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05-1087

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Anti-phospho-IRS1 (Ser307 mouse/ Ser312 human) Antibody, clone 24.6.2

clone 24.6.2, from mouse

Synonym(s):

insulin receptor substrate 1

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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

24.6.2, monoclonal

species reactivity

bovine, pig, mouse, monkey, canine, rat, human

technique(s)

immunocytochemistry: suitable
immunofluorescence: suitable
immunoprecipitation (IP): suitable
western blot: suitable

isotype

IgG2aκ

NCBI accession no.

NP_005535.1

UniProt accession no.

P35568

shipped in

wet ice

target post-translational modification

phosphorylation (pSer307 )

Gene Information

bovine ... Irs1(538598)
dog ... Irs1(486148)
human ... IRS1(3667)
mouse ... Irs1(16367)
pig ... Irs1(100512686)
rat ... Irs1(25467)
rhesus monkey ... Irs1(707870)

General description

IRS1 (Insulin Receptor Substrate 1) transmits insulin signals via metabolic and mitogenic pathways. IRS1 is heavily phosphorylated on both serine and tyrosine residues. These phosphorylated tyrosines enable IRS to act as a docking protein that binds SH2 domains of such proteins as PI3 Kinase (phosphatidylinositol 3-kinase) and GRB2, resulting in activation. Over expression and phosphorylation of serine is associated with insulin resistance and breast cancer. Some of the more notable phosphorylation sites are Ser302 that is phosphorylated following insulin stimulation. Ser307, phosphorylated by JNK and IKK, is a key regulatory site that appears to disrupt the IRS1/IR interaction and inhibits insulin-mediated activation of the PI3 kinase and MAPK pathways, and Ser636/639 that is known to be phosphorylated by p70S6K downstream of mTOR and acts as a negative feedback loop.

Specificity

Predicted to cross-react with many other species based on 100% sequence homology with immunogen.
This antibody recognizes IRS1 phosphorylated at Ser307 (mouse) and Ser312 (human).

Immunogen

Synthetic peptide corresponding to amino acids surrounding phosphorylated Ser307 of mouse IRS1.

Application

This Anti-phospho-IRS1 (Ser307 mouse/ Ser312 human) Antibody, clone 24.6.2 is validated for use in WB, IP, IC, IF for the detection of phospho-IRS1 (Ser307 mouse/ Ser312 human).

Quality

Evaluated by western blot on IR/IRS1 transfected CHO +/- Insulin lysate.

Western Blot Analysis:
1:1,000 dilution of this antibody was used to detect IRS1 in IRS/IR transfected CHO -/+ Calyculin A/ Okadaic Acid-treated cell lysate.

Target description

~185 kDa

Linkage

Replaces: 07-247

Physical form

Format: Purified

Other Notes

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

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Storage Class

12 - Non Combustible Liquids

wgk_germany

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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Xinghui Sun et al.
Circulation research, 118(5), 810-821 (2016-02-03)
The pathogenesis of insulin resistance involves dysregulated gene expression and function in multiple cell types, including endothelial cells (ECs). Post-transcriptional mechanisms such as microRNA-mediated regulation of gene expression could affect insulin action by modulating EC function. To determine whether microRNA-181b
Ashraf Nahle et al.
International journal of molecular sciences, 22(24) (2021-12-25)
The NAD-dependent deacetylase SIRT1 improves β cell function. Accordingly, nicotinamide mononucleotide (NMN), the product of the rate-limiting step in NAD synthesis, prevents β cell dysfunction and glucose intolerance in mice fed a high-fat diet. The current study was performed to
Hua Yan et al.
Molecular medicine reports, 15(1), 180-186 (2016-12-03)
Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disease, the pathological process of which is complex. Activation of the c‑Jun N‑terminal kinase (JNK) signaling pathway is associated with the mechanism underlying obesity-induced insulin resistance. Furthermore, the JNK signaling
Saori Kakehi et al.
Frontiers in physiology, 14, 1198390-1198390 (2023-06-30)
Inactivity causes insulin resistance in skeletal muscle and exacerbates various lifestyle-related diseases. We previously found that 24-h hindlimb cast immobilization (HCI) of the predominantly slow-twitch soleus muscle increased intramyocellular diacylglycerol (IMDG) and insulin resistance by activation of lipin1, and HCI
Alessandro Cannavo et al.
Frontiers in pharmacology, 10, 888-888 (2019-08-27)
Hyperaldosteronism alters cardiac function, inducing adverse left ventricle (LV) remodeling either via increased fibrosis deposition, mitochondrial dysfunction, or both. These harmful effects are due, at least in part, to the activation of the G protein-coupled receptor kinase 2 (GRK2). In
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