clec4e flox (Cyagen Biosciences)
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Cyagen Biosciences
clec4e flox
Clec4e Flox, supplied by Cyagen Biosciences, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cell+transcriptome+sequencing+analysis/Clec4e/pmc12521789-33-12-23
Average 93 stars, based on 1 article reviews
Clec4e Flox, supplied by Cyagen Biosciences, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cell+transcriptome+sequencing+analysis/Clec4e/pmc12521789-33-12-23
Average 93 stars, based on 1 article reviews
clec4e flox - by Bioz Stars,
2026-08
93/100 stars
Images
1) Product Images from "Targeting CLEC4E in immunosuppressive tumour‐associated macrophages via BET inhibition"
Article Title: Targeting CLEC4E in immunosuppressive tumour‐associated macrophages via BET inhibition
Journal: Clinical and Translational Medicine
doi: 10.1002/ctm2.70505
Figure Legend Snippet: Enrichment of C‐type lectin domain family 4 member E (CLEC4E) in tumour‐associated macrophage (TAM) is correlated with unfavourable patient prognosis. (A) Volcano plot of gene enrichment in TAMs by RNA sequencing. (B) Heatmap of gene expressions in M0 and TAM by RNA sequencing, ranked by expression level in TAM. (C) Immunofluorescence of paired tumour and tumour adjacent tissues from melanoma patients. (D) Comparison of CLEC4E fluorescence intensity and macrophage count per field between paired tumour and tumour adjacent tissues. (E) CLEC4E fluorescence comparison between tumours from melanoma patients in stage I/II versus stage III/IV. (F) Overall survival analysis of patients with CLEC4E high and low expressions. Median CLEC4E fluorescence level was determined as the cutoff. (G) Overall survival analysis of patients with high CD68 + infiltration and high CLEC4E expression and patients with low CD68 + infiltration and low CLEC4E expression. Median CLEC4E fluorescence level and median CD68 + infiltration level were determined as the cutoffs.
Techniques Used: RNA Sequencing, Expressing, Immunofluorescence, Comparison, Fluorescence
Figure Legend Snippet: C‐type lectin domain family 4 member E (CLEC4E) expression on tumour‐associated macrophage (TAM) promotes tumour growth in mouse models. (A) Workflow of melanoma mouse model of CLEC4E conditional knockout mice. (B) Tumour growth curve of B16F10 melanoma model. (C) Survival analysis of B16F10 melanoma model. Tumour volume exceeding 500 mm 3 was considered as the endpoint. (D) Pictures of melanoma tissues from CLEC4E knockout and control groups. (E) Body weight gain since intraperitoneal injection of ID8 cells in ovarian cancer model. (F) Survival analysis of ID8 ovarian cancer model. Body weight gain exceeding 4 g was considered as the endpoint. (G) Comparison of celiac tumour implantations in CLEC4E knockout and control groups. (H) Representative pictures of intestinal implantations. (I) Flow cytometry analysis of CD206 and CD68 from melanoma tissues at day 10. (J) Flow cytometry analysis of CD206 and CD68 from ovarian model ascites at week 8.
Techniques Used: Expressing, Knock-Out, Control, Injection, Comparison, Flow Cytometry
Figure Legend Snippet: Single‐cell RNA sequencing analysis of macrophages from melanoma tissues of C‐type lectin domain family 4 member E (CLEC4E) knockout and control mice. (A) Uniform manifold approximation and projection (UMAP) plot of total macrophages. (B) Bar chart showing proportions of macrophage clusters in CLEC4E knockout and control mice. (C) Pseudotime trajectory of macrophages. Cells were divided into five states. (D) Pseudotime trajectories and bar chart showing macrophage distributions of CLEC4E knockout and control mice. (E) Heatmap showing gene markers of each state and the proportion comparison between knockout and control mice. CLEC4E knockout mice had enriched macrophages in states 1 and 4, and decreased macrophages in states 2 and 5 compared to control mice.
