SAB2102995
Anti-IRF6 antibody produced in rabbit
affinity isolated antibody
Synonym(s):
Anti-LPS, Anti-OFC6, Anti-PIT, Anti-PPS, Anti-VWS
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About This Item
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
53 kDa
species reactivity
human, pig, rat, rabbit, dog, horse
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
target post-translational modification
unmodified
Gene Information
human ... IRF6(3664)
Immunogen
Synthetic peptide directed towards the middle region of human IRF6
Application
Applications in which this antibody has been used successfully, and the associated peer-reviewed papers, are given below.
Immunohistochemistry (1 paper)
Immunohistochemistry (1 paper)
Biochem/physiol Actions
IRF6 is a member of the interferon regulatory transcription factor (IRF) family. Family members share a highly-conserved N-terminal helix-turn-helix DNA-binding domain and a less conserved C-terminal protein-binding domain. Mutations in its gene can cause van der Woude syndrome and popliteal pterygium syndrome. This protein is involved in palate formation.The protein encoded by this gene shares strong similarity with Saccharomyces cerevisiae Cdc23, a protein essential for cell cycle progression through the G2/M transition. This protein is a component of anaphase-promoting complex (APC), which is composed of eight protein subunits and highly conserved in eucaryotic cells. APC catalyzes the formation of cyclin B-ubiquitin conjugate that is responsible for the ubiquitin-mediated proteolysis of B-type cyclins. This protein and 3 other members of the APC complex contain the TPR (tetratricopeptide repeat), a protein domain important for protein-protein interaction. This gene encodes a member of the interferon regulatory transcription factor (IRF) family. Family members share a highly-conserved N-terminal helix-turn-helix DNA-binding domain and a less conserved C-terminal protein-binding domain. Mutations in this gene can cause van der Woude syndrome and popliteal pterygium syndrome. This protein is involved in palate formation. Publication Note: This RefSeq record includes a subset of the publications that are available for this gene. Please see the Entrez Gene record to access additional publications.
Sequence
Synthetic peptide located within the following region: GSVRLQISTPDIKDNIVAQLKQLYRILQTQESWQPMQPTPSMQLPPALPP
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 Code
10 - Combustible liquids
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
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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Walid D Fakhouri et al.
Human molecular genetics, 23(10), 2711-2720 (2014-01-21)
DNA variation in Interferon Regulatory Factor 6 (IRF6) causes Van der Woude syndrome (VWS), the most common syndromic form of cleft lip and palate (CLP). However, an etiologic variant in IRF6 has been found in only 70% of VWS families.
Myriam Peyrard-Janvid et al.
American journal of human genetics, 94(1), 23-32 (2013-12-24)
Mutations in interferon regulatory factor 6 (IRF6) account for ∼70% of cases of Van der Woude syndrome (VWS), the most common syndromic form of cleft lip and palate. In 8 of 45 VWS-affected families lacking a mutation in IRF6, we
Youssef A Kousa et al.
Human molecular genetics, 28(10), 1726-1737 (2019-01-29)
Mutations in IRF6, TFAP2A and GRHL3 cause orofacial clefting syndromes in humans. However, Tfap2a and Grhl3 are also required for neurulation in mice. Here, we found that homeostasis of Irf6 is also required for development of the neural tube and
Kazuo Noda et al.
Developmental biology, 415(2), 306-313 (2015-06-28)
Cleft palate is among the most common human birth defects. Submucous cleft palate (SMCP) is a subgroup of cleft palate, which may be as common as overt cleft palate. Despite the high frequency of SMCP in humans, only recently have
Y A Kousa et al.
Journal of dental research, 96(11), 1306-1313 (2017-07-22)
Rare mutations in IRF6 and GRHL3 cause Van der Woude syndrome, an autosomal dominant orofacial clefting disorder. Common variants in IRF6 and GRHL3 also contribute risk for isolated orofacial clefting. Similarly, variants within genes that encode receptor tyrosine kinase (RTK)
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