Journal: iScience

Article Title: Resident vascular Sca1 + progenitors differentiate into endothelial cells in vascular remodeling via miR-145-5p/ERG signaling pathway

doi: 10.1016/j.isci.2024.110080

Figure Lengend Snippet: scRNA-seq analyses revealed Sca1 + cells repopulate ECs in mouse femoral artery after injury (A) Normal femoral arteries (NC) and injured femoral arteries were digested and analyzed by scRNA-seq after 2 (FAI2W) or 4 (FAI4W) weeks. Umap plot showed visualization of unsupervised clustering of all groups. (B) Dot plot of canonical cell markers identified EC cluster ( Kdr , Flt1 , Cdh5 , Pecam1 , and Nos3 ) and SPC cluster ( Cd34 , Ly6a , and Pdgfra ). (C) Bar plot showed the constitution of Ly6a (Sca1) + or Ly6a − cells among ECs of each group. (D) Differentially expressed genes between Ly6a + and Ly6a − cells were identified and analyzed using GO enrichment. The top 10 enriched biological process terms were presented. (E) Trajectory analysis of the differentiation process from SPCs to ECs; the color change from green to blue indicates the cell’s progression from a primitive to a more developed state. (F) The expression levels of canonical EC markers and SPC markers are shown alongside the differentiation trajectory. See also Figure S1 .

Article Snippet: Cells isolated from the aortic arch of C57 wild-type mice were then sorted with Sca1 (Miltenyi Biotec, 130-122-615) microbeads according to manufacturer’s instructions.

Techniques: Expressing

Journal: iScience

Article Title: Resident vascular Sca1 + progenitors differentiate into endothelial cells in vascular remodeling via miR-145-5p/ERG signaling pathway

doi: 10.1016/j.isci.2024.110080

Figure Lengend Snippet: Vascular Sca1 + cells exhibit endothelial differentiation potential in artery injury and repair (A) Immunofluorescence staining of healthy femoral artery for CD31 and Sca1 + lineage marker tdTomato (tdT) using Sca1-CreER T2 ;Rosa26-tdTomato mouse model. The right panel showed magnification of the boxed region. (B) Immunofluorescence staining of injured femoral artery for CD31 and tdTomato (Sca1 + lineage). The right panel and the panel below showed magnification of the boxed regions. For merge images, scale bars, 100 μm. For magnification images, scale bars, 20 μm. (C) Quantification of the percentage of CD31 + tdT + cells in CD31 + cells of healthy femoral artery (HFA) and injured femoral artery (IFA). Data represent mean ± SEM, n = 6 in each group. p value was specified in the graph. Statistical differences between groups were determined by two-tailed Student’s t test for normally distributed values. See also Figure S2 .

Article Snippet: Cells isolated from the aortic arch of C57 wild-type mice were then sorted with Sca1 (Miltenyi Biotec, 130-122-615) microbeads according to manufacturer’s instructions.

Techniques: Immunofluorescence, Staining, Marker, Two Tailed Test

Journal: iScience

Article Title: Resident vascular Sca1 + progenitors differentiate into endothelial cells in vascular remodeling via miR-145-5p/ERG signaling pathway

doi: 10.1016/j.isci.2024.110080

Figure Lengend Snippet: Vascular Sca1 + cells differentiate into ECs in vein graft (A) Immunofluorescence staining of normal vena cava for CD31 and tdTomato (tdT, Sca1 + lineage). The right panel showed magnification of the boxed region. (B) Immunofluorescence staining of vein graft for CD31 and tdTomato. The right panel and the panel below showed magnification of the boxed regions. (C) Quantification of the percentage of CD31 + tdT + cells in CD31 + cells of both groups. (D) Sca1-CreER T2 ; Rosa26-tdTomato mice were bred with Rosa26-iDTR mice. Tamoxifen was given to label Sca1 + cells and diphtheria toxin (DT) injection was performed to ablate certain cells. Immunostaining for tdTomato and CD31 on vein graft sections after DT administration. For merge images, scale bars, 100 μm. For magnification images, scale bars, 20 μm. Data represent mean ± SEM, n = 5 in each group. p value was specified in the graph. Statistical differences between groups were determined by two-tailed Student’s t test for normally distributed values.

Article Snippet: Cells isolated from the aortic arch of C57 wild-type mice were then sorted with Sca1 (Miltenyi Biotec, 130-122-615) microbeads according to manufacturer’s instructions.

