MABE191

Anti-WHSC1/NSD2 Antibody, clone 29D1

Name: Anti-WHSC1/NSD2 Antibody, clone 29D1
Brand: MM
Price: 1560 PLN
Availability: InStock

clone 29D1, from mouse

Synonim(y):

Probable histone-lysine N-methyltransferase NSD2, Multiple myeloma SET domain-containing protein, Nuclear SET domain-containing protein 2, Protein trithorax-5, Wolf-Hirschhorn syndrome candidate 1 protein

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Wybierz wielkość

100 μG

1560,00 zł

Przewidywany termin wysyłki19 stycznia 2026Szczegóły

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Informacje o tej pozycji

UNSPSC Code:

12352203

NACRES:

NA.41

eCl@ss:

32160702

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Nazwa produktu

Anti-WHSC1/NSD2 Antibody, clone 29D1, clone 29D1, from mouse

biological source

mouse

conjugate

unconjugated

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

29D1, monoclonal

species reactivity

human

technique(s)

ChIP: suitable
immunoprecipitation (IP): suitable
western blot: suitable

isotype

IgG2bκ

NCBI accession no.

NP_001035889

UniProt accession no.

O96028

shipped in

wet ice

target post-translational modification

unmodified

Quality Level

100

Gene Information

human ... WHSC1(7468)

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Ta pozycja	ABE490	ABE491	HPA018893
Sigma-Aldrich MABE191 Anti-WHSC1/NSD2 Antibody, clone 29D1	Sigma-Aldrich ABE490 Anti-NSD2 Antibody	Sigma-Aldrich ABE491 Anti-Histone-lysine N-methyltransferase NSD3 Antibody	Sigma-Aldrich HPA018893 Anti-NSD3 antibody produced in rabbit
clone 29D1, monoclonal	clone polyclonal	clone polyclonal	clone polyclonal
species reactivity human	species reactivity human	species reactivity human, mouse	species reactivity human
biological source mouse	biological source rabbit	biological source rabbit	biological source rabbit
antibody form purified immunoglobulin	antibody form affinity isolated antibody	antibody form affinity isolated antibody	antibody form affinity isolated antibody
Gene Information human ... WHSC1(7468)	Gene Information human ... WHSC1(7468)	Gene Information human ... WHSC1L1(54904)	Gene Information human ... WHSC1L1(54904)
isotype IgG2bκ	isotype -	isotype -	isotype -

Analysis Note

Evaluated by Western Blot in HCT116 cell lysate.

Western Blot Analysis: 0.5 µg/mL of this antibody detected WHSC1/NSD2 in 10 µg of HCT116 cell lysate.

Application

Detect WHSC1/NSD2 using this Anti-WHSC1/NSD2 Antibody, clone 29D1 validated for use in Western Blotting, Chromatin Immunoprecipitation (ChIP), Immunoprecipitation.

Western Blot Analysis: 0.5-1 µg/mL from a representative lot detected WHSC1/NSD2 in 10 µg of HeLa nuclear extract and human placenta tissue lysate.

Chromatin Immunoprecipitation Analysis: A representative lot was used by an independent laboratory to detect WHSC1/NSD2 in transfected Gal4-reporter/293T cells. (Marango, J., et al. (2008). Blood. 111:3145-3154.)

Immunoprecipitation Analysis: A representative lot was used by an independent laboratory to detect WHSC1/NSD2 in KMS11 cells. (Marango, J., et al. (2008). Blood. 111:3145-3154.)

General description

Wolf-Hirschhorn syndrome candidate 1 protein (WHSC1), Nuclear SET domain containing protein 2 (NSD2) is a histone lysine methyltransferase that is deregulated in a subgroup of multiple myelomas. NSD proteins have been described to serve as oncogenes; however, little is known about their targets in transcriptional repression or activation. NSD2 is overexpressed in multiple myelomas via translocation between the NSD2 locus on chromosome 4 and the immunoglobulin locus on chromosome 14. NSD2 is under the regulatory control of this immunoglobulin locus. Further research is required to elucidate its roles and mechanisms in cancer.

