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Proteintech irak4
Irak4, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 25 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/irak4+antibody/IRAK4+Antibody/pm41139666-40-10-17
Average 93 stars, based on 25 article reviews
irak4 - by Bioz Stars, 2026-09
93/100 stars

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Article Title: Let-7b-TLR7 Signaling Axis Contributes to the Anesthesia/Surgery-Induced Cognitive Impairment.
Article Snippet: Perioperative neurocognitive disorders (PNDs) are severe and common neurological complications among elderly patients following anesthesia and surgery.. As the first line of defense of the innate immune system, Toll-like receptors (TLRs) have been found to be involved in the occurrence of neurodegenerative diseases in recent years.. However, the role of TLR7 in the pathology and development of PNDs remains largely unclear.



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(A) Left: Graphical representation of the prioritization strategy for candidate drug targets within the inflammatory communities on GN moPDAC-old and GN huPDAC-old . Right: Graphical representation of the prioritization strategy for candidate drug targets within inflammatory-related communities on GN moMalign-old and GN huMalign-old . <t>IRAK4</t> was the only common gene to both prioritization strategies. DGIdb, drug-gene interaction database. CPAT, canSAR.ai protein annotation tool. (B) Representative phospho-IRAK4 (p-IRAK4) stains in moPDAC-young and moPDAC-old. Scale bars, 50 μm. (C) Quantification of p-IRAK4 stain in moPDAC-young and moPDAC-old. Results show mean ± SEM. ***, P < 0.001, Mann-Whitney test. (D) Representative p-IRAK4 stains in huPDAC-young and huPDAC-old. Scale bars, 100 μm. (E) Quantification of p-IRAK4 stain in huPDAC-young and huPDAC-old. Results show mean ± SEM. *, P < 0.05, Mann-Whitney test. (F) Schematic of 2-week study in moPDAC-young and moPDAC-old tumour-bearing orthotopically grafted KPC PDAC organoid-derived mouse models with 100 mg/Kg IRAK4 inhibitor (IRAK4i, emavusertib, CA-4948) or vehicle by daily oral gavage. (G) Representative p-IRAK4 stains in vehicle- and IRAK4i- treated moPDAC-old. Scale bars, 50 μm. (H) Quantification of p-IRAK4 stain in vehicle- and IRAK4i- treated moPDAC-old. Results show mean ± SEM. **, P < 0.01, Mann-Whitney test. (I) Significantly upregulated and downregulated pathways identified by GSEA of IRAK4i-treated moPDAC-old (n=8) compared to vehicle-treated moPDAC-old (n=9). (J) Representative cleaved caspase 3 (CC3) stains in vehicle- and IRAK4i-treated moPDAC-old. Scale bars, 50 μm. (K) Quantification of CC3 stain in vehicle- and IRAK4i-treated moPDAC-old. Results show mean ± SEM. *, P < 0.05, Mann-Whitney test. (L) Number of diaphragm metastases of vehicle- and IRAK4i- treated moPDAC-old. Results show mean ± SEM. *, P < 0.05, Mann-Whitney test. (M) Tumour growth, as measured by ultrasound-based imaging, shown as ratio of tumour volumes at day 14 (d14) over tumour volumes at day -1 (d-1) of vehicle- and IRAK4i- moPDAC-old. Results show mean ± SEM. *, P < 0.05, Mann-Whitney test. (N) Body weight change in vehicle- and IRAK4i- moPDAC-old at day 14 compared to day -1. Results show mean ± SEM. *, P < 0.05, Mann-Whitney test. Body weight at endpoint was calculated by removing the tumour weight. (O) Number of diaphragm metastases of vehicle- and IRAK4i- treated moPDAC-young. Results show mean ± SEM. No significant difference was observed, as assessed by Mann-Whitney test. (P) Tumour growth, as measured by ultrasound-based imaging, shown as ratio of tumour volumes at day 14 (d14) over tumour volumes at day -1 (d-1) of vehicle- and IRAK4i- moPDAC-young. Results show mean ± SEM. No significant difference was observed, as assessed by Mann-Whitney test. (Q) Body weight change in vehicle- and IRAK4i- moPDAC-young at day 14 compared to day -1. Results show mean ± SEM. No significant difference was observed, as assessed by Mann-Whitney test. Body weight at endpoint was calculated by removing the tumour weight.
