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Key Documents

AV31673

Sigma-Aldrich

Anti-FGD1 antibody produced in rabbit

affinity isolated antibody

Sinónimos:

Anti-FYVE, RhoGEF and PH domain containing 1 (faciogenital dysplasia)

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

107 kDa

species reactivity

human

concentration

0.5 mg - 1 mg/mL

technique(s)

immunohistochemistry: suitable
western blot: suitable

NCBI accession no.

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

Gene Information

human ... FGD1(2245)

General description

Facio-genital dysplasia protein (FGD1) is an upstream regulator of Rho GTPases and is involved in the normal development of embryos. It is also known to function as a guanine-nucleotide exchange factor which is specific for Cdc42Hs. FGD1 mutations have been implicated in Aarskog syndrome.
Rabbit Anti-FGD1 antibody recognizes canine, bovine, human, mouse, and rat FGD1.

Immunogen

Synthetic peptide directed towards the C terminal region of human FGD1

Application

Rabbit Anti-FGD1 antibody has been used for western blotting assays at a concentration of 2.0μg/ml.

Biochem/physiol Actions

FGD1 contains Dbl (DH) and pleckstrin (PH) homology domains. It can bind specifically to the Rho family GTPase Cdc42Hs and stimulate the GDP-GTP exchange of the isoprenylated form of Cdc42Hs. It also stimulates the mitogen activated protein kinase cascade leading to c-Jun kinase SAPK/JNK1 activation. FGD1 has an essential role in embryonic development, and FGD1 gene mutations result in the human developmental disorder, Aarskog-Scott syndrome.

Sequence

Synthetic peptide located within the following region: WMAVLGRAGRGDTFCPGPTLSEDREMEEAPVAALGATAEPPESPQTRDKT

Physical form

Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.

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

10 - Combustible liquids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


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C E Schwartz et al.
European journal of human genetics : EJHG, 8(11), 869-874 (2000-11-28)
The Aarskog syndrome or facio-genital dysplasia (FGDY, MIM No. 305400) is an X-linked condition characterized by short stature, macrocephaly, facial, genital and skeletal anomalies. It is caused by mutation of the FGD1 gene mapped to the Xp11.21 region. To date
Y Zheng et al.
The Journal of biological chemistry, 271(52), 33169-33172 (1996-12-27)
The Rho family of small GTP-binding proteins plays important roles in the regulation of actin cytoskeleton organization and cell growth. Activation of these GTPases involves the replacement of bound GDP with GTP, a process catalyzed by the Dbl-like guanine-nucleotide exchange
M F Olson et al.
Current biology : CB, 6(12), 1628-1633 (1996-12-01)
Dbl, a guanine nucleotide exchange factor (GEF) for members of the Rho family of small GTPases, is the prototype of a family of 15 related proteins. The majority of proteins that contain a DH (Dbl homology) domain were isolated as
Peng Hou et al.
Endocrine-related cancer, 18(6), 687-697 (2011-09-23)
The BRAF V600E mutation plays an important role in the tumorigenesis of papillary thyroid cancer (PTC). To explore an epigenetic mechanism involved in this process, we performed a genome-wide DNA methylation analysis using a methylated CpG island amplification (MCA)/CpG island
Peng Hou et al.
Cell cycle (Georgetown, Tex.), 11(2), 286-295 (2011-12-23)
Although BRAF(V600E) is well known to play an important role in the tumorigenesis of melanoma, its molecular mechanism, particularly the epigenetic aspect, has been incompletely understood. Here, we investigated the role of BRAF(V600E) signaling in altering gene methylation in the

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