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Documentos Principais

05-1044

Sigma-Aldrich

Anti-Sin1 Antibody, clone 1C7.2

clone 1C7.2, from mouse

Sinônimo(s):

MEKK2-interacting protein 1, Mitogen-activated protein kinase 2-associated protein 1, SAPK-interacting protein 1, Stress-activated map kinase-interacting protein 1, TORC2 subunit MAPKAP1, mitogen-activated protein kinase associated protein 1, ras inhibit

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About This Item

Código UNSPSC:
12352203
eCl@ss:
32160702
NACRES:
NA.41

fonte biológica

mouse

Nível de qualidade

100

forma do anticorpo

purified antibody

tipo de produto de anticorpo

primary antibodies

clone

1C7.2, monoclonal

reatividade de espécies

rat, mouse, human

técnica(s)

immunofluorescence: suitable
immunohistochemistry: suitable (paraffin)
immunoprecipitation (IP): suitable
western blot: suitable

Isotipo

IgG2aκ

nº de adesão NCBI

NP_001006618

nº de adesão UniProt

Q9BPZ7

Condições de expedição

wet ice

modificação pós-traducional do alvo

unmodified

Informações sobre genes

human ... MAPKAP1(79109)

Descrição geral

Sin1 (stress-activated protein kinase (SAPK)-interacting protein 1, MAPKAP1) is an essential component of the Torc2 complex. mTORC2 is comprised of mTOR, a large Ser/Thr protein kinase along with Sin1, GL (mLST8), Protor1, Protor2, and Rictor. The complex that is activated primarily downstream of PI3 Kinase and is known to affect cell proliferation and survival primarily by phosphorylating Akt on Ser473. Additionally, the mTORC2 complex is also known to effect cytoskeletal organization and migration by exerting its effects through Rac, Rho, and PKC. Sin1 is also known to directly interact without proteins that include Ras, SPAKs, and JNK.
Sin1 is known to have multiple alternative splicing isoforms. Full-length Sin1 is a 522aa protein (59kDa). Sin1 (Isoform 5) (36 kDa) has exon 6 spliced to an alternative exon 7a that results in the loss of both the RBD and PHL domains. Sin1Isoform 2) (55 kDa) lacks exon 7 and lacks the RBD. Sin1 (Isoform 3) (53 kDa) lacks exon 8 lacks the PHL domain. Sin1 (Isoform 4) (37 kDa) lacks exon 1.

Especificidade

Detects Sin-1 and its isoforms.
Other species have not been tested.

Imunogênio

Full-length Human Sin1 GST-fusion protein.

Aplicação

Detect Sin1 using this Anti-Sin1 Antibody, clone 1C7.2 validated for use in WB, IP, IH(P) & IF.

Qualidade

Western Blot Analysis:
This lot detected Sin1 at 1:1,000 dilution in A431 cell lysate resolved via SDS-PAGE and transferred to PVDF.

Descrição-alvo

Sin1 is 59 kDa Isoforms are 36, 37, 41, 53, 54, and 55 kDa

forma física

Format: Purified
Purified mouse monoclonal in 0.1M Tris-Glycine (pH 7.4), 150mM NaCl with 0.05% NaN3.

Outras notas

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

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Código de classe de armazenamento

12 - Non Combustible Liquids

Classe de risco de água (WGK)

WGK 1

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable

Certificados de análise (COA)

Busque Certificados de análise (COA) digitando o Número do Lote do produto. Os números de lote e remessa podem ser encontrados no rótulo de um produto após a palavra “Lot” ou “Batch”.

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MicroRNA-7 regulates the mTOR pathway and proliferation in adult pancreatic ?-cells.
Wang, Y; Liu, J; Liu, C; Naji, A; Stoffers, DA
Diabetes null
Isolation of the mTOR complexes by affinity purification.
Dos D Sarbassov,Olga Bulgakova,Rakhmet I Bersimbaev,Tattym Shaiken
Methods in Molecular Biology null
PPIP5K1 modulates ligand competition between diphosphoinositol polyphosphates and PtdIns(3,4,5)P3 for polyphosphoinositide-binding domains.
Gokhale, NA; Zaremba, A; Janoshazi, AK; Weaver, JD; Shears, SB
The Biochemical Journal null
Suree Kim et al.
Cancers, 13(10) (2021-06-03)
The serine/threonine kinase AKT is a major effector during phosphatidylinositol 3-kinase (PI3K)-driven cell signal transduction in response to extracellular stimuli. AKT activation mechanisms have been extensively studied; however, the mechanism underlying target of rapamycin complex 2 (mTORC2) phosphorylation of AKT
J Mathieu et al.
Nature communications, 10(1), 632-632 (2019-02-09)
To reveal how cells exit human pluripotency, we designed a CRISPR-Cas9 screen exploiting the metabolic and epigenetic differences between naïve and primed pluripotent cells. We identify the tumor suppressor, Folliculin(FLCN) as a critical gene required for the exit from human
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