Techniques: Immunofluorescence, Staining, Injection, Immunostaining, Two Tailed Test

Journal: iScience

Article Title: Resident vascular Sca1 + progenitors differentiate into endothelial cells in vascular remodeling via miR-145-5p/ERG signaling pathway

doi: 10.1016/j.isci.2024.110080

Figure Lengend Snippet: Isolated Sca1 + cells could differentiate into ECs with VEGF treatment in vitro (A) The morphological changes in Sca1 + cells after treatment with 50 ng/ml VEGF for 0–5 days. (B) mRNA expression level of EC markers Kdr , Flt1 , and Pecam1 as determined by RT-PCR at different time points after culture with VEGF. (C) Protein expression level of PECAM1, CDH5, and KDR as determined by western blotting assay. (D) Protein bands were quantified by densitometry and normalized to the density of Tubulin. (E) Immunofluorescence staining of CD31 in Sca1 + cells treated with VEGF at different time points. Scale bars, 25 μm. Data represent mean ± SEM. ∗∗∗ p < 0.001, ∗∗ p < 0.01, ns p ≥ 0.05. n = 3 in each group. Statistical differences between groups were determined by one-way ANOVA analysis of variance with method of multiple comparisons.

Article Snippet: Cells isolated from the aortic arch of C57 wild-type mice were then sorted with Sca1 (Miltenyi Biotec, 130-122-615) microbeads according to manufacturer’s instructions.

Techniques: Isolation, In Vitro, Expressing, Reverse Transcription Polymerase Chain Reaction, Western Blot, Immunofluorescence, Staining

Journal: iScience

Article Title: Resident vascular Sca1 + progenitors differentiate into endothelial cells in vascular remodeling via miR-145-5p/ERG signaling pathway

doi: 10.1016/j.isci.2024.110080

Figure Lengend Snippet: The effect of miR-145-5p on the differentiation of Sca1 + cells to ECs with VEGF treatment (A) RT-PCR analysis for the expression of miR-145-5p in Sca1 + cells treated with VEGF at different time points. (B) RT-PCR showed expression of miR-145-5p in Sca1 + cells after transfection with mimic control/miR-145-5p mimic and inhibitor control/miR-145-5p inhibitor. (C) and (D) RT-PCR analysis for the expression of Pecam1 , Flt1 , and Cdh5 in Sca1 + cells transfected with mimic control/miR-145 mimic or inhibitor control/miR-145 inhibitor and cultured in VEGF. (E) the protein expression level of PECAM1, CDH5 and KDR as determined by western blotting assay in each group. (F) Protein bands were quantified by densitometry and normalized to the density of Tubulin. (G) Immunofluorescence staining of CD31 ( Pecam1 ) in Sca1 + cells and (H) analysis for fluorescence intensity of CD31 in each group, n = 3. scale bars, 25 μm. Data represent mean ± SEM. ∗∗ p < 0.01, ∗∗∗ p < 0.001, ns p ≥ 0.05. Statistical differences between groups were determined by one-way analysis of variance with method of multiple comparisons. See also Figure S3 .

Article Snippet: Cells isolated from the aortic arch of C57 wild-type mice were then sorted with Sca1 (Miltenyi Biotec, 130-122-615) microbeads according to manufacturer’s instructions.

Techniques: Reverse Transcription Polymerase Chain Reaction, Expressing, Transfection, Control, Cell Culture, Western Blot, Immunofluorescence, Staining, Fluorescence

Journal: iScience

Article Title: Resident vascular Sca1 + progenitors differentiate into endothelial cells in vascular remodeling via miR-145-5p/ERG signaling pathway

doi: 10.1016/j.isci.2024.110080

Figure Lengend Snippet: The effects of miR-145-5p on the proliferation and migration of Sca1 + cells (A) CCK8 assay for the effect of miR-145-5p overexpression on the proliferation of Sca1 + cells. Transwell migration assay (B) and wound healing assay (C) for the effect of miR-145-5p overexpression on the migration of Sca1 + cells. n = 3 in each group. Scale bars, 25 μm. Data represent mean ± SEM. ∗ p < 0.05, ∗∗ p < 0.01, ns p ≥ 0.05. Statistical differences between groups were determined by two-tailed Student’s t test for normally distributed values.

