2006). Together, these studies implicate CXCL5 in the pathogenesis of endometriosis.


Epithelial-neutrophil activating peptide (ENA-78) is an important angiogenic factor in non-small cell lung cancer.
Arenberg DA, Keane MP, DiGiovine B, Kunkel SL, Morris SB, Xue YY, Burdick MD, Glass MC, Iannettoni MD, Strieter RM.
J Clin Invest. 1998 Aug 1;102(3):465-72.
PMID 9691082
CXC chemokines in angiogenesis.
Belperio JA, Keane MP, Arenberg DA, Addison CL, Ehlert JE, Burdick MD, Strieter RM.
J Leukoc Biol. 2000 Jul;68(1):1-8. (REVIEW)
PMID 10914483
Macrophage-specific metalloelastase (MMP-12) truncates and inactivates ELR+ CXC chemokines and generates CCL2, -7, -8, and -13 antagonists: potential role of the macrophage in terminating polymorphonuclear leukocyte influx.
Dean RA, Cox JH, Bellac CL, Doucet A, Starr AE, Overall CM.
Blood. 2008 Oct 15;112(8):3455-64. doi: 10.1182/blood-2007-12-129080. Epub 2008 Jul 25.
PMID 18660381
Enhanced ENA-78 and IL-8 expression in patients with malignant pancreatic diseases.
Frick VO, Rubie C, Wagner M, Graeber S, Grimm H, Kopp B, Rau BM, Schilling MK.
Pancreatology. 2008;8(4-5):488-97. doi: 10.1159/000151776. Epub 2008 Sep 3.
PMID 18765953
The role of an epithelial neutrophil-activating peptide-78-like protein in rat adjuvant-induced arthritis.
Halloran MM, Woods JM, Strieter RM, Szekanecz Z, Volin MV, Hosaka S, Haines GK 3rd, Kunkel SL, Burdick MD, Walz A, Koch AE.
J Immunol. 1999 Jun 15;162(12):7492-500.
PMID 10358204
Enterocytes are the primary source of the chemokine ENA-78 in normal colon and ulcerative colitis.
Keates S, Keates AC, Mizoguchi E, Bhan A, Kelly CP.
Am J Physiol. 1997 Jul;273(1 Pt 1):G75-82.
PMID 9252512
Epithelial neutrophil activating peptide-78: a novel chemotactic cytokine for neutrophils in arthritis.
Koch AE, Kunkel SL, Harlow LA, Mazarakis DD, Haines GK, Burdick MD, Pope RM, Walz A, Strieter RM.
J Clin Invest. 1994 Sep;94(3):1012-8.
PMID 8083342
CXCL5/ENA78 increased cell migration and epithelial-to-mesenchymal transition of hormone-independent prostate cancer by early growth response-1/snail signaling pathway.
Kuo PL, Chen YH, Chen TC, Shen KH, Hsu YL.
J Cell Physiol. 2011 May;226(5):1224-31. doi: 10.1002/jcp.22445.
PMID 20945384
Overexpression of CXCL5 is associated with poor survival in patients with pancreatic cancer.
Li A, King J, Moro A, Sugi MD, Dawson DW, Kaplan J, Li G, Lu X, Strieter RM, Burdick M, Go VL, Reber HA, Eibl G, Hines OJ.
Am J Pathol. 2011 Mar;178(3):1340-9. doi: 10.1016/j.ajpath.2010.11.058.
PMID 21356384
Mast cells produce ENA-78, which can function as a potent neutrophil chemoattractant during allergic airway inflammation.
Lukacs NW, Hogaboam CM, Kunkel SL, Chensue SW, Burdick MD, Evanoff HL, Strieter RM.
J Leukoc Biol. 1998 Jun;63(6):746-51.
PMID 9620668
Down-regulation of CXCL5 inhibits squamous carcinogenesis.
Miyazaki H, Patel V, Wang H, Edmunds RK, Gutkind JS, Yeudall WA.
Cancer Res. 2006 Apr 15;66(8):4279-84.