Techniques Used: RNA Sequencing, Knock-Out, Control, Comparison
Figure Legend Snippet: C‐type lectin domain family 4 member E (CLEC4E) deletion suppresses tumour‐associated macrophage (TAM) proliferation and abundance in tumour microenvironment (TME). (A) Immunofluorescence of CD68 and Ki67 with B16F10 melanoma tumours from CLEC4E knockout and control mice. (B) Column charts comparing Ki67 + cells in TAM and macrophage count between control and CLEC4E knockout groups. (C) Macrophage sorting chart and qRT‐PCR comparing proliferation markers in macrophages from control and CLEC4E knockout mice. (D) qRT‐PCR of CLEC4E silencing efficiency and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis with CLEC4E silencing in TAM. (E) RT‐PCR verification of proliferation gene markers enriched in KEGG analysis. (F) Top 10 differentially expressed phosphorylated proteins between CLEC4E knockout and control macrophages. (G) Protein‒protein interaction (PPI) analysis of differentially expressed phosphorylated proteins in CLEC4E knockout versus control macrophages. (H) Western blot of PLC‐γ2, Syk and Erk phosphorylation with CLEC4E ligation in macrophages. (Trehalose‐6,6‐dibehenate) TDB concentrations were 0, 10, 25 and 50 µg/mL sequentially. (I) Cell counting kit‐8 assay of M0 and TAMs differentiated from RAW264.7 with TDB or Erk inhibitor (Erki). (j) Cell counting kit‐8 assay of peritoneal macrophages from CLEC4E knockout and control mice.
Techniques Used: Immunofluorescence, Knock-Out, Control, Quantitative RT-PCR, Reverse Transcription Polymerase Chain Reaction, Western Blot, Phospho-proteomics, Ligation, Cell Counting
Figure Legend Snippet: C‐type lectin domain family 4 member E (CLEC4E) knockout strengthens macrophage‒T cell interaction and T‐cell cytotoxicity. (A) Interactions of all cell clusters in control and CLEC4E knockout mice. (B) Bar charts showing the number and strength of total interactions. (C) Bar chart of interaction numbers of tumour‐associated macrophage (TAM)‒T cells. (D) Selective ligand‒receptor pair expressions between TAM and T cells. (E) Bar chart of RT‐PCR with sorted macrophages from mouse melanoma tissues. (F) Expressions of selective genes in T‐cell population. (G) Flow cytometry of granzyme B and CD8 in ovarian cancer ascites at week 18. (H) Flow cytometry of CD4 and CD8 in melanoma tissues at day 10. (I) Immunohistochemistry of granzyme B with intestinal implantation of ovarian cancer. (J) Immunofluorescence images of melanoma tumour tissues from two patients and the correlation between the area of mean fluorescence of CLEC4E and CD8 of 18 patients.
Techniques Used: Knock-Out, Control, Reverse Transcription Polymerase Chain Reaction, Flow Cytometry, Immunohistochemistry, Immunofluorescence, Fluorescence
Figure Legend Snippet: BET inhibitor strongly suppresses C‐type lectin domain family 4 member E (CLEC4E) expression on tumour‐associated macrophage (TAM). (A) Screening of 132 drugs for CLEC4E inhibition in RAW264.7 TAM induced by B16‐CM. (B) RT‐PCR of CLEC4E expression on BMDM with B16‐CM and NHWD‐870 treatment. (C) Western blot of CLEC4E expression on BMDM with B16‐CM and NHWD‐870 treatment. (D) Western blot of CLEC4E expression on THP‐1 TAM induced with SK28‐CM or A2780‐CM. (E) Immunofluorescence of Yumm1.7 melanoma tissues with BET inhibitor NHWD‐870 treatment.
Techniques Used: Expressing, Inhibition, Reverse Transcription Polymerase Chain Reaction, Western Blot, Immunofluorescence
Figure Legend Snippet: BET inhibitor downregulates C‐type lectin domain family 4 member E (CLEC4E) by targeting on BRD4/CEBPβ. (A) RT‐PCR showing the efficiency of RNA silencing of BRD2, BRD3 and BRD4 on BMDM‐TAM. (B) Western blot of CLEC4E with BRD2/3/4 silenced in BMDM‐TAM. (C) CHIP sequencing (CHIP‐seq) of A375 showing no BRD4 binding on CLEC4E. (D) Western blot of CLEC4E with CEBPβ silenced in BMDM‐TAM. (E) Western blot of CEBPβ with BRD2/3/4 silenced in BMDM‐TAM. (F) Western blot of CEBPβ with BRD4 silenced in THP‐1 tumour‐associated macrophage (TAM). (G) Western blot of CEBPβ with BET inhibitor NHWD‐870 (20 nM) treatment in THP‐1 TAM induced by indicated tumour conditioned medium. (H) Luciferase assay with 293T cells transfected with pGL3‐CEBPB or pLG3‐basic and BRD4 or NC plasmids. (I) CHIP‐seq of A375 showing BRD4 binding on the promoter of CEBPB.
Techniques Used: Reverse Transcription Polymerase Chain Reaction, Western Blot, ChIP-sequencing, Binding Assay, Luciferase, Transfection