Редактирование: CCL1

C-C motif chemokine 1 precursor (Small-inducible cytokine A1) (T lymphocyte-secreted protein I-309) [SCYA1]

==Publications==

{{medline-entry
|title=Differential gene expression profile between cord blood progenitor-derived and adult progenitor-derived human mast cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/15860227
|abstract=In order to better understand the mechanisms governing the display of mast cell characteristics in human mast cells (MCs), such as cord blood (CB)-derived cultured mast cells, peripheral blood (PB)-derived cultured MCs, and differentiated adult-lung cultured MCs, we examined the transcriptomes of these three types MCs using oligonucleotide microarray (GeneChip) and hierarchical clustering analysis. The expression profile of CB-derived MCs substantially differed from those of PB- and lung-derived MCs. In CB-derived MCs, we identified 132 up-regulated transcripts, such as [[MARCKS]], [[KRT1]], [[TIMP2]], [[SERPINA1]], and [[TLR2]], and 428 down-regulated transcripts, such as [[LTBP3]], [[CDC42BPA]], [[DDO]], [[DICER1]], and [[FCER1A]]. Moreover, using RT-PCR and FACS analysis, we confirmed the expression of [[TLR2]], which plays an important role in innate immunity, in CB-derived MCs but not in PB-derived MCs. In addition, it was observed that CB-derived MCs uniquely release histamine and [[CCL1]], which are produced by human MCs but not by human monocytes, in response to peptidoglycan (PGN), although it had been controversy issue whether CB-derived MCs could, in fact, induce degranulation in response to PGN. These results indicated that in innate immunity MCs derived from neonatal hemopoietic cells might have unique functions compared to their adult counterparts because of different gene profiles.
|mesh-terms=* Adult
* Aging
* Cell Differentiation
* Cluster Analysis
* Down-Regulation
* Fetal Blood
* Gene Expression Profiling
* Histamine Release
* Humans
* Mast Cells
* Membrane Glycoproteins
* Oligonucleotide Array Sequence Analysis
* RNA, Messenger
* Receptors, Cell Surface
* Stem Cells
* Toll-Like Receptor 2
* Toll-Like Receptors
* Transcription, Genetic
* Up-Regulation

|full-text-url=https://sci-hub.do/10.1016/j.imlet.2004.12.001
}}