mProX™ Human RPS6KA1 Stable Cell Line

Sub Cat	Product Name	Target Protein Species	Host Cell Type	Assay Types	Inquiry	Datasheet
S01YF-1222-KX480	Magic™ Human RSK1(RPS6KA1) in Vitro Assay	Human		Kinase Assay

Product Information

Target Family

Kinases/Enzyme

Target Protein Species

Human

Host Cell Type

HEK293;CHO-K1;HEL

Target Classification

Kinase Cell Lines

Target Research Area

Pain and Addiction Research;Cancer Research

Related Diseases

Coffin-Lowry Syndrome; Sarcoma

Gene ID

Human:6195

UniProt ID

Human:Q15418

Product Properties

Biosafety Level

Level 1

Activity

Yes

Quantity

10⁶ cells per vial

Applications

RPS6KA1, a member of the RSK gene family, has various applications in different fields. In the context of acute myeloid leukemia (AML), RPS6KA1 and other RSK gene family members can be used to predict prognosis and treatment responses. They can help classify patients into different risk groups and determine overall survival rates. Additionally, RPS6KA1 may serve as a potential drug target for AML treatment. In the field of cancer treatment, RPS6KA1 has been implicated in resistance to therapy in AML. Inhibiting RPS6KA1 can enhance the sensitivity of cancer cells to this combination therapy. Furthermore, RPS6KA1 inhibition can target specific subclones of cancer cells and prevent relapse. In pancreatic and liver cancer, blocking miR-1976, which is regulated by RPS6KA1, can enhance chemosensitivity and improve treatment outcomes. In hepatocellular carcinoma (HCC), copy number variation (CNV) of RPS6KB1, along with BCL9, detected from circulating free DNA, can be used as prognostic markers and independent predictors of patient survival. Finally, in the field of cognitive decline, environmental enrichment, which includes physical, social, and mental activities, can improve cognitive abilities in aged mice. Late-onset environmental enrichment can restore deficits in spatial learning and memory in older mice, and this improvement is associated with specific changes in the hippocampal transcriptome, including the regulation of RPS6KA1. Overall, RPS6KA1 has diverse applications in the fields of leukemia, cancer treatment, hepatocellular carcinoma, and cognitive decline.

Protocols

Please visit our protocols page.

Customer Reviews

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FAQ

chat Morgan Garcia (Verified Customer)

How is RPS6KA1 associated with steroid-resistant asthma? Oct 08 2021

chat Patrick Liam (Creative Biolabs Scientific Support)

RPS6KA1 is hypomethylated in patients with steroid-resistant asthma, suggesting a role in the development of this condition via the MAPK signaling pathway. Oct 08 2021

chat Cameron Davis (Verified Customer)

What is the relationship between RPS6KA1 and acute myeloid leukemia (AML) prognosis? Mar 01 2022

chat Patrick Liam (Creative Biolabs Scientific Support)

The interaction of FLT3-ITD mutation and the CXCL12/CXCR4 axis in AML leads to increased RPS6KA1 expression, which is associated with drug resistance and poor prognosis. Mar 01 2022

Published Data

Fig.1 Significant reduction in viability was observed upon knockdown of RPS6KA1.

The viability of HEL cells was assessed after RPS6KA1 knockdown, relative to the control vector, with cells being cultured for 96 hours, and viability was normalized to the pLKO control vector. A total of six independently treated cell cultures, pooled from two independent experiments per construct, were analyzed. Mean and standard deviation were provided, and statistical analysis was conducted using a two-tailed Student's t-test.

Ref: Kong, Tim, et al. "DUSP6 mediates resistance to JAK2 inhibition and drives leukemic progression." Nature Cancer 4.1 (2023): 108-127.

Pubmed: 36581736

DOI: 10.1038/s43018-022-00486-8

Research Highlights

Wu, Shasha. et al. "Comprehensive analysis of the RSK gene family in acute myeloid leukemia determines a prognostic signature for the prediction of clinical prognosis and treatment responses." Hematology (Amsterdam, Netherlands), 2023.
Despite significant advancements in basic and translational research that have improved our understanding of the genetics and pathopoiesis of acute myeloid leukemia (AML), the prognosis for this disease remains poor. This is despite the development of numerous targeted therapies. Therefore, there is a need to continue to deepen our understanding of the molecular pathogenesis of AML in order to further advance treatment options.
Wu, Shasha. et al. "Comprehensive analysis of the RSK gene family in acute myeloid leukemia determines a prognostic signature for the prediction of clinical prognosis and treatment responses." Hematology (Amsterdam, Netherlands), 2023.
Pubmed: 37462338 DOI: 10.1080/16078454.2023.2235833

Weidenauer, Katharina. et al. "The ribosomal protein S6 kinase alpha-1 (RPS6KA1) induces resistance to venetoclax/azacitidine in acute myeloid leukemia." Leukemia, 2023.
The combined therapy of venetoclax and azacitidine has proven to be effective and tolerable in treating acute myeloid leukemia (AML) in older, multimorbid patients. However, despite promising results, many patients do not experience a sustained remission or are resistant to the treatment. To address this issue, a team conducted a genome-wide CRISPR/Cas9 library screen and identified various genes responsible for conferring resistance to this combination therapy. The ribosomal protein S6 kinase A1 (RPS6KA1) was found to be among the most significantly depleted genes in venetoclax/azacitidine-treated AML cells. Further studies using the RPS6KA1 inhibitor BI-D1870 showed a decrease in proliferation and colony-forming ability compared to using venetoclax/azacitidine alone. In addition, BI-D1870 was able to fully restore the sensitivity of AML cells with acquired resistance to venetoclax/azacitidine. It was also observed that RPS6KA1 inhibition effectively targeted monocytic blast subclones, which could potentially lead to relapse following venetoclax/azacitidine treatment. These findings suggest that RPS6KA1 plays a crucial role in mediating resistance to venetoclax/azacitidine and that RPS6KA1 inhibition could be a potential strategy to prevent or overcome resistance in AML treatment.
Weidenauer, Katharina. et al. "The ribosomal protein S6 kinase alpha-1 (RPS6KA1) induces resistance to venetoclax/azacitidine in acute myeloid leukemia." Leukemia, 2023.
Pubmed: 37414921 DOI: 10.1038/s41375-023-01951-8