PMID 16618752
Epithelial neutrophil-activating peptide 78 concentrations are elevated in the peritoneal fluid of women with endometriosis.
Mueller MD, Mazzucchelli L, Buri C, Lebovic DI, Dreher E, Taylor RN.
Fertil Steril. 2003 Mar;79 Suppl 1:815-20.
PMID 12620496
CXCL5 overexpression is associated with late stage gastric cancer.
Park JY, Park KH, Bang S, Kim MH, Lee JE, Gang J, Koh SS, Song SY.
J Cancer Res Clin Oncol. 2007 Nov;133(11):835-40. Epub 2007 May 4.
PMID 17479287
Differential expression of chemokines in normal pancreas and in chronic pancreatitis.
Saurer L, Reber P, Schaffner T, Buchler MW, Buri C, Kappeler A, Walz A, Friess H, Mueller C.
Gastroenterology. 2000 Feb;118(2):356-67.
PMID 10648464
Levels of the chemokines growth-related oncogene alpha and epithelial neutrophil-activating protein 78 are raised in patients with severe acute pancreatitis.
Shokuhi S, Bhatia M, Christmas S, Sutton R, Neoptolemos JP, Slavin J.
Br J Surg. 2002 May;89(5):566-72.
PMID 11972545
Disrupted expression of CXCL5 in colorectal cancer is associated with rapid tumor formation in rats and poor prognosis in patients.
Speetjens FM, Kuppen PJ, Sandel MH, Menon AG, Burg D, van de Velde CJ, Tollenaar RA, de Bont HJ, Nagelkerke JF.
Clin Cancer Res. 2008 Apr 15;14(8):2276-84. doi: 10.1158/1078-0432.CCR-07-4045.
PMID 18413816
Biochemical characterization and N-terminomics analysis of leukolysin, the membrane-type 6 matrix metalloprotease (MMP25): chemokine and vimentin cleavages enhance cell migration and macrophage phagocytic activities.
Starr AE, Bellac CL, Dufour A, Goebeler V, Overall CM.
J Biol Chem. 2012 Apr 13;287(16):13382-95. doi: 10.1074/jbc.M111.314179. Epub 2012 Feb 24.
PMID 22367194
The role of CXC chemokines in pulmonary fibrosis.
Strieter RM, Gomperts BN, Keane MP.
J Clin Invest. 2007 Mar;117(3):549-56.
PMID 17332882
Elevated levels of interferon gamma-inducible protein-10 and epithelial neutrophil-activating peptide-78 in patients with pulmonary sarcoidosis.
Sugiyama K, Mukae H, Ishii H, Kakugawa T, Ishimoto H, Nakayama S, Shirai R, Fujii T, Mizuta Y, Kohno S.
Respirology. 2006 Nov;11(6):708-14.
PMID 17052298
Gelatinase B/MMP-9 and neutrophil collagenase/MMP-8 process the chemokines human GCP-2/CXCL6, ENA-78/CXCL5 and mouse GCP-2/LIX and modulate their physiological activities.
Van Den Steen PE, Wuyts A, Husson SJ, Proost P, Van Damme J, Opdenakker G.
Eur J Biochem. 2003 Sep;270(18):3739-49.
PMID 12950257
Structure and neutrophil-activating properties of a novel inflammatory peptide (ENA-78) with homology to interleukin 8.
Walz A, Burgener R, Car B, Baggiolini M, Kunkel SL, Strieter RM.
J Exp Med. 1991 Dec 1;174(6):1355-62.
PMID 1744577
Blockade of the chemokine receptor CXCR2 inhibits pancreatic cancer cell-induced angiogenesis.
Wente MN, Keane MP, Burdick MD, Friess H, Buchler MW, Ceyhan GO, Reber HA, Strieter RM, Hines OJ.
Cancer Lett. 2006 Sep 28;241(2):221-7. Epub 2006 Feb 3.
PMID 16458421
Increased ENA-78 in the follicular fluid of patients with endometriosis.
