DNAH5, Polyclonal Antibody

Dynein heavy chain 5; axonemal; Axonemal beta dynein heavy chain 5; Ciliary dynein heavy chain 5; DNAH5; DNAHC5; HL1; KIAA1603

For Research Use Only. Not for use in diagnostic procedures.

Polyclonal

IgG

Rabbit

>95%, Protein G purified

Liquid

Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.

Manufactured in an ISO 13485:2003 and EN ISO 13485:2012 Certified Laboratory.

Small volumes of anti-DNAH5 antibody vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

Force generating protein of respiratory cilia. Produces force towards the minus ends of microtubules. Dynein has ATPase activity; the force-producing power stroke is thought to occur on release of ADP. Required for structural and functional integrity of the cilia of ependymal cells lining the brain ventricles.

ELISA (EIA)

dynein axonemal heavy chain 5

dynein heavy chain 5, axonemal

Dynein heavy chain 5, axonemal

DNAHC5; HL1; KIAA1603  [Similar Products]

DYH5_HUMAN

This gene encodes a dynein protein, which is part of a microtubule-associated motor protein complex consisting of heavy, light, and intermediate chains. This protein is an axonemal heavy chain dynein. It functions as a force-generating protein with ATPase activity, whereby the release of ADP is thought to produce the force-producing power stroke. Mutations in this gene cause primary ciliary dyskinesia type 3, as well as Kartagener syndrome, which are both diseases due to ciliary defects. [provided by RefSeq, Oct 2009]

DNAH5: Force generating protein of respiratory cilia. Produces force towards the minus ends of microtubules. Dynein has ATPase activity; the force-producing power stroke is thought to occur on release of ADP. Required for structural and functional integrity of the cilia of ependymal cells lining the brain ventricles. Defects in DNAH5 are the cause of primary ciliary dyskinesia type 3 (CILD3). CILD3 is an autosomal recessive disorder characterized by axonemal abnormalities of motile cilia. Respiratory infections leading to chronic inflammation and bronchiectasis are recurrent, due to defects in the respiratory cilia; reduced fertility is often observed in male patients due to abnormalities of sperm tails. Half of the patients exhibit situs inversus, due to dysfunction of monocilia at the embryonic node and randomization of left-right body asymmetry. Primary ciliary dyskinesia associated with situs inversus is referred to as Kartagener syndrome. Defects in DNAH5 are a cause of Kartagener syndrome (KTGS). KTGS is an autosomal recessive disorder characterized by the association of primary ciliary dyskinesia with situs inversus. Clinical features include recurrent respiratory infections, bronchiectasis, infertility, and lateral transposition of the viscera of the thorax and abdomen. The situs inversus is most often total, although it can be partial in some cases (isolated dextrocardia or isolated transposition of abdominal viscera). Belongs to the dynein heavy chain family.

Protein type: Microtubule-binding; Motility/polarity/chemotaxis; Motor

Chromosomal Location of Human Ortholog: 5p15.2

Cellular Component: axoneme

Biological Process: determination of left/right symmetry; sperm motility

Disease: Ciliary Dyskinesia, Primary, 3

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