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Key Documents

SAB4300397

Sigma-Aldrich

Anti-MYOD1 (Ab-200) antibody produced in rabbit

affinity isolated antibody

Synonyma:

Anti-MYF3 antibody produced in rabbit, Anti-MYOD antibody produced in rabbit, Anti-PUM antibody produced in rabbit, Anti-bHLHc1 antibody produced in rabbit, Anti-myogenic differentiation 1 antibody produced in rabbit

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About This Item

MDL number:
MFCD01323984
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

~40 kDa

species reactivity

mouse, human, rat

concentration

1 mg/mL

technique(s)

western blot: 1:500-1:1000

isotype

IgG

immunogen sequence

(A-S-S-P-R)

NCBI accession no.

NP_002469.2

UniProt accession no.

P15172

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... MYOD1(4654)

General description

MYOD1 (myogenic differentiation 1) gene codes for a nuclear protein, that is a member of the basic helix-loop-helix (bHLH) family of transcription factors and the myogenic factors subfamily. It is located on human chromosome 11p15.1.

Immunogen

Peptide sequence around aa. 198!202 (A-S-S-P-R), according to the protein MYOD1.

Biochem/physiol Actions

Lack of MyoD (myogenic differentiation) results in a perinatally lethal fetal akinesia. It brings histone-modifying enzymes, which help to induce muscle differentiation.

Features and Benefits

Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.

Target description

MyoD encodes a nuclear protein that belongs to the basic helix-loop-helix family of transcription factors and the myogenic factors subfamily. It regulates muscle cell differentiation by inducing cell cycle arrest, a prerequisite for myogenic initiation. The protein is also involved in muscle regeneration. It activates its own transcription which may stabilize commitment to myogenesis.

Physical form

Solution in phosphate-buffered saline containing 0.02% sodium azide and 50% glycerol

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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recommended

Č. produktu
Popis
Stanovení ceny

Storage Class

10 - Combustible liquids

wgk_germany

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable

Osvědčení o analýze (COA)

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Navštívit knihovnu dokumentů

Deficiency of the myogenic factor MyoD causes a perinatally lethal fetal akinesia
Watson CM, et al.
Journal of medical Genetics, 53(4), 264-269 (2016)
A recurrent neomorphic mutation in MYOD1 defines a clinically aggressive subset of embryonal rhabdomyosarcoma associated with PI3K-AKT pathway mutations
Kohsaka S, et al.
Nature Genetics, 46(6), 595-600 (2014)
Katalin Gyurina et al.
International journal of molecular sciences, 24(23) (2023-12-09)
Stimulation of thermogenesis by inducing uncoupling protein 1 (UCP1) expression in adipocytes is thought to promote weight loss by increasing energy expenditure, and it is postulated that the human newborn has thermogenic subcutaneous fat depots. However, it remains unclear whether
Manuela Dos Santos et al.
Advances in rheumatology (London, England), 62(1), 27-27 (2022-07-23)
Clinical evidence of skeletal muscle involvement is not uncommon in systemic lupus erythematosus (SLE). Because of the poor understanding of signaling pathways involved in SLE muscle wasting, the  aim of this study was to evaluate the effects of vitamin D supplementation
Narasimhan P Agaram et al.
Genes, chromosomes & cancer, 53(9), 779-787 (2014-05-16)
Sclerosing and spindle cell rhabdomyosarcoma (RMS) are rare types of RMS recently reclassified as a stand-alone pathologic entity, separate from embryonal RMS (ERMS). Although sclerosing and spindle cell RMS share clinical and morphologic features, a pathogenetic link based on shared
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