Article Snippet: Cells isolated from the aortic arch of C57 wild-type mice were then sorted with Sca1 (Miltenyi Biotec, 130-122-615) microbeads according to manufacturer’s instructions.

Techniques: Migration, CCK-8 Assay, Over Expression, Transwell Migration Assay, Wound Healing Assay, Two Tailed Test

Journal: iScience

Article Title: Resident vascular Sca1 + progenitors differentiate into endothelial cells in vascular remodeling via miR-145-5p/ERG signaling pathway

doi: 10.1016/j.isci.2024.110080

Figure Lengend Snippet: MiR-145-5p targets ERG to regulate differentiation of Sca1 + cells into ECs (A) The database TargetScan shows the combining site of miR-145-5p on ERG’s 3′-UTR region. (B) Luciferase activity of 293T cells co-transfected with wild type ERG-3′UTR and mimic control/miR-145-5p mimic or inhibitor control/miR-145-5p inhibitor. (C) Luciferase activity of Sca1 + cells co-transfected with mutant ERG-3′UTR and mimic control/miR-145-5p mimic or inhibitor control/miR-145-5p inhibitor. (D) Erg mRNA expression in Sca1 + cells transfected with mimic control or miR-145-5p mimic as measured by RT-PCR. (E) ERG expression of Sca1 + cells transfected with control plasmid vector (pcDNA-control) or plasmid to overexpress ERG (pcDNA-ERG) as measured by RT-PCR. (F) mRNA expression of Kdr , Pecam1 and Flt1 in Sca1 + cells transfected with pcDNA-control or pcDNA-ERG after treated with VEGF. (G) Protein expression level of KDR, PECAM1, and CDH5 in Sca1 + cells transfected with pcDNA-control or pcDNA-ERG after treated with VEGF. (H) mRNA expression of Kdr , Pecam1 and Flt1 in Sca1 + cells of each group as indicated. (I) Protein expression level of KDR, PECAM1, and CDH5 in Sca1 + cells of each group as indicated. (J) Protein bands were quantified by densitometry and normalized to the density of Tubulin. (K) Expression level of miR-145-5p in healthy cephalic vein and arteriovenous fistula (AVF) as determined by RT-PCR. p value between the 2 groups were specified in the graph. n = 12 in the healthy group and n = 8 in the AVF group. Data represent mean ± SEM. Statistical differences between groups were determined by one-way ANOVA analysis of variance with method of multiple comparisons or (D,E,K) two-tailed Student’s t test for normally distributed values.∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗∗ p < 0.0001, ns p ≥ 0.05. See also Figure S4 - .

Article Snippet: Cells isolated from the aortic arch of C57 wild-type mice were then sorted with Sca1 (Miltenyi Biotec, 130-122-615) microbeads according to manufacturer’s instructions.

Techniques: Luciferase, Activity Assay, Transfection, Control, Mutagenesis, Expressing, Reverse Transcription Polymerase Chain Reaction, Plasmid Preparation, Two Tailed Test

Journal: iScience

Article Title: Resident vascular Sca1 + progenitors differentiate into endothelial cells in vascular remodeling via miR-145-5p/ERG signaling pathway

doi: 10.1016/j.isci.2024.110080

Figure Lengend Snippet:

Article Snippet: Cells isolated from the aortic arch of C57 wild-type mice were then sorted with Sca1 (Miltenyi Biotec, 130-122-615) microbeads according to manufacturer’s instructions.

Techniques: Recombinant, Lysis, Purification, Luciferase, Reporter Assay, CCK-8 Assay, Plasmid Preparation, Software

Journal: Journal of Virology

Article Title: N-acetyltransferase 10 regulates alphavirus replication via N4-acetylcytidine (ac4C) modification of the lymphocyte antigen six family member E (LY6E) mRNA

doi: 10.1128/jvi.01350-23

Figure Lengend Snippet: Primer sequences used for molecular cloning

Article Snippet: Antibodies against NAT10 (cat. no. 13365-1-AP, 1:2,000, ProteinTech, Wuhan, China), LY6E (cat. no. A09496-2, 1:1,000, Boster, Wuhan, China), dsRNA/J2 (cat. no. 10010200, 1:400, Scicons, Szirak, Hungary), β-tubulin (cat. no. D198906, 1:5,000, Sangon Biotech, Shanghai, China), and ac4C (cat. no. ab25251125, 1:500, Abcam, Cambridge, USA) were also used.