Wunder DM, Mueller MD, Birkhauser MH, Bersinger NA.
Acta Obstet Gynecol Scand. 2006;85(3):336-42.
PMID 16553183
Epithelial neutrophil-activating peptide (ENA-78), acute coronary syndrome prognosis, and modulatory effect of statins.
Zineh I, Beitelshees AL, Welder GJ, Hou W, Chegini N, Wu J, Cresci S, Province MA, Spertus JA.
PLoS One. 2008 Sep 3;3(9):e3117. doi: 10.1371/journal.pone.0003117.
PMID 18769620


This paper should be referenced as such :
Bulysheva, AA ; Yeudall, WA
CXCL5 (chemokine (C-X-C motif) ligand 5)
Atlas Genet Cytogenet Oncol Haematol. 2013;17(11):749-752.
Free journal version : [ pdf ]   [ DOI ]

External links


HGNC (Hugo)CXCL5   10642
Entrez_Gene (NCBI)CXCL5    C-X-C motif chemokine ligand 5
AliasesENA-78; SCYB5
GeneCards (Weizmann)CXCL5
Ensembl hg19 (Hinxton)ENSG00000163735 [Gene_View]
Ensembl hg38 (Hinxton)ENSG00000163735 [Gene_View]  ENSG00000163735 [Sequence]  chr4:73995642-73998677 [Contig_View]  CXCL5 [Vega]
ICGC DataPortalENSG00000163735
TCGA cBioPortalCXCL5
Genatlas (Paris)CXCL5
SOURCE (Princeton)CXCL5
Genetics Home Reference (NIH)CXCL5
Genomic and cartography
GoldenPath hg38 (UCSC)CXCL5  -     chr4:73995642-73998677 -  4q13.3   [Description]    (hg38-Dec_2013)
GoldenPath hg19 (UCSC)CXCL5  -     4q13.3   [Description]    (hg19-Feb_2009)
GoldenPathCXCL5 - 4q13.3 [CytoView hg19]  CXCL5 - 4q13.3 [CytoView hg38]
Genome Data Viewer NCBICXCL5 [Mapview hg19]  
Gene and transcription
Genbank (Entrez)AK026546 AK312128 BC008376 BT006807 BU169770
RefSeq transcript (Entrez)NM_002994
Consensus coding sequences : CCDS (NCBI)CXCL5
Gene ExpressionCXCL5 [ NCBI-GEO ]   CXCL5 [ EBI - ARRAY_EXPRESS ]   CXCL5 [ SEEK ]   CXCL5 [ MEM ]
Gene Expression Viewer (FireBrowse)CXCL5 [ Firebrowse - Broad ]
GenevisibleExpression of CXCL5 in : [tissues]  [cell-lines]  [cancer]  [perturbations]  
BioGPS (Tissue expression)6374
GTEX Portal (Tissue expression)CXCL5
Human Protein AtlasENSG00000163735-CXCL5 [pathology]   [cell]   [tissue]
Protein : pattern, domain, 3D structure
UniProt/SwissProtP42830   [function]  [subcellular_location]  [family_and_domains]  [pathology_and_biotech]  [ptm_processing]  [expression]  [interaction]
NextProtP42830  [Sequence]  [Exons]  [Medical]  [Publications]
With graphics : InterProP42830
Domaine pattern : Prosite (Expaxy)SMALL_CYTOKINES_CXC (PS00471)   
Domains : Interpro (EBI)Chemokine_CXC    Chemokine_CXC_CS    Chemokine_IL8-like_dom    CXC_Chemokine_domain    Interleukin_8-like_sf   
Domain families : Pfam (Sanger)IL8 (PF00048)   
Domain families : Pfam (NCBI)pfam00048   
Domain families : Smart (EMBL)SCY (SM00199)  
Conserved Domain (NCBI)CXCL5
PDB Europe2MGS   
Structural Biology KnowledgeBase2MGS   
SCOP (Structural Classification of Proteins)2MGS   
CATH (Classification of proteins structures)2MGS   
AlphaFold pdb e-kbP42830   
Human Protein Atlas [tissue]ENSG00000163735-CXCL5 [tissue]
Protein Interaction databases
IntAct (EBI)P42830
Ontologies - Pathways
