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HPA018418

Sigma-Aldrich

Anti-IFT27 antibody produced in rabbit

enhanced validation

Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution

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Synonym(s):
Anti-BBS19, Anti-RABL4, Anti-RAYL
UNSPSC Code:
12352203
Human Protein Atlas Number:
NACRES:
NA.41

biological source

rabbit

Quality Level

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

product line

Prestige Antibodies® Powered by Atlas Antibodies

form

buffered aqueous glycerol solution

species reactivity

human

enhanced validation

recombinant expression
orthogonal RNAseq
Learn more about Antibody Enhanced Validation

technique(s)

immunoblotting: 0.04-0.4 μg/mL

immunogen sequence

TNEESFNNCSKWLEKARSQAPGISLPGVLVGNKTDLAGRRAVDSAEARAWALGQGLECFETSVKEMENFEAPFHCLAKQFHQLYREKVEV

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... RABL4(11020)

General description

Orthologs of intraflagellar transport protein-27 (IFT27) are present in genomes of Chlamydomonas, zebrafish and mouse. In Chlamydomonas IFT27 is localized along entire length of flagella.

Immunogen

intraflagellar transport 27

Application

All Prestige Antibodies Powered by Atlas Antibodies are developed and validated by the Human Protein Atlas (HPA) project and as a result, are supported by the most extensive characterization in the industry.

The Human Protein Atlas project can be subdivided into three efforts: Human Tissue Atlas, Cancer Atlas, and Human Cell Atlas. The antibodies that have been generated in support of the Tissue and Cancer Atlas projects have been tested by immunohistochemistry against hundreds of normal and disease tissues and through the recent efforts of the Human Cell Atlas project, many have been characterized by immunofluorescence to map the human proteome not only at the tissue level but now at the subcellular level. These images and the collection of this vast data set can be viewed on the Human Protein Atlas (HPA) site by clicking on the Image Gallery link. We also provide Prestige Antibodies® protocols and other useful information.

Biochem/physiol Actions

Intraflagellar transport protein-27 (IFT27) is a component of IFT complex B (IFT-B). Cargo exit and entry into cilia is mediated by BBSome, a complex of Bardet-Biedl syndrome (BBS) proteins. IFT27 is crucial for exit of BBSome and cargoes from cilia. IFT27 dissociates from the IFT-B and binds the ARF-like GTPase, ARL6. The binding causes activation of ARL6, BBSome coat assembly and subsequent ciliary exit. BBS is a rare autosomal recessive disorder characterized by multisystem involvement caused due to ciliary defects. Mutations in IFT27 are associated with BBS. IFT27 interacts with IFT25 and both are crucial for hair follicle morphogenesis. Absence of IFT27 disrupts hedgehog signaling, which causes hair follicle morphogenesis defects.

Features and Benefits

Prestige Antibodies® are highly characterized and extensively validated antibodies with the added benefit of all available characterization data for each target being accessible via the Human Protein Atlas portal linked just below the product name at the top of this page. The uniqueness and low cross-reactivity of the Prestige Antibodies® to other proteins are due to a thorough selection of antigen regions, affinity purification, and stringent selection. Prestige antigen controls are available for every corresponding Prestige Antibody and can be found in the linkage section.

Every Prestige Antibody is tested in the following ways:
  • IHC tissue array of 44 normal human tissues and 20 of the most common cancer type tissues.
  • Protein array of 364 human recombinant protein fragments.

Linkage

Corresponding Antigen APREST74563

Physical form

Solution in phosphate-buffered saline, pH 7.2, containing 40% glycerol and 0.02% sodium azide

Legal Information

Prestige Antibodies is a registered trademark of Merck KGaA, Darmstadt, Germany

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.

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Regulatory Information

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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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Zhaohui Wang et al.
PloS one, 4(5), e5384-e5384 (2009-05-05)
Intraflagellar transport (IFT) is the bidirectional movement of IFT particles between the cell body and the distal tip of a flagellum. Organized into complexes A and B, IFT particles are composed of at least 18 proteins. The function of IFT
Hongmin Qin et al.
Current biology : CB, 17(3), 193-202 (2007-02-06)
Intraflagellar transport (IFT) is a motility process operating between the ciliary/flagellar (interchangeable terms) membrane and the microtubular axoneme of motile and sensory cilia. Multipolypeptide IFT particles, composed of complexes A and B, carry flagellar precursors to their assembly site at
Mohammed A Aldahmesh et al.
Human molecular genetics, 23(12), 3307-3315 (2014-02-04)
Bardet-Biedl syndrome (BBS) is an autosomal recessive ciliopathy with multisystem involvement. So far, 18 BBS genes have been identified and the majority of them are essential for the function of BBSome, a protein complex involved in transporting membrane proteins into
Ning Yang et al.
Development (Cambridge, England), 142(12), 2194-2202 (2015-05-30)
Hair follicle morphogenesis requires precisely controlled reciprocal communications, including hedgehog (Hh) signaling. Activation of the Hh signaling pathway relies on the primary cilium. Disrupting ciliogenesis results in hair follicle morphogenesis defects due to attenuated Hh signaling; however, the loss of

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