Techniques: Sequencing

Journal: Journal of Virology

Article Title: N-acetyltransferase 10 regulates alphavirus replication via N4-acetylcytidine (ac4C) modification of the lymphocyte antigen six family member E (LY6E) mRNA

doi: 10.1128/jvi.01350-23

Figure Lengend Snippet: Primer sequences used for qRT-PCR

Article Snippet: Antibodies against NAT10 (cat. no. 13365-1-AP, 1:2,000, ProteinTech, Wuhan, China), LY6E (cat. no. A09496-2, 1:1,000, Boster, Wuhan, China), dsRNA/J2 (cat. no. 10010200, 1:400, Scicons, Szirak, Hungary), β-tubulin (cat. no. D198906, 1:5,000, Sangon Biotech, Shanghai, China), and ac4C (cat. no. ab25251125, 1:500, Abcam, Cambridge, USA) were also used.

Techniques: Sequencing

Journal: Journal of Virology

Article Title: N-acetyltransferase 10 regulates alphavirus replication via N4-acetylcytidine (ac4C) modification of the lymphocyte antigen six family member E (LY6E) mRNA

doi: 10.1128/jvi.01350-23

Figure Lengend Snippet: NAT10 targets LY6E, which mediates ac4C modifications during SINV infection. ( A ) Validation of candidate genes from the RNAseq data using qRT-PCR in NAT10-KD cells infected with SINV. ( B ) Predicted ac4C modification sites for the LY6E pre-mRNA and mature mRNA. ( C ) IP of 293T cells transfected with the NAT10-Myc plasmid and anti-Myc antibody; enriched LY6E mRNA was analyzed using qRT-PCR; the interactions between the NAT10 and LY6E mRNA were also analyzed. ( D ) ( Upper panel ) Immunoblot of the NAT10 immunoprecipitate in panel C. ( Lower panel ) Agarose gel electrophoresis images of the LY6E amplified using qRT-PCR in panel C. ( E ) After incubating with the anti-ac4C antibody and normal rabbit IgG mixed with protein A/G beads at 4°C for 2 h, respectively, incubation was continued with the NAT10-KD Huh7 cell lysate for 2 h. The bound ac4C-modified RNA was eluted and analyzed using qRT-PCR. ( Left panel ) The ac4C-modified RNA was also analyzed using qRT-PCR. ( Right panel ) Agarose gel electrophoresis images of the LY6E amplified using qRT-PCR. Equal amounts of RNA fragments not subjected to immunoprecipitation were used as the input controls. ( F ) ( Upper panel ) Schematic of the 4xS1m aptamer. ( Lower panel ) WT or ac4C site mutated (C–T mut) LY6E mRNA tagged with 4xS1m aptamer was incubated with cell lysates overexpressing NAT10 and separated via streptavidin-conjugated beads. NAT10 in the cell lysate was pulled down, and the LY6E mRNA was detected using an immunoblot. Cells transfected with vectors were used as negative controls. ( G ) ( Upper panel ) Schematic diagram of the dual-luciferase reporter plasmid pmirGLO. ( Lower panel ) Luciferase activity in the NAT10-KD Huh7 ( I ) or A549 (ii) cells transfected with pmirGLO with the WT or ac4C-modifier-site-mutated (C–T mut) the 3′-UTR of the LY6E mRNA. Firefly luciferase activity was normalized to Renilla luciferase activity. ( H, I ) Stability of LY6E mRNA in NAT10-KD Huh7 ( H ) and A549 ( I ) cells after treatment with actinomycin D (5 µg/mL) was analyzed using qRT-PCR at different time points. ( J ) Ly6E mRNA levels were analyzed in Huh7 cells using qRT-PCR at different time points after 24 h of Remodelin treatment with actinomycin D. Blots were quantified with ImageJ software and normalized to control levels. Data are presented as the means ± SEM ( n = 3). * P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.001, and NS, not significant (A, E, G, H, I, and J, two-way ANOVA with Bonferroni post-test; C, unpaired Student’s t -tests).

