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SAB5600116

Sigma-Aldrich

Anti-HA-Tag antibody, Rabbit Monoclonal

recombinant, expressed in HEK 293 cells, clone RM305, purified immunoglobulin

Synonym(s):

Human influenza hemagglutinin amino acids 98-106

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

recombinant

expressed in HEK 293 cells

Quality Level

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

RM305, monoclonal
recombinant monoclonal

form

buffered aqueous glycerol solution

technique(s)

flow cytometry: 0.1-1 μg/mL
immunocytochemistry: 0.1-1 μg/mL
immunohistochemistry: 0.01-0.5 μg/mL
immunoprecipitation (IP): 0.5-2 μg/mL
western blot: 0.1-1 μg/mL

isotype

IgG

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Related Categories

General description

The hemagglutinin (HA) gene is mapped to segment 4 of Influenza B viral genome. HA is a dominant antigen present on the influenza viral surface. It is a homotrimer and each monomer is produced as a single polypeptide.

Specificity

This antibody reacts to recombinant proteins containing a HA-Tag fused to either the amino or carboxy terminus. No cross reactivity with other endogenous protein.

Immunogen

A peptide corresponding to HA-tag (Human influenza hemagglutinin amino acids 98-106).

Application

Anti-HA-Tag antibody, Rabbit Monoclonal has been used in western blotting.

Biochem/physiol Actions

Hemagglutinin (HA) regulates membrane fusion and receptor-binding functions during viral entry and infection. The virus gains entry into the host cell via endocytosis and successive membrane fusion mediated by the HA antigen. HA plays a crucial role in viral pathogenesis and host response to viral infection.

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

Solution in phosphate buffered saline containing 50% glycerol, 1% BSA and 0.09% sodium azide.

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Storage Class Code

10 - Combustible liquids

WGK

WGK 3

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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Entry, Replication, Immune Evasion, and Neurotoxicity of Synthetically Engineered Bat-Borne Mumps Virus
Kruger N, et al.
Cell Reports, 25(2), 312-320 (2018)
Sandi Shen et al.
Biology, 12(4) (2023-04-28)
We previously demonstrated that mice with targeted deletion of the leucine repeat rich kinase 1 (Lrrk1) gene were osteopetrotic due to the failure of osteoclasts to resorb bone. To determine how LRRK1 regulates osteoclast activity, we examined the intracellular and
Nirut Leela et al.
PeerJ, 12, e16595-e16595 (2024-01-19)
Plasmodium falciparum possesses a cobalamin-dependent methionine synthase (MS). MS is putatively encoded by the PF3D7_1233700 gene, which is orthologous and syntenic in Plasmodium. However, its vulnerability as an antimalarial target has not been assessed. We edited the PF3D7_1233700 and PF3D7_0417200
Musadiq A Bhat et al.
International journal of molecular sciences, 24(17) (2023-09-09)
GABAB receptor-mediated inhibition is indispensable for maintaining a healthy neuronal excitation/inhibition balance. Many neurological diseases are associated with a disturbed excitation/inhibition balance and downregulation of GABAB receptors due to enhanced sorting of the receptors to lysosomal degradation. A key event
On the origin of the human influenza virus subtypes H2N2 and H3N2.
Scholtissek C, et al.
Virology, 87(1), 13-20 (1978)

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