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Key Documents

05-1044

Sigma-Aldrich

Anti-Sin1 Antibody, clone 1C7.2

clone 1C7.2, from mouse

Synonyme(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

Code UNSPSC :
12352203
eCl@ss :
32160702
Nomenclature NACRES :
NA.41

Source biologique

mouse

Niveau de qualité

Forme d'anticorps

purified antibody

Type de produit anticorps

primary antibodies

Clone

1C7.2, monoclonal

Espèces réactives

rat, mouse, human

Technique(s)

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

Isotype

IgG2aκ

Numéro d'accès NCBI

Numéro d'accès UniProt

Conditions d'expédition

wet ice

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... MAPKAP1(79109)

Description générale

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.

Spécificité

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

Immunogène

Full-length Human Sin1 GST-fusion protein.

Application

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

Qualité

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

Description de la cible

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

Forme physique

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

Autres remarques

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

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Code de la classe de stockage

12 - Non Combustible Liquids

Classe de danger pour l'eau (WGK)

WGK 1

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Retrouvez la documentation relative aux produits que vous avez récemment achetés dans la Bibliothèque de documents.

Consulter la Bibliothèque de documents

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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