Article Snippet: Antibodies against NAT10 (cat. no. 13365-1-AP, 1:2,000, ProteinTech, Wuhan, China), LY6E (cat. no. A09496-2, 1:1,000, Boster, Wuhan, China), dsRNA/J2 (cat. no. 10010200, 1:400, Scicons, Szirak, Hungary), β-tubulin (cat. no. D198906, 1:5,000, Sangon Biotech, Shanghai, China), and ac4C (cat. no. ab25251125, 1:500, Abcam, Cambridge, USA) were also used.

Techniques: Infection, Biomarker Discovery, Quantitative RT-PCR, Modification, Transfection, Plasmid Preparation, Western Blot, Agarose Gel Electrophoresis, Amplification, Incubation, Immunoprecipitation, Luciferase, Activity Assay, Software, Control

Journal: Journal of Virology

Article Title: N-acetyltransferase 10 regulates alphavirus replication via N4-acetylcytidine (ac4C) modification of the lymphocyte antigen six family member E (LY6E) mRNA

doi: 10.1128/jvi.01350-23

Figure Lengend Snippet: Predicted ac4C modification sites in the LY6E mRNA determined using PACES ^a

Article Snippet: Antibodies against NAT10 (cat. no. 13365-1-AP, 1:2,000, ProteinTech, Wuhan, China), LY6E (cat. no. A09496-2, 1:1,000, Boster, Wuhan, China), dsRNA/J2 (cat. no. 10010200, 1:400, Scicons, Szirak, Hungary), β-tubulin (cat. no. D198906, 1:5,000, Sangon Biotech, Shanghai, China), and ac4C (cat. no. ab25251125, 1:500, Abcam, Cambridge, USA) were also used.

Techniques: Modification, Sequencing

Journal: Journal of Virology

Article Title: N-acetyltransferase 10 regulates alphavirus replication via N4-acetylcytidine (ac4C) modification of the lymphocyte antigen six family member E (LY6E) mRNA

doi: 10.1128/jvi.01350-23

Figure Lengend Snippet: Mutations in the predicted ac4C modification sites of the LY6E mRNA ^a , ^b

Article Snippet: Antibodies against NAT10 (cat. no. 13365-1-AP, 1:2,000, ProteinTech, Wuhan, China), LY6E (cat. no. A09496-2, 1:1,000, Boster, Wuhan, China), dsRNA/J2 (cat. no. 10010200, 1:400, Scicons, Szirak, Hungary), β-tubulin (cat. no. D198906, 1:5,000, Sangon Biotech, Shanghai, China), and ac4C (cat. no. ab25251125, 1:500, Abcam, Cambridge, USA) were also used.

Techniques: Modification, Sequencing

Journal: Journal of Virology

Article Title: N-acetyltransferase 10 regulates alphavirus replication via N4-acetylcytidine (ac4C) modification of the lymphocyte antigen six family member E (LY6E) mRNA

doi: 10.1128/jvi.01350-23

Figure Lengend Snippet: SINV is positively affected by NAT10 as it regulates the stability of the LY6E mRNA. ( A ) qRT-PCR analysis of LY6E mRNA expression in LY6E-KD Huh7 cells. ( B ) qRT-PCR analysis of the SINV RNA expression levels in LY6E-KD Huh7 cells at 24 hpi (MOI = 1). ( C ) Immunoblot analysis of the SINV capsid protein expression in LY6E-KD Huh7 cells at 6, 12, and 24 hpi (MOI = 1). ( D ) Plaque formation assay using the SINV infectious virions obtained from the LY6E-KD Huh7 cell culture medium at 24 hpi (MOI = 1). ( E ) qRT-PCR analysis of the SINV RNA expression levels in LY6E-KD Huh7 cells ectopically expressing LY6E and infected with SINV, 24 hpi (MOI = 1). ( F ) Immunoblot analysis of the SINV capsid protein abundance described in panel ( E ). ( G ) Plaque formation assay using the SINV infectious virions obtained from the culture supernatant described in panel ( E ). ( H ) qRT-PCR analysis of the SINV RNA expression levels in NAT10-KD Huh7 cells ectopically expressing LY6E and infected with SINV, 24 hpi (MOI = 1). ( I ) Immunoblot analysis of the SINV capsid protein abundance as described in panel ( H ). ( J ) Plaque formation assay for the SINV infectious virions obtained from the culture supernatant described in panel ( H ). Blots were quantified with ImageJ software and normalized to control levels. Data are presented as the means ± SEM ( n = 3). * P ≤ 0.05 and *** P ≤ 0.001 (A, B, and D, unpaired Student’s t -tests; E, G, H, and J, one-way ANOVA with Tukey’s multiple comparisons test).