~152 kDa observed. There are seven isoforms ranging between ~30 and ~152 kDa Different lysates may indicate different isoforms in Western Blots.

Immunogen

GST-tagged recombinant protein corresponding to human WHSC1/NSD2.

Other Notes

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

Physical form

Format: Purified

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Klasa składowania

12 - Non Combustible Liquids

wgk

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable

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Dokumenty związane z niedawno zakupionymi produktami zostały zamieszczone w Bibliotece dokumentów.

Odwiedź Bibliotekę dokumentów

Impaired H3K36 methylation defines a subset of head and neck squamous cell carcinomas.

Simon Papillon-Cavanagh et al.

Nature genetics, 49(2), 180-185 (2017-01-10)

Human papillomavirus (HPV)-negative head and neck squamous cell carcinomas (HNSCCs) are deadly and common cancers. Recent genomic studies implicate multiple genetic pathways, including cell signaling, cell cycle and immune evasion, in their development. Here we analyze public data sets and

The H3K36me2 writer-reader dependency in H3K27M-DIPG.

Jia-Ray Yu et al.

Science advances, 7(29) (2021-07-16)

Histone H3K27M is a driving mutation in diffuse intrinsic pontine glioma (DIPG), a deadly pediatric brain tumor. H3K27M reshapes the epigenome through a global inhibition of PRC2 catalytic activity and displacement of H3K27me2/3, promoting oncogenesis of DIPG. As a consequence

H3K27M in Gliomas Causes a One-Step Decrease in H3K27 Methylation and Reduced Spreading within the Constraints of H3K36 Methylation.

Ashot S Harutyunyan et al.

Cell reports, 33(7), 108390-108390 (2020-11-19)

The discovery of H3K27M mutations in pediatric gliomas marked a new chapter in cancer epigenomics. Numerous studies have investigated the effect of this mutation on H3K27 trimethylation, but only recently have we started to realize its additional effects on the

Global Regulation of the Histone Mark H3K36me2 Underlies Epithelial Plasticity and Metastatic Progression.

Salina Yuan et al.

Cancer discovery, 10(6), 854-871 (2020-03-20)

Epithelial plasticity, reversible modulation of a cell's epithelial and mesenchymal features, is associated with tumor metastasis and chemoresistance, leading causes of cancer mortality. Although different master transcription factors and epigenetic modifiers have been implicated in this process in various contexts

Powiązane treści

White Paper - The Message in the Marks: Deciphering Cancer Epigenetics

Cancer is a complex disease manifestation. At its core, it remains a disease of abnormal cellular proliferation and inappropriate gene expression. In the early days, carcinogenesis was viewed simply as resulting from a collection of genetic mutations that altered the gene expression of key oncogenic genes or tumor suppressor genes leading to uncontrolled growth and disease (Virani, S et al 2012). Today, however, research is showing that carcinogenesis results from the successive accumulation of heritable genetic and epigenetic changes. Moreover, the success in how we predict, treat and overcome cancer will likely involve not only understanding the consequences of direct genetic changes that can cause cancer, but also how the epigenetic and environmental changes cause cancer (Johnson C et al 2015; Waldmann T et al 2013). Epigenetics is the study of heritable gene expression as it relates to changes in DNA structure that are not tied to changes in DNA sequence but, instead, are tied to how the nucleic acid material is read or processed via the myriad of protein-protein, protein-nucleic acid, and nucleic acid-nucleic acid interactions that ultimately manifest themselves into a specific expression phenotype (Ngai SC et al 2012, Johnson C et al 2015). This review will discuss some of the principal aspects of epigenetic research and how they relate to our current understanding of carcinogenesis. Because epigenetics affects phenotype and changes in epigenetics are thought to be key to environmental adaptability and thus may in fact be reversed or manipulated, understanding the integration of experimental and epidemiologic science surrounding cancer and its many manifestations should lead to more effective cancer prognostics as well as treatments (Virani S et al 2012).

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