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SAB4502878

Sigma-Aldrich

Anti-STAT5A antibody produced in rabbit

affinity isolated antibody

Synonym(s):

MGF, MPF, Mammary gland factor, STA5A, STAT5

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About This Item

MDL number:
MFCD00803569
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

100

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen 90 kDa

species reactivity

rat, human, mouse

concentration

~1 mg/mL

technique(s)

ELISA: 1:5000
western blot: 1:500-1:1000

NCBI accession no.

P42229

UniProt accession no.

P42229

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... STAT5A(6776)

General description

Anti-STAT5A Antibody detects endogenous levels of total STAT5A protein.

Immunogen

The antiserum was produced against synthesized peptide derived from human STAT5A.

Immunogen Range: 386-435

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.

Physical form

Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.

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wgk_germany

nwg

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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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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