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Documenti fondamentali

PLA0307

Goat anti-Sp1 Antibody, Affinity Purified

Name: Goat anti-Sp1 Antibody, Affinity Purified
Brand: SIGMA

Powered by Bethyl Laboratories, Inc.

Sinonimo/i:

specificity protein 1

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About This Item

Codice UNSPSC:

12352203

NACRES:

NA.41

Origine biologica

goat

Livello qualitativo

100

Forma dell’anticorpo

affinity purified immunoglobulin

Tipo di anticorpo

primary antibodies

Grado

Reattività contro le specie

mouse, human

Concentrazione

1 mg/mL

tecniche

immunohistochemistry: 1:1,000-1:5,000
immunoprecipitation (IP): 2- 10 μg/mg
western blot: 1:2,000- 1:10,000

Numero d’accesso

NP_612482.2

N° accesso UniProt

P08047

Condizioni di spedizione

wet ice

Temperatura di conservazione

2-8°C

modifica post-traduzionali bersaglio

unmodified

Informazioni sul gene

goat ... Sp1(6667)

Immunogeno

The epitope recognized by PLA0307 maps to a region between residue 735 to 785 of human Sp1 Transcription Factor using the numbering given in entry NP_612482.2 (GeneID 6667).

Stato fisico

Tris-citrate/phosphate buffer, pH 7 to 8 containing 0.09% Sodium Azide

Altre note

Specificity protein 1 (Sp1) is the original member of the Sp1-like/KLF family of zinc-finger transcription factors that binds GC-rich DNA elements to regulate transcription of genes involved in a variety of cellular functions. Sp-1 interacts with coactivators such as p300/CBP, TAFII130, and CRSP.

Esclusione di responsabilità

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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Codice della classe di stoccaggio

12 - Non Combustible Liquids

Classe di pericolosità dell'acqua (WGK)

nwg

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°C)

Not applicable

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miR-2909-mediated regulation of KLF4: a novel molecular mechanism for differentiating between B-cell and T-cell pediatric acute lymphoblastic leukemias.

Deepti Malik et al.

Molecular cancer, 13, 175-175 (2014-07-20)

microRNAs (miRNAs) play both oncogenic and oncostatic roles in leukemia. However, the molecular details underlying miRNA-mediated regulation of their target genes in pediatric B- and T-cell acute lymphoblastic leukemias (ALLs) remain unclear. The present study investigated the relationship between miR-2909

Genome-wide modulation of gene transcription in ovarian carcinoma cells by a new mithramycin analogue.

Carolina Vizcaíno et al.

PloS one, 9(8), e104687-e104687 (2014-08-12)

Ovarian cancer has a poor prognosis due to intrinsic or acquired resistance to some cytotoxic drugs, raising the interest in new DNA-binding agents such as mithramycin analogues as potential chemotherapeutic agents in gynecological cancer. Using a genome-wide approach, we have

Extracellular signal-related kinase 2/specificity protein 1/specificity protein 3/repressor element-1 silencing transcription factor pathway is involved in Aroclor 1254-induced toxicity in SH-SY5Y neuronal cells.

Luigi Formisano et al.

Journal of neuroscience research, 93(1), 167-177 (2014-08-06)

Polychlorinated biphenyls (PCBs) cause a wide spectrum of toxic effects in the brain through undefined mechanisms. Exposure to the PCB mixture Aroclor-1254 (A1254) increases the repressor element-1 silencing transcription factor (REST) expression, leading to neuronal death. This study sought to

Proteasome inhibitors exert cytotoxicity and increase chemosensitivity via transcriptional repression of Notch1 in T-cell acute lymphoblastic leukemia.

D Koyama et al.

Leukemia, 28(6), 1216-1226 (2013-12-05)

The Notch signaling pathway has been recognized as a key factor for the pathogenesis of T-cell acute lymphoblastic leukemia (T-ALL), because of the high incidence of activating mutations of Notch1. Notch inhibition could serve as a new treatment strategy for

Flavonoid ingredients of Ginkgo biloba leaf extract regulate lipid metabolism through Sp1-mediated carnitine palmitoyltranferase 1A up-regulation.

Ting Wei et al.

Journal of biomedical science, 21, 87-87 (2014-09-04)

Lipid accumulation is the primary evidence of non-alcoholic fatty liver disease (NAFLD). Ginkgo biloba extract (GBE) and its flavonoid ingredients (quercetin, kaempferol, and isorhamnetin) could lessen the lipid accumulation associated with up-regulation of the rate-limiting enzyme, carnitine palmitoyltransferase 1A (CPT1A)

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