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Rab43 regulates MyD88 by controlling its ubiquitination. ( A , B ) The level of MyD88 protein and mRNA was detected by western blot and qPCR in both Rab43-WT and Rab43-KO BMDMs. * p < 0.05 vs. Rab43-WT BMDMs. N.s., not statistically significant. ( C ) Co-IP detected the <t>MyD88-IRAK4</t> interaction in LPS Rab43-WT and Rab43-KO BMDMs. * p < 0.05 vs. Rab43-WT BMDMs. ( D ) The level of Ub protein was detected using western blot after Rab43-WT and Rab43-KO BMDMs were treated with 1 µg/mL LPS for 0, 1, and 2 h. * p < 0.05 vs. Rab43-WT BMDMs. ( E ) The levels of Ub and MyD88 proteins were detected using western blot after Rab43-WT, and Rab43-KO BMDMs were treated with 100 nM MG132 for 0 and 2 h. * p < 0.05 vs. Rab43-WT BMDMs. ( F ) Co-IP detected the MyD88-Ub interaction in Rab43-WT and Rab43-KO BMDMs. * p < 0.05 vs. Rab43-WT BMDMs. ( G ) qPCR detected the expression of A20, SPOP, HOIL-1, OTUD4, ABCF1, NRDP1, CYLD, RNP215, SMURF1, and SMURF2 in Rab43-WT and Rab43-KO BMDMs. * p < 0.05 vs. the Rab43-WT BMDMs. H. Rab43 and MyD88 protein expression were detected after RAW264.7 cells had been transfected with pcDNA3.1-Rab43-flag or vector plasmid. * p < 0.05 vs. vector group. The data were from at least three separate experiments.
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Rab43 regulates MyD88 by controlling its ubiquitination. ( A , B ) The level of MyD88 protein and mRNA was detected by western blot and qPCR in both Rab43-WT and Rab43-KO BMDMs. * p < 0.05 vs. Rab43-WT BMDMs. N.s., not statistically significant. ( C ) Co-IP detected the <t>MyD88-IRAK4</t> interaction in LPS Rab43-WT and Rab43-KO BMDMs. * p < 0.05 vs. Rab43-WT BMDMs. ( D ) The level of Ub protein was detected using western blot after Rab43-WT and Rab43-KO BMDMs were treated with 1 µg/mL LPS for 0, 1, and 2 h. * p < 0.05 vs. Rab43-WT BMDMs. ( E ) The levels of Ub and MyD88 proteins were detected using western blot after Rab43-WT, and Rab43-KO BMDMs were treated with 100 nM MG132 for 0 and 2 h. * p < 0.05 vs. Rab43-WT BMDMs. ( F ) Co-IP detected the MyD88-Ub interaction in Rab43-WT and Rab43-KO BMDMs. * p < 0.05 vs. Rab43-WT BMDMs. ( G ) qPCR detected the expression of A20, SPOP, HOIL-1, OTUD4, ABCF1, NRDP1, CYLD, RNP215, SMURF1, and SMURF2 in Rab43-WT and Rab43-KO BMDMs. * p < 0.05 vs. the Rab43-WT BMDMs. H. Rab43 and MyD88 protein expression were detected after RAW264.7 cells had been transfected with pcDNA3.1-Rab43-flag or vector plasmid. * p < 0.05 vs. vector group. The data were from at least three separate experiments.
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Rab43 regulates MyD88 by controlling its ubiquitination. ( A , B ) The level of MyD88 protein and mRNA was detected by western blot and qPCR in both Rab43-WT and Rab43-KO BMDMs. * p < 0.05 vs. Rab43-WT BMDMs. N.s., not statistically significant. ( C ) Co-IP detected the <t>MyD88-IRAK4</t> interaction in LPS Rab43-WT and Rab43-KO BMDMs. * p < 0.05 vs. Rab43-WT BMDMs. ( D ) The level of Ub protein was detected using western blot after Rab43-WT and Rab43-KO BMDMs were treated with 1 µg/mL LPS for 0, 1, and 2 h. * p < 0.05 vs. Rab43-WT BMDMs. ( E ) The levels of Ub and MyD88 proteins were detected using western blot after Rab43-WT, and Rab43-KO BMDMs were treated with 100 nM MG132 for 0 and 2 h. * p < 0.05 vs. Rab43-WT BMDMs. ( F ) Co-IP detected the MyD88-Ub interaction in Rab43-WT and Rab43-KO BMDMs. * p < 0.05 vs. Rab43-WT BMDMs. ( G ) qPCR detected the expression of A20, SPOP, HOIL-1, OTUD4, ABCF1, NRDP1, CYLD, RNP215, SMURF1, and SMURF2 in Rab43-WT and Rab43-KO BMDMs. * p < 0.05 vs. the Rab43-WT BMDMs. H. Rab43 and MyD88 protein expression were detected after RAW264.7 cells had been transfected with pcDNA3.1-Rab43-flag or vector plasmid. * p < 0.05 vs. vector group. The data were from at least three separate experiments.
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Image Search Results


