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AB258548

Human NSD1 (KMT3B) knockout HEK-293T cell lysate

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NSD1 KO cell lysate available now. KO validated. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, Homozygous: 22 bp deletion in exon4.
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Sanger Sequencing - Human NSD1 (KMT3B) knockout HEK-293T cell lysate (AB258548)
  • Sanger seq

Unknown

Sanger Sequencing - Human NSD1 (KMT3B) knockout HEK-293T cell lysate (AB258548)

Homozygous : 22 bp deletion in exon4

Key facts

Cell type

HEK-293T

Species or organism

Human

Tissue

Kidney

Knockout validation

Sanger Sequencing

Mutation description

Knockout achieved by using CRISPR/Cas9, Homozygous: 22 bp deletion in exon4.

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Complementary Products

Primary Antibodies

AB222145

Anti-KMT3B / NSD1 antibody

Immunocytochemistry/ Immunofluorescence - Anti-KMT3B / NSD1 antibody (AB222145)

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Proteins & Peptides

AB196419

Recombinant human KMT3B / NSD1 protein

Functional Studies - Recombinant human KMT3B / NSD1 protein (AB196419)

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Cell Lines & Lysates

AB266306

Human NSD1 (KMT3B) knockout HEK-293T cell line

Sanger Sequencing - Human NSD1 (KMT3B) knockout HEK-293T cell line (AB266306)

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Product details

Knockout cell lysate achieved by CRISPR/Cas9.

REACH authorisation
Abcam has not and does not intend to apply for the REACH Authorisation of customers' uses of products that contain European Authorisation list (Annex XIV) substances.
It is the responsibility of our customers to check the necessity of application of REACH Authorisation, and any other relevant authorisations, for their intended uses.

Lysate preparation: Our lysates are made using RIPA buffer to which we add a protease inhibitor cocktail and phosphatase inhibitor cocktail (ratio: 300:100:10). This means that the protein of interest is denatured. If you require a native form of the protein please use the live cell version. Please refer to our lysis protocol for further details on how our lysates are prepared.

User storage instructions: Lyophilizate may be stored at 4°C. After reconstitution, store at -20°C for short-term storage or -80°C for long-term storage.

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.

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What's included?

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Properties and storage information

Gene name
NSD1
Gene editing type
Knockout
Gene editing method
CRISPR technology
Knockout validation
Sanger Sequencing
Zygosity
Homozygous
Shipped at conditions
Ambient - Can Ship with Ice
Appropriate short-term storage conditions
-20°C
Appropriate long-term storage conditions
-20°C
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Supplementary information

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

KMT3B also known as NSD1 is a histone methyltransferase enzyme with a significant role in chromatin modification. This protein adds methyl groups to histone H3 at lysine 36 (H3K36). With a molecular mass around 280 kDa NSD1 is mostly expressed in tissues such as the brain and skeletal muscle. It plays an integral role in controlling gene expression and maintaining genomic stability through its actions on chromatin.
Biological function summary

NSD1 modulates transcription regulation by interacting with other nuclear proteins. As a part of the epigenetic regulation mechanism it is involved in complex processes of genome organization. By methylating H3K36 NSD1 affects chromatin dynamics and influences transcriptional activation and repression. NSD1 supports the orchestration of transcriptional changes in response to cellular signals and environmental stimuli.

Pathways

NSD1 interfaces with transcriptional regulation and chromatin remodeling pathways. Its enzymatic action on H3K36 links NSD1 to pathways governing cell growth and differentiation. Through its interactions NSD1 associates with proteins like MLL and SETD2 highlighting its role in the regulation of gene expression and cellular developmental pathways.

NSD1's dysfunction associates with Sotos syndrome and acute myeloid leukemia. Mutations in NSD1 lead to overgrowth and developmental delay characteristics observed in Sotos syndrome. In leukemia disrupted methylation patterns arise from NSD1 alterations affecting proteins like NUP98 contributing to oncogenic transformation and malignancy progression.
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Quality control

STR analysis

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

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Cell culture

Biosafety level

EU: 2 US: 2

Adherent/suspension

Adherent

Gender

Female

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Product protocols

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Product promise

We are committed to supporting your work with high-quality reagents, and we're here for you every step of the way. In the unlikely event that one of our products does not perform as expected, you're protected by our Product Promise.
For full details, please see our Terms & Conditions

Please note: All products are 'FOR RESEARCH USE ONLY. NOT FOR USE IN DIAGNOSTIC OR THERAPEUTIC PROCEDURES'.

For licensing inquiries, please contact partnerships@abcam.com