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MAP3K11 KO cell line available to order. KO validated by Western blot. Free of charge wild type control provided. Knockout achieved by using CRISPR/Cas9, 1 bp insertion in exon 5 and 2 bp deletion in exon 5 and 7 bp deletion in exon 5.

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Images

Western blot - Human MAP3K11 (MLK3) knockout A549 cell line (AB267168), expandable thumbnail
  • Sanger Sequencing - Human MAP3K11 (MLK3) knockout A549 cell line (AB267168), expandable thumbnail
  • Sanger Sequencing - Human MAP3K11 (MLK3) knockout A549 cell line (AB267168), expandable thumbnail
  • Sanger Sequencing - Human MAP3K11 (MLK3) knockout A549 cell line (AB267168), expandable thumbnail

Key facts

Cell type
A549
Species or organism
Human
Tissue
Lung
Form
Liquid
Knockout validation
Sanger Sequencing, Western blot
Mutation description
Knockout achieved by using CRISPR/Cas9, 1 bp insertion in exon 5 and 2 bp deletion in exon 5 and 7 bp deletion in exon 5

Alternative names

2610017K16Rik, EC 2.7.11.25, M3K11_HUMAN, MEKK11, MGC17114, Map3k11, Mitogen-activated protein kinase kinase kinase 11, Mixed lineage kinase 3, Mixed lineage protein kinase 3, PTK1, Protein tyrosine kinase PTK1, RHOE, SH3 domain containing proline rich kinase, SPRK, Src-homology 3 domain-containing proline-rich kinase

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MAP3K11 KO cell line available to order. KO validated by Western blot. Free of charge wild type control provided. Knockout achieved by using CRISPR/Cas9, 1 bp insertion in exon 5 and 2 bp deletion in exon 5 and 7 bp deletion in exon 5.

Key facts

Cell type
A549
Form
Liquid
Mutation description
Knockout achieved by using CRISPR/Cas9, 1 bp insertion in exon 5 and 2 bp deletion in exon 5 and 7 bp deletion in exon 5
Antibiotic resistance
Puromycin 1µg/mL
Disease
Carcinoma
Concentration
Loading...

Properties

Gene name
MAP3K11
Gene editing type
Knockout
Gene editing method
CRISPR technology
Knockout validation
Sanger Sequencing, Western blot

Quality control

STR analysis
CSF1PO, D13S317, D7S820, D5S818, TH01, D16S539, TPOX

Cell culture

Biosafety level
EU: 1 US: 1
Adherent/suspension
Adherent
Gender
Male

Handling procedures

Initial handling guidelines

Upon arrival, the vial should be stored in liquid nitrogen vapor phase and not at -80°C. Storage at -80°C may result in loss of viability.

1. Thaw the vial in 37°C water bath for approximately 1-2 minutes.
2. Transfer the cell suspension (0.8 mL) to a 15 mL/50 mL conical sterile polypropylene centrifuge tube containing 8.4 mL pre-warmed culture medium, wash vial with an additional 0.8 mL culture medium (total volume 10 mL) to collect remaining cells, and centrifuge at 201 x g (rcf) for 5 minutes at room temperature. 10 mL represents minimum recommended dilution. 20 mL represents maximum recommended dilution.
3. Resuspend the cell pellet in 5 mL pre-warmed culture medium and count using a haemocytometer or alternative cell counting method seed all remaining cells into a T25.
4. Incubate the culture at 37°C incubator with 5% CO2. Check the culture one day after revival and continue to check until 80% confluent. Media change can be given if needed.
5. Once confluent passage into an appropriate flask at a density of 2x104 cells/cm2. Seeding density is given as a guide only and should be scaled to align with individual lab schedules. Cultures should be monitored daily.

Subculture guidelines
  • All seeding densities should be based on cell counts gained by established methods.
  • A guide seeding density of 2x104 cells/cm2 is recommended.
  • Cells should be passaged when they have achieved 80-90% confluence.
  • Do not allow the cell density to exceed 7x104 cells/cm2.
Culture medium
F-12K + 10% FBS
Cryopreservation medium
Cell Freezing Medium-DMSO Serum free media, contains 8.7% DMSO in MEM supplemented with methyl cellulose.

Storage

Shipped at conditions
Dry Ice
Appropriate short-term storage conditions
-196°C
Appropriate long-term storage conditions
-196°C

Notes

Recommended control: Human wild-type A549 cell line (ab255450). Please note a wild-type cell line is not automatically included with a knockout cell line order, if required please add recommended wild-type cell line at no additional cost using the code WILDTYPE-TMTK1.

We will provide viable cells that proliferate on revival.

This product is subject to limited use licenses from The Broad Institute, ERS Genomics Limited and Sigma-Aldrich Co. LLC, and is developed with patented technology. For full details of the licenses and patents please refer to our limited use license and patent pages.

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.
Activity summary

MLK3 also known as MEKK11 is a kinase widely expressed in human tissues. This protein with a molecular mass of approximately 97 kDa functions as a mitogen-activated protein kinase kinase kinase (MAP3K). MLK3 mechanically activates the c-Jun N-terminal kinase (JNK) and p38 MAP kinase pathways by phosphorylating downstream MAP2Ks. It is involved in various cell processes including apoptosis and inflammation.

Biological function summary

MLK3 plays a critical role in cellular response to stress and inflammation. It acts as part of a signaling complex that regulates the JNK and p38 pathways key mediators in immune responses. These pathways control the production of pro-inflammatory cytokines and the cellular stress response. Through its kinase activity MLK3 supports the activation of transcription factors such as AP-1 which drive gene expression changes needed for its biological functions.

Pathways

MLK3 is intricately involved in the MAPK signaling cascade. It connects with other MAP3Ks like MLK1 and MLK2 contributing to the complexity of MAPK signaling. MLK3’s participation in the JNK and p38 pathways links it to cytokine signaling and cellular stress responses. These pathways are significant for maintaining cellular homeostasis and coordinating responses to external stimuli.

Associated diseases and disorders

MLK3 has implications in cancer and neurodegenerative diseases. In cancer MLK3 modulates pathways that influence cell proliferation and survival potentially leading to tumor growth and metastasis when dysregulated. Similarly altered MLK3 signaling is observed in neurodegenerative diseases possibly due to its role in managing cellular stress. MLK3 interacts with proteins like JNK and p38 which are important in disease mechanisms and progression.

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