(A) Left: Graphical representation of the prioritization strategy for candidate drug targets within the inflammatory communities on GN moPDAC-old and GN huPDAC-old . Right: Graphical representation of the prioritization strategy for candidate drug targets within inflammatory-related communities on GN moMalign-old and GN huMalign-old . IRAK4 was the only common gene to both prioritization strategies. DGIdb, drug-gene interaction database. CPAT, canSAR.ai protein annotation tool. (B) Representative phospho-IRAK4 (p-IRAK4) stains in moPDAC-young and moPDAC-old. Scale bars, 50 μm. (C) Quantification of p-IRAK4 stain in moPDAC-young and moPDAC-old. Results show mean ± SEM. ***, P < 0.001, Mann-Whitney test. (D) Representative p-IRAK4 stains in huPDAC-young and huPDAC-old. Scale bars, 100 μm. (E) Quantification of p-IRAK4 stain in huPDAC-young and huPDAC-old. Results show mean ± SEM. *, P < 0.05, Mann-Whitney test. (F) Schematic of 2-week study in moPDAC-young and moPDAC-old tumour-bearing orthotopically grafted KPC PDAC organoid-derived mouse models with 100 mg/Kg IRAK4 inhibitor (IRAK4i, emavusertib, CA-4948) or vehicle by daily oral gavage. (G) Representative p-IRAK4 stains in vehicle- and IRAK4i- treated moPDAC-old. Scale bars, 50 μm. (H) Quantification of p-IRAK4 stain in vehicle- and IRAK4i- treated moPDAC-old. Results show mean ± SEM. **, P < 0.01, Mann-Whitney test. (I) Significantly upregulated and downregulated pathways identified by GSEA of IRAK4i-treated moPDAC-old (n=8) compared to vehicle-treated moPDAC-old (n=9). (J) Representative cleaved caspase 3 (CC3) stains in vehicle- and IRAK4i-treated moPDAC-old. Scale bars, 50 μm. (K) Quantification of CC3 stain in vehicle- and IRAK4i-treated moPDAC-old. Results show mean ± SEM. *, P < 0.05, Mann-Whitney test. (L) Number of diaphragm metastases of vehicle- and IRAK4i- treated moPDAC-old. Results show mean ± SEM. *, P < 0.05, Mann-Whitney test. (M) Tumour growth, as measured by ultrasound-based imaging, shown as ratio of tumour volumes at day 14 (d14) over tumour volumes at day -1 (d-1) of vehicle- and IRAK4i- moPDAC-old. Results show mean ± SEM. *, P < 0.05, Mann-Whitney test. (N) Body weight change in vehicle- and IRAK4i- moPDAC-old at day 14 compared to day -1. Results show mean ± SEM. *, P < 0.05, Mann-Whitney test. Body weight at endpoint was calculated by removing the tumour weight. (O) Number of diaphragm metastases of vehicle- and IRAK4i- treated moPDAC-young. Results show mean ± SEM. No significant difference was observed, as assessed by Mann-Whitney test. (P) Tumour growth, as measured by ultrasound-based imaging, shown as ratio of tumour volumes at day 14 (d14) over tumour volumes at day -1 (d-1) of vehicle- and IRAK4i- moPDAC-young. Results show mean ± SEM. No significant difference was observed, as assessed by Mann-Whitney test. (Q) Body weight change in vehicle- and IRAK4i- moPDAC-young at day 14 compared to day -1. Results show mean ± SEM. No significant difference was observed, as assessed by Mann-Whitney test. Body weight at endpoint was calculated by removing the tumour weight.

