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Merck
CN

05-1044

Anti-Sin1 Antibody, clone 1C7.2

clone 1C7.2, from mouse

别名:

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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关于此项目

UNSPSC Code:
12352203
NACRES:
NA.41
eCl@ss:
32160702
Conjugate:
unconjugated
Clone:
1C7.2, monoclonal
Application:
immunofluorescence
immunohistochemistry
immunoprecipitation (IP)
western blot
Species reactivity:
rat, mouse, human
Citations:
14
Technique(s):
immunofluorescence: suitable
immunohistochemistry: suitable (paraffin)
immunoprecipitation (IP): suitable
western blot: suitable
Uniprot accession no.:
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产品名称

Anti-Sin1 Antibody, clone 1C7.2, clone 1C7.2, from mouse

biological source

mouse

conjugate

unconjugated

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.

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Quality Level

Gene Information

human ... MAPKAP1(79109)

Analysis Note

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

Application

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

Biochem/physiol Actions

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

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

Immunogen

Full-length Human Sin1 GST-fusion protein.

Other Notes

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

Physical form

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

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存储类别

12 - Non Combustible Liquids

wgk

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable


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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
Ruizhi Li et al.
Cell death discovery, 8(1), 357-357 (2022-08-14)
Proliferating cancer cells are dependent on glutamine metabolism for survival when challenged with oxidative stresses caused by reactive oxygen species, hypoxia, nutrient deprivation and matrix detachment. ATF4, a key stress responsive transcription factor, is essential for cancer cells to sustain
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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