SAB2102760
Anti-ZEB2 antibody produced in rabbit
affinity isolated antibody
Synonym(s):
Anti-KIAA0569, Anti-SIP1, Anti-SMADIP1, Anti-Zinc finger E-box binding homeobox 2
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All Photos(4)
About This Item
Recommended Products
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
136 kDa
species reactivity
human, pig
concentration
0.5 mg - 1 mg/mL
technique(s)
immunohistochemistry: suitable
western blot: suitable
UniProt accession no.
shipped in
wet ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... ZEB2(9839)
Immunogen
Synthetic peptide directed towards the N terminal region of human ZEB2
Biochem/physiol Actions
The ZFHX1B gene is a member of the delta-EF1/Zfh1 family of 2-handed zinc finger/homeodomain proteins. ZFHX1B is strongly transcribed at an early stage in the developing peripheral and central nervous systems of both mice and humans, in all neuronal regions of the brains of 25-week human fetuses and adult mice, and in numerous nonneural tissues. The SMADIP1 gene (also known as SIP1) is a member of the delta-EF1 (ZEB1; MIM 189909)/Zfh1 family of 2-handed zinc finger/homeodomain proteins. SMADIP1 interacts with receptor-mediated, activated full-length SMADs (see MIM 605568) (Verschueren et al., 1999 [PubMed 10400677]).[supplied by OMIM]. 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. PRIMARYREFSEQ_SPAN PRIMARY_IDENTIFIER PRIMARY_SPAN COMP 1-58 AB056507.1 1-58 59-553 AL118674.1 57-551 554-5558 AB056507.1 553-5557 5559-5583 AI858477.1 1-25 c
Physical properties
Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.
Sequence
Synthetic peptide located within the following region: SETDEEDKLHIAEDDGIANPLDQETSPASVPNHESSPHVSQALLPREEEE
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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Abisola Abisoye-Ogunniyan et al.
Cancer letters, 431, 1-10 (2018-05-12)
The loss of miR-200 family, through DNA methylation, results in cancer cells undergoing an epithelial to mesenchymal transition (EMT), and metastasis. In this study, we established that the transcriptional repressor Kaiso directly binds methylated regions of the miR-200 family, and
C Depner et al.
Nature communications, 7, 12329-12329 (2016-07-30)
Diffuse invasion of the surrounding brain parenchyma is a major obstacle in the treatment of gliomas with various therapeutics, including anti-angiogenic agents. Here we identify the epi-/genetic and microenvironmental downregulation of ephrinB2 as a crucial step that promotes tumour invasion
Mingxia Xiong et al.
American journal of physiology. Renal physiology, 302(3), F369-F379 (2011-10-21)
Most chronic kidney injuries inevitably progress to irreversible renal fibrosis. Tubular epithelial-to-mesenchymal transition (EMT) is recognized to play pivotal roles in the process of renal fibrosis. However, a comprehensive understanding of the pathogenesis of renal scar formation and progression remains
Michaël H Meel et al.
Clinical cancer research : an official journal of the American Association for Cancer Research, 26(13), 3319-3332 (2020-03-14)
Diffuse intrinsic pontine glioma (DIPG) is an incurable type of pediatric brain cancer, which in the majority of cases is driven by mutations in genes encoding histone 3 (H3K27M). We here determined the preclinical therapeutic potential of combined AXL and
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