Human CD164 Antibody

Detection of CD164 by Immunohistochemistry

The downregulation of CD164 impedes breast cancer progression in vivo. (A) Schematic representation of the tumor implantation and therapeutic protocol. (B) Measurement of tumor volume and (C) assessment of tumor growth rates comparing the si-CD164 treatment group to the control group throughout the treatment period in nude mice. (D) Monitoring alterations in body weight of nude mice during the treatment duration. (E) Immunohistochemical staining of tumor tissues for Ki67, a marker of proliferation. (F) Histological analysis of primary internal organs to evaluate potential toxicity (scale bars = 50 μm). (G) Western blot analysis evaluating the knockdown efficiency of siRNA-Cd164 in the 4T1 cell line. (H) Measurement of tumor volume and (I) assessment of tumor growth rates comparing the si-Cd164 treatment group to the control group throughout the treatment period in Balb/c mice. (J) Immunohistochemical staining of tumor tissues for Ki67 and CD164 (scale bars = 50 μm). (K) Monitoring alterations in body weight of Balb/c mice during the treatment duration. Data are expressed as mean ± SD. Statistical significance was assessed utilizing two-way ANOVA and t-tests. Image collected and cropped by CiteAb from the following open publication (https://www.frontiersin.org/articles/10.3389/fimmu.2025.1601547/full), licensed under a CC-BY license. Not internally tested by R&D Systems.

Detection of CD164 by Flow Cytometry

Chemosensitivity and functional enrichment analyses of CD164 in breast carcinoma. (A) Chemosensitivity analysis of breast cancer specimens utilizing drug response data from the GDSC database. The pharmacological sensitivity profiles of four targeted agents—YK-4-279 (RNA helicase A inhibitor), BMS-345541 (IKK inhibitor), AZ960 (JAK2/3 inhibitor), and Talazoparib (PARP inhibitor)—were stratified by CD164 expression status (Low Expression [Lexp] vs. High Expression [Hexp]). Violin plot distributions revealed consistently lower IC50 values (indicating greater sensitivity) in CD164-low tumors across above compounds. (B) The pharmacological sensitivity profiles of two targeted agents—SB505124 (TGF-beta receptor inhibitor) and EPZ004777 (DOT1L inhibitor)—were also stratified by CD164 expression status (Lexp vs. Hexp). Violin plot distributions revealed consistently lower IC50 values (indicating greater sensitivity) in CD164-high tumors across above compounds. (C) GSEA analysis revealed CD164’s involvement in regulating the AMPK signaling pathway, Butanoate metabolism, and Circadian rhythm pathways. (D) GSVA analysis was performed to investigate the molecular mechanisms through which CD164 facilitates tumor progression. The gene sets were ranked based on the GSVA scores. Data was acquired from the Molecular Signatures Database. Image collected and cropped by CiteAb from the following open publication (https://www.frontiersin.org/articles/10.3389/fimmu.2025.1601547/full), licensed under a CC-BY license. Not internally tested by R&D Systems.