Article Snippet: Antibodies against NAT10 (cat. no. 13365-1-AP, 1:2,000, ProteinTech, Wuhan, China), LY6E (cat. no. A09496-2, 1:1,000, Boster, Wuhan, China), dsRNA/J2 (cat. no. 10010200, 1:400, Scicons, Szirak, Hungary), β-tubulin (cat. no. D198906, 1:5,000, Sangon Biotech, Shanghai, China), and ac4C (cat. no. ab25251125, 1:500, Abcam, Cambridge, USA) were also used.

Techniques: Quantitative RT-PCR, Expressing, RNA Expression, Western Blot, Plaque Formation Assay, Cell Culture, Infection, Quantitative Proteomics, Software, Control

Journal: Journal of Virology

Article Title: N-acetyltransferase 10 regulates alphavirus replication via N4-acetylcytidine (ac4C) modification of the lymphocyte antigen six family member E (LY6E) mRNA

doi: 10.1128/jvi.01350-23

Figure Lengend Snippet: Working model showing how the loss of NAT10 reduces alphavirus replication. Alphavirus (SINV) infection upregulates NAT10 in host cells and promotes NAT10-mediated ac4C acetylation of LY6E mRNA transcripts, increasing LY6E expression and enhancing alphavirus replication.

Article Snippet: Antibodies against NAT10 (cat. no. 13365-1-AP, 1:2,000, ProteinTech, Wuhan, China), LY6E (cat. no. A09496-2, 1:1,000, Boster, Wuhan, China), dsRNA/J2 (cat. no. 10010200, 1:400, Scicons, Szirak, Hungary), β-tubulin (cat. no. D198906, 1:5,000, Sangon Biotech, Shanghai, China), and ac4C (cat. no. ab25251125, 1:500, Abcam, Cambridge, USA) were also used.

Techniques: Infection, Expressing

Journal: bioRxiv

Article Title: SuperCell2.0 enables semi-supervised construction of multimodal metacell atlases

doi: 10.64898/2026.02.19.706848

Figure Lengend Snippet: A WNN UMAP of monocytes from the CITE-seq PBMC metacells atlas. Metacells are colored by refined blood monocyte subtypes derived from multimodal clustering. B Selected Protein and RNA markers as well as signature scores (based on RNA) in the different monocyte subtypes. C Proportion of monocyte subtypes at the different time points of the HIV vaccine trial for the 8 donors. D Violin plot of LY6E , SIGLEC1 RNA expression and CD169 (encoded by SIGLEC1 ) protein expression in metacells from healthy donors (day 0 of the vaccination trial) in CD14 monocytes compared to interferon-primed CD14 monocyte clusters. (***) indicates an EdgeR FDR < 0.001 and (NS.) indicates a non-significant difference. E Experimental workflow implemented to test LY6E and CD169 as surface markers to study interferon-primed CD14 monocytes. A classical FACS strategy was used to gate CD14 monocytes from four healthy blood donors. Four CD14 subpopulations were defined by CD169 and LY6E surface expression, sorted and subjected to bulk RNA-sequencing. F Monocyte subtype proportions in each donor were measured by FACS. G Upper panel: Heatmap of the protein coding differentially expressed genes between the main CD14+,CD169-,LY6E- monocyte subpopulation and the three other CD14 monocyte subtypes. Lower panel: Selected signature scores differentially expressed between the main CD14+,CD169-,LY6E- monocyte subpopulation and the three other CD14 monocyte subtypes.

Article Snippet: Cells were blocked with human TrueStain FcX (BioLegend, 422302) for 20 minutes and subsequently stained in 50 μL/million cells of Brilliant Stain Buffer (25% v/v in FACS buffer, BD Horizon, 566349) with antibodies against CD169 (PE, BioLegend, 346003, 1:100), CD45 (PE/Cy7, BioLegend, 304015, 1:200), CD14 (FITC, BioLegend, 325604, 1:200), CD11b (BV421, BioLegend, 101236, 1:200), CD15 (BV510, BioLegend, 323028, 1:200), CD16 (BV785, BioLegend, 302045, 1:200), and LY6E (APC, Creative Biolabs, MOB-636, 1:100).

Techniques: Derivative Assay, RNA Expression, Expressing, RNA Sequencing