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Sigma-Aldrich

Anti-Sin1 Antibody, clone 1C7.2

clone 1C7.2, from mouse

Synonym(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

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

biological source

mouse

Quality Level

100

antibody form

purified antibody

antibody product type

primary antibodies

clone

1C7.2, monoclonal

species reactivity

rat, mouse, human

technique(s)

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

isotype

IgG2aκ

NCBI accession no.

NP_001006618

UniProt accession no.

Q9BPZ7

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

human ... MAPKAP1(79109)

General description

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.

Specificity

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

Immunogen

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.

Quality

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

Target description

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

Physical form

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

Other Notes

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

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WGK

WGK 1

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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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
Isolation of the mTOR complexes by affinity purification.
Dos D Sarbassov,Olga Bulgakova,Rakhmet I Bersimbaev,Tattym Shaiken
Methods in Molecular Biology null
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
Zhenbo Tu et al.
Proceedings of the National Academy of Sciences of the United States of America, 119(43), e2203180119-e2203180119 (2022-10-22)
The phosphoinositide 3-kinase (PI3K) pathway represents the most hyperactivated oncogenic pathway in triple-negative breast cancer (TNBC), a highly aggressive tumor subtype encompassing ∼15% of breast cancers and which possesses no targeted therapeutics. Despite critical contributions of its signaling arms to
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