Human HOOK1 ELISA Matched Antibody Pair

Name: Human HOOK1 ELISA Matched Antibody Pair
SKU: ABPR-0435
Rating: 5 (1 reviews)

Regulatory status: For research use only, not for use in diagnostic procedures.

COA

SDS

Datasheet

Summary

Species Reactivity

Human

Intended Use

This antibody pair set comes with matched antibody pair to detect and quantify protein level of human HOOK1.

General Description

This gene encodes a member of the hook family of coiled-coil proteins, which bind to microtubules and organelles through their N- and C-terminal domains, respectively. The encoded protein localizes to discrete punctuate subcellular structures, and interacts with several members of the Rab GTPase family involved in endocytosis. It is thought to link endocytic membrane trafficking to the microtubule cytoskeleton. Several alternatively spliced transcript variants have been identified, but the full-length nature of some of these variants has not been determined.

Reconstitution And Storage

Store reagents of the antibody pair set at -20°C or lower. Please aliquot to avoid repeated freeze thaw cycle. Reagents should be returned to -20°C storage immediately after use.

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

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References

Hypoxia increases amyloid-beta level in exosomes by enhancing the interaction between CD147 and Hook1

AMERICAN JOURNAL OF TRANSLATIONAL RESEARCH

Authors: Xie, Jun-Chao; Ma, Xiao-Ye; Liu, Xiao-Hui; Yu, Jia; Zhao, Yi-Chen; Tan, Yan; Liu, Xue-Yuan; Zhao, Yan-Xin

Abstract

Hypoxia promotes the accumulation of amyloid-beta (A beta), which is related to the pathogenesis of Alzheimer's disease (AD). CD147 is considered as an additional subunit of.-secretase regulated by hypoxia, and has been identified in exosomes. A beta is also found in exosomes that participate in the intercellular communication and amyloids propagation. This study was to investigate the role of CD147 in hypoxia-induced accumulation of A beta in exosomes. Our results showed that hypoxia increased the levels of A beta 40 and A beta 42 in exosomes and enhanced the interaction between CD147 and Hook1 in SH-SY5YAPP695 cells. Moreover, hypoxia increased the interaction between amyloid precursor protein (APP) and CD147 as well as the expression of CD147 in isolated membrane. After we interfered the interaction between CD147 and Hook1 by decreasing Rab22a expression, the hypoxia induced A beta accumulation in exosomes was significantly suppressed. In addition, the increased interaction between CD147 and Hook1 was further confirmed in hypoxia exposed C57BL/6 mice. Our findings reveal that hypoxia may increase exosome A beta level by enhancing the interaction between CD147 and Hook1.

The Hook1 gene is non-functional in the abnormal spermatozoon head shape (azh) mutant mouse

HUMAN MOLECULAR GENETICS

Authors: Mendoza-Lujambio, I; Burfeind, P; Dixkens, C; Meinhardt, A; Hoyer-Fender, S; Engel, W; Neesen, J

Abstract

In mice carrying the autosomal recessive mutation 'abnormal spermatozoon head shape' (azh) all spermatozoa display a highly abnormal head morphology that differs drastically from the compact and hook-shaped head of the normal murine sperm. Moreover, the azh mutation causes tail abnormalities often resulting in coiled sperm tails or in the decapitation of the sperm head from the flagellum. We have isolated and characterized murine Hook1 cDNA and analyzed the corresponding genomic structure. Furthermore, the Hook1 gene was mapped to the same region on chromosome 4 to which the azh locus was previously linked. The Hook1 gene is predominantly expressed in haploid male germ cells, and immunohistochemical analysis revealed that Hook1 is responsible for the linkage of the microtubular manchette and the flagellum to cellular structures. Here, we report that the azh mutation is due to a deletion of exons 10 and 11 in the murine Hook1 gene leading to a non-functional protein. Our results indicate that loss of Hook1 function results in ectopic positioning of microtubular structures within the spermatid and causes the azh phenotype. Therefore, the human HOOK1 gene could serve as a candidate gene for male infertility due to teratozoospermia or decapitation defects.