mProX™ Human CAMK2B Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Kinase Cell Lines
To download a Certificate of Analysis, please enter a lot number in the search box below. Note: Certificate of Analysis not available for kit components.
Lot Number
Made to Order Inquiry
InquiryBased on this stable cell line, we also provide cell-based in vitro assays to evaluate the effects of your compounds or antibodies.
Sub Cat | Product Name | Target Protein Species | Host Cell Type | Assay Types | Inquiry | Datasheet |
---|---|---|---|---|---|---|
S01YF-1122-KX1051 | Magic™ Human CaMK2β(CAMK2B) in Vitro Assay | Human | Kinase Assay |
Product Information
Product Properties
Protocols
Please visit our protocols page.
Customer Reviews
Deborah
Verified Customer
Amanda
Verified Customer
Any questions about our products? Please visit our frequently asked questions page.
Published Data
Fig.1 Upregulation of CAMK2B is associated with decreases in proliferation and fibroblast infiltration.
With lentiviral transfection, CAMK2B was either overexpressed or subjected to short-hairpin (sh) RNA-mediated silencing in SK-RC-39 cells. As demonstrated by migration experiments, migration is improved following CAMK2B silencing, although less CAMK2B overexpressing cells traverse the basement membrane than SK-RC-39 control cells.
Ref: Jia, Qingan, et al. "Anti-tumor role of CAMK2B in remodeling the stromal microenvironment and inhibiting proliferation in papillary renal cell carcinoma." Frontiers in oncology 12 (2022): 740051.
Pubmed: 35127542
DOI: 10.3389/fonc.2022.740051
Research Highlights
This paper illustrates the intrafamilial heterogeneity of CAMK2B mutant expression and broadens the clinical phenotypic spectrum of the disease.
Heiman, Paige, Sarah Drewes, and Lina Ghaloul-Gonzalez. "A familial case of CAMK2B mutation with variable expressivity." SAGE Open Medical Case Reports 9 (2021): 2050313X21990982.
Pubmed:
33796307
DOI:
10.1177/2050313X21990982
The significance of CaMKIIα and CaMKIIβ, along with their autoinhibitory control, in human brain function is underscored by these observations, which also point to the potential pathological basis of the amplification of A-type K+ currents.
Akita, Tenpei, et al. "De novo variants in CAMK 2A and CAMK 2B cause neurodevelopmental disorders." Annals of clinical and translational neurology 5.3 (2018): 280-296.