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HMOX1 KO cell line available to order. KO validated by Next Generation Sequencing, Western blot. Free of charge wild type control provided. Knockout achieved by CRISPR/Cas9 X = 4 bp deletion Frameshift: 100%.

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Images

Western blot - Human HMOX1 (Heme Oxygenase 1) knockout A549 cell line (AB269503), expandable thumbnail
  • Western blot - Human HMOX1 (Heme Oxygenase 1) knockout A549 cell line (AB269503), expandable thumbnail
  • Next Generation Sequencing - Human HMOX1 (Heme Oxygenase 1) knockout A549 cell line (AB269503), expandable thumbnail
  • Next Generation Sequencing - Human HMOX1 (Heme Oxygenase 1) knockout A549 cell line (AB269503), expandable thumbnail

Publications

Key facts

Cell type
A549
Species or organism
Human
Tissue
Lung
Form
Liquid
Knockout validation
Next Generation Sequencing, Western blot
Mutation description
Knockout achieved by CRISPR/Cas9 X = 4 bp deletion Frameshift: 100%

Alternative names

32 kD, D8Wsu38e, HMOX1_HUMAN, HO, HO-1, HSP32, Heat shock protein, Heat shock protein 32 kD, Heme oxygenase (decycling) 1, Heme oxygenase 1, Hemox, Hmox, bK286B10

Recommended products

HMOX1 KO cell line available to order. KO validated by Next Generation Sequencing, Western blot. Free of charge wild type control provided. Knockout achieved by CRISPR/Cas9 X = 4 bp deletion Frameshift: 100%.

Key facts

Cell type
A549
Form
Liquid
Mutation description
Knockout achieved by CRISPR/Cas9 X = 4 bp deletion Frameshift: 100%
Disease
Carcinoma
Concentration
Loading...

Properties

Gene name
HMOX1
Gene editing type
Knockout
Gene editing method
CRISPR technology
Knockout validation
Next Generation 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 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.

Supplementary info

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

Heme Oxygenase 1 also known as HO-1 or HMOX1 is an enzyme that plays an important mechanistic role in heme catabolism. It catalyzes the degradation of heme into biliverdin carbon monoxide and free iron. This process involves the cleavage of the heme ring. HO-1 has a molecular weight of approximately 32 kDa. It is widely expressed in numerous tissues but is especially abundant in the liver and spleen. Its expression is induced by heme and other stress stimuli such as heavy metals cytokines and reactive oxygen species.

Biological function summary

Heme Oxygenase 1 serves important protective functions in the body. It is not part of a larger complex but its products such as carbon monoxide and biliverdin have their own biological activities. Carbon monoxide produced by HO-1 has antiflammatory properties and can modulate apoptotic pathways. Biliverdin is reduced to bilirubin which acts as an antioxidant. The enzyme therefore directly influences cellular stress responses and maintains cellular homeostasis through these processes.

Pathways

Heme Oxygenase 1 is integrally involved in oxidative stress response and heme metabolism. It participates in the cellular response to oxidative damage by reducing oxidative stress and promoting cytoprotection. Through its heme degradation activity it is connected with the synthesis of biologically active molecules like bilirubin and carbon monoxide. Heme Oxygenase 1 activity is related to other proteins in oxidative stress pathways such as Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2) which regulates its expression and globins which are sources of heme for HO-1 activity.

Associated diseases and disorders

Heme Oxygenase 1 has been linked to conditions like cardiovascular diseases and neurodegenerative disorders. Its expression can attenuate the severity of atherosclerosis where oxidative stress is an important factor. In neurodegenerative diseases HO-1’s antioxidant properties may provide neuroprotection by mitigating oxidative damage. The protein's interactions with inflammatory cytokines such as Interleukin-6 and tumor necrosis factor-alpha influence its activity in these disease contexts.

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