Journal: bioRxiv

Article Title: Cross-species graph-embedding unmasks the ageing microenvironment as a key determinant of pancreatic cancer malignant cell biology and therapy response

doi: 10.64898/2026.02.02.703350

Figure Lengend Snippet: (A) Left: Graphical representation of the prioritization strategy for candidate drug targets within the inflammatory communities on GN moPDAC-old and GN huPDAC-old . Right: Graphical representation of the prioritization strategy for candidate drug targets within inflammatory-related communities on GN moMalign-old and GN huMalign-old . IRAK4 was the only common gene to both prioritization strategies. DGIdb, drug-gene interaction database. CPAT, canSAR.ai protein annotation tool. (B) Representative phospho-IRAK4 (p-IRAK4) stains in moPDAC-young and moPDAC-old. Scale bars, 50 μm. (C) Quantification of p-IRAK4 stain in moPDAC-young and moPDAC-old. Results show mean ± SEM. ***, P < 0.001, Mann-Whitney test. (D) Representative p-IRAK4 stains in huPDAC-young and huPDAC-old. Scale bars, 100 μm. (E) Quantification of p-IRAK4 stain in huPDAC-young and huPDAC-old. Results show mean ± SEM. *, P < 0.05, Mann-Whitney test. (F) Schematic of 2-week study in moPDAC-young and moPDAC-old tumour-bearing orthotopically grafted KPC PDAC organoid-derived mouse models with 100 mg/Kg IRAK4 inhibitor (IRAK4i, emavusertib, CA-4948) or vehicle by daily oral gavage. (G) Representative p-IRAK4 stains in vehicle- and IRAK4i- treated moPDAC-old. Scale bars, 50 μm. (H) Quantification of p-IRAK4 stain in vehicle- and IRAK4i- treated moPDAC-old. Results show mean ± SEM. **, P < 0.01, Mann-Whitney test. (I) Significantly upregulated and downregulated pathways identified by GSEA of IRAK4i-treated moPDAC-old (n=8) compared to vehicle-treated moPDAC-old (n=9). (J) Representative cleaved caspase 3 (CC3) stains in vehicle- and IRAK4i-treated moPDAC-old. Scale bars, 50 μm. (K) Quantification of CC3 stain in vehicle- and IRAK4i-treated moPDAC-old. Results show mean ± SEM. *, P < 0.05, Mann-Whitney test. (L) Number of diaphragm metastases of vehicle- and IRAK4i- treated moPDAC-old. Results show mean ± SEM. *, P < 0.05, Mann-Whitney test. (M) Tumour growth, as measured by ultrasound-based imaging, shown as ratio of tumour volumes at day 14 (d14) over tumour volumes at day -1 (d-1) of vehicle- and IRAK4i- moPDAC-old. Results show mean ± SEM. *, P < 0.05, Mann-Whitney test. (N) Body weight change in vehicle- and IRAK4i- moPDAC-old at day 14 compared to day -1. Results show mean ± SEM. *, P < 0.05, Mann-Whitney test. Body weight at endpoint was calculated by removing the tumour weight. (O) Number of diaphragm metastases of vehicle- and IRAK4i- treated moPDAC-young. Results show mean ± SEM. No significant difference was observed, as assessed by Mann-Whitney test. (P) Tumour growth, as measured by ultrasound-based imaging, shown as ratio of tumour volumes at day 14 (d14) over tumour volumes at day -1 (d-1) of vehicle- and IRAK4i- moPDAC-young. Results show mean ± SEM. No significant difference was observed, as assessed by Mann-Whitney test. (Q) Body weight change in vehicle- and IRAK4i- moPDAC-young at day 14 compared to day -1. Results show mean ± SEM. No significant difference was observed, as assessed by Mann-Whitney test. Body weight at endpoint was calculated by removing the tumour weight.

Article Snippet: Primary antibodies were anti-mouse αSMA (ab5694; Abcam; RRID:AB_2223021), anti-human αSMA (M0851, DAKO; RRID:AB_2223500), CC3 (9664; Cell signaling technologies; RRID:AB_2070042), IRAK4 (4363; Cell Signaling Technologies; RRID:AB 2126429), and p-IRAK4 (MAB2538; Abnova; RRID:AB_10555313).

