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SAB2501370

Anti-SNAI1 (N-terminal) antibody produced in goat

Name: Anti-SNAI1 (N-terminal) antibody produced in goat
Brand: SIGMA

affinity isolated antibody, buffered aqueous solution

Synonym(s):

Anti-SLUGH2, Anti-SNA, Anti-SNAH, Anti-dJ710H13.1, Snail homolog 1 (Drosophila)

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About This Item

UNSPSC Code:

12352203

NACRES:

NA.41

biological source

goat

Quality Level

100

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

species reactivity

rat, human

technique(s)

indirect ELISA: suitable

UniProt accession no.

O95863

application(s)

research pathology

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... SNAI1(6615)

General description

Snail family transcriptional repressor 1 (SNAIL) is a transcription factor and the gene encoding it is localized on human chromosome 20q13.13.

Immunogen

Peptide with sequence RKPSDPNRKPNY-C, from the N-terminal region of the protein sequence according to NP_005976.2

Biochem/physiol Actions

Snail family transcriptional repressor 1 (SNAIL) acts as a repressor of genes associated with the epithelial phenotype like E-cadherin and increases the expression of genes linked with the mesenchymal phenotype. It has a role in epithelial-mesenchymal transition. The protein aids in G1 transition (early to late) in the cell cycle. SNAIL also modulates cell-matrix adhesion.

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.

Physical form

Supplied at 0.5 mg/mL in 20mM Tris (pH 7.3) and 150mM NaCl with 0.02% sodium azide and 0.5% bovine serum albumin.

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 2

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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SNAIL transcription factor increases the motility and invasive capacity of prostate cancer cells.

Osorio LA

Molecular Medicine Reports (2016)

CRISPR/Cas9n-Mediated Deletion of the Snail 1Gene (SNAI1) Reveals Its Role in Regulating Cell Morphology, Cell-Cell Interactions, and Gene Expression in Ovarian Cancer (RMG-1) Cells.

Haraguchi M

PLoS ONE (2015)

TP53 Mutation, Epithelial-Mesenchymal Transition, and StemlikeFeatures in Breast Cancer Subtypes

Danila Coradini

Journal of Biomedicine and Biotechnology (2012)

Acquired drug resistance interferes with the susceptibility of prostate cancer cells to metabolic stress.

Jessica Catapano et al.

Cellular & molecular biology letters, 27(1), 100-100 (2022-11-20)

Metformin is an inhibitor of oxidative phosphorylation that displays an array of anticancer activities. The interference of metformin with the activity of multi-drug resistance systems in cancer cells has been reported. However, the consequences of the acquired chemoresistance for the

Metabolic reprogramming of poly(morpho)nuclear giant cells determines glioblastoma recovery from doxorubicin-induced stress.

Maciej Pudełek et al.

Journal of translational medicine, 22(1), 757-757 (2024-08-13)

Multi-drug resistance of poly(morpho)nuclear giant cells (PGCs) determines their cytoprotective and generative potential in cancer ecosystems. However, mechanisms underlying the involvement of PGCs in glioblastoma multiforme (GBM) adaptation to chemotherapeutic regimes remain largely obscure. In particular, metabolic reprogramming of PGCs

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