Ontology : AmiGOprotein binding  extracellular region  extracellular space  chemotaxis  inflammatory response  signal transduction  G protein-coupled receptor signaling pathway  cell-cell signaling  chemokine activity  positive regulation of cell population proliferation  neutrophil chemotaxis  identical protein binding  CXCR chemokine receptor binding  antimicrobial humoral immune response mediated by antimicrobial peptide  chemokine-mediated signaling pathway  cellular response to lipopolysaccharide  
Ontology : EGO-EBIprotein binding  extracellular region  extracellular space  chemotaxis  inflammatory response  signal transduction  G protein-coupled receptor signaling pathway  cell-cell signaling  chemokine activity  positive regulation of cell population proliferation  neutrophil chemotaxis  identical protein binding  CXCR chemokine receptor binding  antimicrobial humoral immune response mediated by antimicrobial peptide  chemokine-mediated signaling pathway  cellular response to lipopolysaccharide  
Pathways : KEGGCytokine-cytokine receptor interaction    Chemokine signaling pathway    TNF signaling pathway    Pertussis    Rheumatoid arthritis   
REACTOMEP42830 [protein]
REACTOME PathwaysR-HSA-418594 [pathway]   
NDEx NetworkCXCL5
Atlas of Cancer Signalling NetworkCXCL5
Wikipedia pathwaysCXCL5
Orthology - Evolution
GeneTree (enSembl)ENSG00000163735
Phylogenetic Trees/Animal Genes : TreeFamCXCL5
Homologs : HomoloGeneCXCL5
Homology/Alignments : Family Browser (UCSC)CXCL5
Gene fusions - Rearrangements
Fusion : QuiverCXCL5
Polymorphisms : SNP and Copy number variants
NCBI Variation ViewerCXCL5 [hg38]
dbSNP Single Nucleotide Polymorphism (NCBI)CXCL5
Exome Variant ServerCXCL5
GNOMAD BrowserENSG00000163735
Varsome BrowserCXCL5
ACMGCXCL5 variants
Genomic Variants (DGV)CXCL5 [DGVbeta]
DECIPHERCXCL5 [patients]   [syndromes]   [variants]   [genes]  
CONAN: Copy Number AnalysisCXCL5 
ICGC Data PortalCXCL5 
TCGA Data PortalCXCL5 
Broad Tumor PortalCXCL5
OASIS PortalCXCL5 [ Somatic mutations - Copy number]
Somatic Mutations in Cancer : COSMICCXCL5  [overview]  [genome browser]  [tissue]  [distribution]  
Somatic Mutations in Cancer : COSMIC3DCXCL5
Mutations and Diseases : HGMDCXCL5
LOVD (Leiden Open Variation Database)[gene] [transcripts] [variants]
DgiDB (Drug Gene Interaction Database)CXCL5
DoCM (Curated mutations)CXCL5
CIViC (Clinical Interpretations of Variants in Cancer)CXCL5
NCG (London)CXCL5
Impact of mutations[PolyPhen2] [Provean] [Buck Institute : MutDB] [Mutation Assessor] [Mutanalyser]
Genetic Testing Registry CXCL5
NextProtP42830 [Medical]
Target ValidationCXCL5
Huge Navigator CXCL5 [HugePedia]
Clinical trials, drugs, therapy
Protein Interactions : CTDCXCL5
Pharm GKB GenePA35573
Clinical trialCXCL5
DataMed IndexCXCL5
PubMed137 Pubmed reference(s) in Entrez
GeneRIFsGene References Into Functions (Entrez)
REVIEW articlesautomatic search in PubMed
Last year publicationsautomatic search in PubMed

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indexed on : Fri Oct 8 21:15:44 CEST 2021

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