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WH0006662M2

Sigma-Aldrich

Monoclonal Anti-SOX9 antibody produced in mouse

clone 3C10, purified immunoglobulin, buffered aqueous solution

Synonym(s):

Anti-CMD1, Anti-CMPD1, Anti-SRA1, Anti-SRY (sex determining region Y)-box 9 (campomelic dysplasia, autosomal sex-reversal)

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

mouse

conjugate

unconjugated

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

3C10, monoclonal

form

buffered aqueous solution

species reactivity

human

technique(s)

immunoprecipitation (IP): suitable
indirect ELISA: suitable
indirect immunofluorescence: suitable
western blot: 1-5 μg/mL

isotype

IgG2aκ

GenBank accession no.

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... SOX9(6662)

General description

The protein encoded by this gene recognizes the sequence CCTTGAG along with other members of the HMG-box class DNA-binding proteins. It acts during chondrocyte differentiation and, with steroidogenic factor 1, regulates transcription of the anti-Muellerian hormone (AMH) gene. Deficiencies lead to the skeletal malformation syndrome campomelic dysplasia, frequently with sex reversal. (provided by RefSeq)

Immunogen

SOX9 (NP_000337, 400 a.a. ~ 509 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa.

Sequence
EQLSPSHYSEQQQHSPQQIAYSPFNLPHYSPSYPPITRSQYDYTDHQNSSSYYSHAAGQGTGLYSTFTYMNPAQRPMYTPIADTSGVPSIPQTHSPQHWEQPVYTQLTRP

Application

Monoclonal Anti-SOX9 antibody produced in mouse has been used in immunofluorescence.

Biochem/physiol Actions

Sex determining region Y-box 9 (SOX9), a transcription factor, is associated with the testis-determining factor sex determining region Y (SRY). It is expressed mainly in adult tissues and also in fetal testis and skeletal tissue. SOX9 consists of two functional domains: a high-mobility group (HMG) DNA-binding domain and a C-terminal transactivation domain. It plays a major role in cartilage differentiation and early testis development. It has been reported that SOX9 might play a role in chondrogenesis. Mutation of SOX9 gene in human causes campomelic dysplasia, a severe dwarfism syndrome and autosomal XY sex reversal.

Physical form

Solution in phosphate buffered saline, pH 7.4

Legal Information

GenBank is a registered trademark of United States Department of Health and Human Services

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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Storage Class Code

10 - Combustible liquids

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Personal Protective Equipment

dust mask type N95 (US), Eyeshields, Gloves

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Autosomal sex reversal and campomelic dysplasia are caused by mutations in and around the SRY-related gene SOX9
T Wagner
Cell, 79 (1994)
Toward understanding SOX9 function in chondrocyte differentiation. V Lefebvre and B de Crombrugghe Matrix biology : journal of the International Society for Matrix Biology
V Lefebvre
INTERNATIONAL CONFERENCE ON MATHEMATICS, ENGINEERING AND INDUSTRIAL APPLICATIONS 2014 (ICoMEIA 2014), 16 (1998)
SOX9 is a potent activator of the chondrocyte-specific enhancer of the pro alpha1(II) collagen gene
V Lefebvre
Molecular and Cellular Biology, 17 (1997)
Sox9-Positive Progenitor Cells Play a Key Role in Renal Tubule Epithelial Regeneration in Mice
Hyun MiKang
Cell Reports (2016)
Loss of DNA-dependent dimerization of the transcription factor SOX9 as a cause for campomelic dysplasia
Elisabeth Sock
Human Molecular Genetics, 12 (2003)

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