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Key Documents

SAB4300329

Sigma-Aldrich

Anti-STAT5A (Ab-694) antibody produced in rabbit

affinity isolated antibody

Sinónimos:

Anti-MGF antibody produced in rabbit, Anti-STAT5 antibody produced in rabbit, Anti-signal transducer and activator of transcription 5A antibody produced in rabbit

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About This Item

MDL number:
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

~90 kDa

species reactivity

rat, human, mouse

concentration

1 mg/mL

technique(s)

immunohistochemistry (formalin-fixed, paraffin-embedded sections): 1:50-1:100
western blot: 1:500-1:1000

isotype

IgG

immunogen sequence

(D-G-Y-V-K)

NCBI accession no.

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... STAT5A(6776)

Immunogen

Peptide sequence around aa. 692-696 (D-G-Y-V-K), according to the protein STAT5A.

Features and Benefits

Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.

Target description

Carries out a dual function: signal transduction and activation of transcription. Binds to the GAS element and activates PRL-induced transcription.

Physical form

Solution in phosphate-buffered saline containing 0.02% sodium azide and 50% glycerol

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Storage Class

10 - Combustible liquids

wgk_germany

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable


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Alex Man Lai Wu et al.
American journal of physiology. Endocrinology and metabolism, 307(7), E596-E610 (2014-08-15)
The multidrug resistance efflux transporter ATP-binding cassette subfamily G member 2 (ABCG2) is not only overexpressed in certain drug-resistant cancers but is also highly expressed in the mammary gland during lactation, carrying xenobiotics and nutrients into milk. We sought to
Liting Xue et al.
Blood, 124(3), 426-436 (2014-06-05)
Acute myeloid leukemia (AML) results from the activity of driver mutations that deregulate proliferation and survival of hematopoietic stem cells (HSCs). The fusion protein CBFβ-SMMHC impairs differentiation in hematopoietic stem and progenitor cells and induces AML in cooperation with other

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