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Key Documents

ABT65

Sigma-Aldrich

Anti-HAX-1 Antibody

from rabbit, purified by affinity chromatography

Synonym(s):

HCLS1-associated protein X-1, HS1-associating protein X-1, HAX-1, HS1-binding protein 1, HSP1BP-1

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

rabbit

Quality Level

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

purified by

affinity chromatography

species reactivity

mouse, rat, human

technique(s)

immunocytochemistry: suitable
western blot: suitable

NCBI accession no.

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

human ... HAX1(10456)

General description

HAX-1 (HS1-associated protein X-1) is a mitochondrial anti-apoptotic protein and is thought to be regulated by Omi/HtrA2. HAX-1 has been found to associate with BSEP, MDR1 and MDR2 ABC-transporters and interacts with cortactin to play a role in BSEP internalization from the apical membrane. HAX-1 and alphavbeta6 are found to be highly expressed in certain oral cancers and work together to enhance tumor invasion and progression. High expression of HAX-1 in many other cancer tissues shows that HAX-1 is important in neoplastic transformation.

Specificity

This antibody recognizes HAX-1 at the domains involved in HCLS1-, CASP9-, and GNA13-binding.

Immunogen

Epitope: HCLS1-, CASP9-, and GNA13-binding domains
KLH-conjugated linear peptide corresponding to the domain of human HAX-1 that is involved in HCLS1-, CASP9-, and GNA13-bindings.

Application

Anti-HAX-1 Antibody is an antibody against HAX-1 for use in WB & IC.
Research Category
Apoptosis & Cancer
Research Sub Category
Apoptosis - Additional

Cytoskeleton
Western Blot Analysis: 0.1 µg/mL from a representative lot detected HAX-1 in 10 µg of HeLa cell lysate and rat liver tissue lysate.

Immunocytochemistry Analysis: A 1:500 dilution from a representative lot detected HAX-1 in NIH/3T3 and HeLa cells.

Quality

Evaluated by Western Blot in Jurkat cell lysate.

Western Blot Analysis: 0.1 µg/mL of this antibody detected HAX-1 in 10 µg of Jurkat cell lysate.

Target description

~35 kDa observed.
HAX-1 has been shown to migrate as a ~34-36 kDa band in WB (Ortiz, D.F., et al. (2004). JBC. 279(31):32761-32770).

Physical form

Affinity purified
Purified rabbit polyclonal in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.

Storage and Stability

Stable for 1 year at 2-8°C from date of receipt.

Analysis Note

Control
Jurkat cell lysate

Other Notes

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

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

12 - Non Combustible Liquids

WGK

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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Keqing Huang et al.
Frontiers in pharmacology, 10, 107-107 (2019-03-06)
The chemotherapeutic drug doxorubicin (DOX) provokes a dose-related cardiotoxicity. Thus, there is an urgent need to identify the underlying mechanisms and develop strategies to overcome them. Here we demonstrated that glabridin (GLA), an isoflavone from licorice root, prevents DOX-induced cardiotoxicity
Ke Wang et al.
Scientific reports, 6, 37927-37927 (2016-12-08)
Myocardial apoptosis is a significant problem underlying ischemic heart disease. We previously reported significantly elevated expression of cytoplasmic Omi/HtrA2, triggers cardiomyocytes apoptosis. However, whether increased Omi/HtrA2 within mitochondria itself influences myocardial survival in vivo is unknown. We aim to observe

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