CD44 Knockout Cell Lysate

Name: CD44 Knockout Cell Lysate
SKU: DAG-KO007
Rating: 5 (1 reviews)

CD44 Knockout Cell Lysate from HeLa cell line for anti-CD44 antibody specificity validation.

COA

SDS

Datasheet

Summary

Product Overview

HeLa cell lines were engineered into double-knockout lines by CRISPR technology. The double knockout genotype was verified by PCR followed by sequencing. The CD44 knockout cell lysate are the cell homogenate in RIPA buffer made from the KO cell lines. A vial of lysate from the parental cell line was also provided as an internal control.

Nature

Cell Lysate

Alternative Names

CD44; Cd44 molecule; CD44A; METAA; RHAMM; CD44 antigen; PGP-1; PGP-I; HUTCH-I; ECMR-III; hermes antigen; hyaluronate receptor; phagocytic glycoprotein 1; phagocytic glycoprotein I; extracellular matrix receptor III; GP90 lymphocyte homing/adhesion receptor; Cell surface glycoprotein CD44 (hyaluronate binding protein);

Application Notes

Prior to SDS-PAGE fractionation, boil the lysate for 5 minutes.

Dilution

Lysate samples can be diluted with 2x SDS Sample Buffer.
After dilution, the protein sample should be aliquoted and stored at -20°C for long term storage.

Format

Lyophilized

Concentration

The protein concentration was determined with BCA assay.

Buffer

RIPA buffer

Preservative

None

Storage

Store at -20°C. Avoid repeated freeze-thaw cycles.

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Hyaluronic-Acid-Presenting Self-Assembled Nanoparticles Transform a Hyaluronidase HYAL1 Substrate into an Efficient and Selective Inhibitor

ANGEWANDTE CHEMIE-INTERNATIONAL EDITION

Authors: Duan, Haohao; Donovan, Mark; Hernandez, Franck; Di Primo, Carmelo; Garanger, Elisabeth; Schultze, Xavier; Lecommandoux, Sebastien

Abstract

In this study, an original method of macromolecular design was used to develop a hyaluronidase-1 (HYAL1) inhibitor from its principal substrate, hyaluronic acid (HA). HA-based nanoparticles (HA-NP) were obtained by copolymer self-assembly and their effects on HYAL1 activity were investigated by combining different analytical tools. Compared to HA, HA-NP exhibited an enhanced stability against HYAL1 degradation while maintaining its interaction with the HA receptors CD44 and aggrecan. HA-NP displayed a strong and selective inhibition of HYAL1 activity and retarded the hydrolysis of higher-molar-mass HA in solution. A co-nanoprecipitation process was used to formulate a range of hybrid nanoparticle samples, which demonstrated the specificity and efficiency of HA-NP in HYAL1 inhibition.

ILC2 Proliferated by IL-33 Stimulation Alleviates Acute Colitis in Rag1(-/-)Mouse through Promoting M2 Macrophage Polarization

JOURNAL OF IMMUNOLOGY RESEARCH

Authors: You, Yong; Zhang, Xiaoqing; Wang, Xiao; Yue, Dan; Meng, Fanxiang; Zhu, Junfeng; Wang, Yuanyuan; Sun, Xun

Abstract

This study was to identify functions of ILC2, a newly found innate lymphoid cell which mainly locates in mucosa organs like lungs and intestines, in IBD. We injected rIL-33 protein to C57/BL6 mouse to explore how IL-33 induces ILC2 proliferation. The results showed that ILC2 reached a proliferation peak at day 5 and expressed multiple surface markers like CD127, C-kit, CD69, CD44, ST2, CD27, DR3, MHCII, and CD90.2. ILC2 also expressed high quantity of IL-13 and IL-5 and few IL-17A which indicates a potentially immunological function in IBD development. Afterwards, we transferred sort purified ILC2 to Rag1(-/-)mouse given DSS to induce acute colitis in order to explore the innate function of ILC2. Data showed that ILC2 alleviates DSS-induced acute innate colitis by repairing epithelial barrier and restore body weight. Furthermore, we found that ILC2 can cause macrophages polarizing to M2 macrophages in the gut. Therefore, we concluded that ILC2 played a therapeutic role in mouse acute colitis.