Techniques: Staining, MANN-WHITNEY, Derivative Assay, Imaging

Rab43 regulates MyD88 by controlling its ubiquitination. ( A , B ) The level of MyD88 protein and mRNA was detected by western blot and qPCR in both Rab43-WT and Rab43-KO BMDMs. * p < 0.05 vs. Rab43-WT BMDMs. N.s., not statistically significant. ( C ) Co-IP detected the MyD88-IRAK4 interaction in LPS Rab43-WT and Rab43-KO BMDMs. * p < 0.05 vs. Rab43-WT BMDMs. ( D ) The level of Ub protein was detected using western blot after Rab43-WT and Rab43-KO BMDMs were treated with 1 µg/mL LPS for 0, 1, and 2 h. * p < 0.05 vs. Rab43-WT BMDMs. ( E ) The levels of Ub and MyD88 proteins were detected using western blot after Rab43-WT, and Rab43-KO BMDMs were treated with 100 nM MG132 for 0 and 2 h. * p < 0.05 vs. Rab43-WT BMDMs. ( F ) Co-IP detected the MyD88-Ub interaction in Rab43-WT and Rab43-KO BMDMs. * p < 0.05 vs. Rab43-WT BMDMs. ( G ) qPCR detected the expression of A20, SPOP, HOIL-1, OTUD4, ABCF1, NRDP1, CYLD, RNP215, SMURF1, and SMURF2 in Rab43-WT and Rab43-KO BMDMs. * p < 0.05 vs. the Rab43-WT BMDMs. H. Rab43 and MyD88 protein expression were detected after RAW264.7 cells had been transfected with pcDNA3.1-Rab43-flag or vector plasmid. * p < 0.05 vs. vector group. The data were from at least three separate experiments.

Journal: Scientific Reports

Article Title: Rab43 mitigates the inflammatory response in acute lung injury via MyD88 ubiquitination

doi: 10.1038/s41598-026-35187-0

Figure Lengend Snippet: Rab43 regulates MyD88 by controlling its ubiquitination. ( A , B ) The level of MyD88 protein and mRNA was detected by western blot and qPCR in both Rab43-WT and Rab43-KO BMDMs. * p < 0.05 vs. Rab43-WT BMDMs. N.s., not statistically significant. ( C ) Co-IP detected the MyD88-IRAK4 interaction in LPS Rab43-WT and Rab43-KO BMDMs. * p < 0.05 vs. Rab43-WT BMDMs. ( D ) The level of Ub protein was detected using western blot after Rab43-WT and Rab43-KO BMDMs were treated with 1 µg/mL LPS for 0, 1, and 2 h. * p < 0.05 vs. Rab43-WT BMDMs. ( E ) The levels of Ub and MyD88 proteins were detected using western blot after Rab43-WT, and Rab43-KO BMDMs were treated with 100 nM MG132 for 0 and 2 h. * p < 0.05 vs. Rab43-WT BMDMs. ( F ) Co-IP detected the MyD88-Ub interaction in Rab43-WT and Rab43-KO BMDMs. * p < 0.05 vs. Rab43-WT BMDMs. ( G ) qPCR detected the expression of A20, SPOP, HOIL-1, OTUD4, ABCF1, NRDP1, CYLD, RNP215, SMURF1, and SMURF2 in Rab43-WT and Rab43-KO BMDMs. * p < 0.05 vs. the Rab43-WT BMDMs. H. Rab43 and MyD88 protein expression were detected after RAW264.7 cells had been transfected with pcDNA3.1-Rab43-flag or vector plasmid. * p < 0.05 vs. vector group. The data were from at least three separate experiments.

Article Snippet: IRAK4 Antibody (#4363, CST).

Techniques: Ubiquitin Proteomics, Western Blot, Co-Immunoprecipitation Assay, Expressing, Transfection, Plasmid Preparation

When ALI takes place in mice, the membrane surface receptor TLR4 of lung macrophages recognizes LPS, activates the downstream MyD88 to recruit IRAK4 and other forms of myddosome, and subsequently generates inflammatory factors to eliminate invading pathogens. The active MyD88 is degraded by the ubiquitin-proteasome system after modification. Knockdown of Rab43 inhibited the ubiquitination modification and degradation of MyD88, and the non-degraded myddosome continuously activated the downstream inflammatory pathway, resulting in a considerable quantity of inflammatory factors that damaged lung tissue and exacerbated ALI.

Journal: Scientific Reports

Article Title: Rab43 mitigates the inflammatory response in acute lung injury via MyD88 ubiquitination

doi: 10.1038/s41598-026-35187-0

Figure Lengend Snippet: When ALI takes place in mice, the membrane surface receptor TLR4 of lung macrophages recognizes LPS, activates the downstream MyD88 to recruit IRAK4 and other forms of myddosome, and subsequently generates inflammatory factors to eliminate invading pathogens. The active MyD88 is degraded by the ubiquitin-proteasome system after modification. Knockdown of Rab43 inhibited the ubiquitination modification and degradation of MyD88, and the non-degraded myddosome continuously activated the downstream inflammatory pathway, resulting in a considerable quantity of inflammatory factors that damaged lung tissue and exacerbated ALI.

Article Snippet: IRAK4 Antibody (#4363, CST).

Techniques: Membrane, Ubiquitin Proteomics, Modification, Knockdown