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AB266326

Human SMAD9 knockout HEK-293T cell line

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SMAD9 KO cell line available to order. KO validated by. Free of charge wild type control provided. Knockout achieved by using CRISPR/Cas9, 17 bp deletion in exon 2 and 8 bp deletion in exon 2.

View Alternative Names

MAD homolog 9, MADH6, Mothers against DPP homolog 9, Mothers against decapentaplegic, Mothers against decapentaplegic homolog 9, SMAD family member 9, SMAD, mothers against DPP homolog 9 (Drosophila), SMAD8A, SMAD8B, SMAD9_HUMAN

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Sanger Sequencing - Human SMAD9 knockout HEK-293T cell line (AB266326)
  • Sanger seq

Unknown

Sanger Sequencing - Human SMAD9 knockout HEK-293T cell line (AB266326)

Allele-1 : 17 bp deletion in exon2

Sanger Sequencing - Human SMAD9 knockout HEK-293T cell line (AB266326)
  • Sanger seq

Unknown

Sanger Sequencing - Human SMAD9 knockout HEK-293T cell line (AB266326)

Allele-2 : 8 bp deletion in exon 2.

Key facts

Cell type

HEK-293T

Species or organism

Human

Tissue

Kidney

Form

Liquid

form

Knockout validation

Sanger Sequencing

Mutation description

Knockout achieved by using CRISPR/Cas9, 17 bp deletion in exon 2 and 8 bp deletion in exon 2

Product details

Recommended control: Human wild-type HEK293T cell line (ab255449). 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 and ERS Genomics Limited, and is developed with patented technology. For full details of the limited use licenses and relevant patents please refer to our limited use license and patent pages.

What's included?

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Properties and storage information

Gene name
SMAD9
Gene editing type
Knockout
Gene editing method
CRISPR technology
Knockout validation
Sanger Sequencing
Shipped at conditions
Dry Ice
Appropriate short-term storage conditions
-196°C
Appropriate long-term storage conditions
-196°C

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.
Culture medium

DMEM (High Glucose) + 10% FBS

Cryopreservation medium

Cell Freezing Medium-DMSO Serum free media, contains 8.7% DMSO in MEM supplemented with methyl cellulose.

Supplementary information

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

SMAD9 also known as Mothers against decapentaplegic homolog 9 or MADH9 is a transcription factor involved in signal transduction and transcriptional activity. It has a molecular mass of approximately 50 kDa. SMAD9 is widely expressed in various tissues including the heart brain and skeletal muscle. In its mechanical function SMAD9 becomes activated through phosphorylation by type I receptor serine/threonine kinases and forms part of the SMAD protein family that transmits extracellular signals to the nucleus affecting gene expression.
Biological function summary

SMAD9 plays a role in the cellular processes of growth and differentiation particularly within the bone morphogenetic protein (BMP) signaling pathway. It operates as part of a complex with other SMAD proteins such as SMAD1 and SMAD5 forming heteromeric complexes that regulate the transcription of BMP-responsive genes. This gene transcription is vital for the development and repair of tissues as well as the maintenance of cellular homeostasis.

Pathways

SMAD9 participates significantly in the BMP and transforming growth factor-beta (TGF-β) signaling pathways. These pathways are important for a variety of cellular responses including proliferation apoptosis and differentiation. SMAD9 associates with BMP receptors to mediate the BMP signaling cascade acting synergistically with other SMAD family members like SMAD4 which is a common mediator in these pathways. This interrelation places SMAD9 at a pivotal point within the regulation of multiple cellular responses.

Research indicates that SMAD9 mutations or dysregulation can associate with pulmonary arterial hypertension (PAH) and certain forms of cancer. In PAH altered SMAD9 signaling disrupts normal vascular remodeling resulting in elevated pulmonary artery pressure. Additionally it can interact with other proteins like BMPR2 a receptor for BMP which also plays a significant role in the pathogenesis of PAH. Understanding the involvement of SMAD9 in these conditions can provide insights into potential therapeutic targets for treatment.

Quality control

STR analysis

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

Cell culture

Biosafety level

EU: 2 US: 2

Adherent/suspension

Adherent

Gender

Female

Product protocols

Product promise

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