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Merck

ABD51

Anti-BMPR-1A Antibody

from rabbit, purified by affinity chromatography

Synonyme(s) :

Bone morphogenetic protein receptor type-1A, BMP type-1A receptor, BMPR-1A, Activin receptor-like kinase 3, ALK-3, Serine/threonine-protein kinase receptor R5, SKR5, CD_antigen=CD292

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A propos de cet article

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

Principaux documents

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Nom du produit

Anti-BMPR-1A Antibody, from rabbit, purified by affinity chromatography

biological source

rabbit

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

purified by

affinity chromatography

species reactivity

rat, human, mouse

technique(s)

western blot: suitable

NCBI accession no.

NP_004320

UniProt accession no.

P36894

shipped in

wet ice

target post-translational modification

unmodified

Quality Level

100

Gene Information

human ... BMPR1A(657)

Analysis Note

Control
NIH/3T3 cell lysate
Evaluated by Western Blot in NIH/3T3 cell lysate.

Western Blot Analysis: 0.1 µg/mL of this antibody detected BMPR-1A on 10 µg of NIH/3T3 cell lysate.

Application

Anti-BMPR-1A Antibody is an antibody against BMPR-1A for use in WB.
Research Category
Stem Cell Research
Research Sub Category
Kinases & Phosphatases

Biochem/physiol Actions

This antibody recognizes BMPR-1A at the extracellular domain.

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.

General description

BMPR-1A (bone morphogenic protein receptor type 1A) signaling is known to be important for inner root sheath differentiation, hair follicle cycling and tooth development. Mutations in BMPR-1A are a common cause of juvenile polyposis syndrome (JPS). BMPR-1A is expressed in a high quantity during the formation of the primary and secondary palate and the loss of BMPR-1A could be a cause for the cleft palate birth defect.
~75 kDa observed. The calculated molecular weight is 67 kDa; however, BMPR-1A has been shown as a ~77 kDa band in western blots (Koenig, B., et al. (1994). Molecular and Cellular Biology. 14(9):5961-5974).

Immunogen

Epitope: Extracellular domain
KLH-conjugated linear peptide corresponding to the extracellular domain of human BMPR-1A.

Other Notes

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

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.

Preparation Note

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

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Classe de stockage

12 - Non Combustible Liquids

wgk

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable

Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Consulter la Bibliothèque de documents

Joohwee Kim et al.
Biochimica et biophysica acta, 1853(2), 500-512 (2014-12-17)
Prostaglandins are a group of lipid signaling molecules involved in various physiological processes. In addition, prostaglandins have been implicated in the development and progression of diseases including cancer, cardiovascular disease, and arthritis. Prostaglandins exert their effects through the activation of
Guillermo Agustín Videla Richardson et al.
Brain pathology (Zurich, Switzerland), 26(1), 43-61 (2015-03-27)
Although BMP4-induced differentiation of glioma stem cells (GSCs) is well recognized, details of the cellular responses triggered by this morphogen are still poorly defined. In this study, we established several GSC-enriched cell lines (GSC-ECLs) from high-grade gliomas. The expansion of
Xing-Gang Wu et al.
Blood, 124(8), 1335-1343 (2014-06-07)
Mutations in HFE are the most common cause of hereditary hemochromatosis (HH). HFE mutations result in reduced expression of hepcidin, a hepatic hormone, which negatively regulates iron absorption from the duodenum and iron release from macrophages. However, the mechanism by

Numéro d'article de commerce international

RéférenceGTIN
ABD5104053252632174

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