HSP27 (Human) ELISA Kit (DEIA3601)

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

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Size
96T
Sample
cell culture supernatant, plasma, serum, tissues
Species Reactivity
Human
Intended Use
The Human HSP27 ELISA kit is designed for detection of human HSP27 in plasma, serum, milk, tissue extract, and cell culture samples.
Contents of Kit
1. Human Hsp27 Microplate
2. Sealing Tapes
3. Human Hsp27 Standard
4. Biotinylated Hsp27 Antibody (100x)
5. EIA Diluent Concentrate (10x)
6. Wash Buffer Concentrate (20X)
7. Streptavidin-Peroxidase Conjugate
8. Chromogen Substrate
9. Stop Solution
Storage
Store components of the kit at 2-8°C or -20°C upon arrival up to the expiration date. For more detailed information, please download the following document on our website.
Sensitivity
0.3 ng/mL

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References


An insulator-like sequence acts as a negative regulatory element in between the mouse Shsp/alpha B-crystallin enhancer and Mkbp/HspB2 promoter

INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE

Authors: Swamynathan, SK; Piatigorsky, J

Behavioral Defects in Chaperone-Deficient Alzheimer's Disease Model Mice

PLOS ONE

Authors: Ojha, Juhi; Karmegam, Rajalakshmi V.; Masilamoni, J. Gunasingh; Terry, Alvin V., Jr.; Cashikar, Anil G.

Molecular chaperones protect cells from the deleterious effects of protein misfolding and aggregation. Neurotoxicity of amyloid-beta (A beta) aggregates and their deposition in senile plaques are hallmarks of Alzheimer's disease (AD). We observed that the overall content of alpha B-crystallin, a small heat shock protein molecular chaperone, decreased in AD model mice in an age-dependent manner. We hypothesized that alpha B-crystallin protects cells against A beta toxicity. To test this, we crossed alpha B-crystallin/HspB2 deficient (CRYAB(-/-) HSPB2(-/-)) mice with AD model transgenic mice expressing mutant human amyloid precursor protein. Transgenic and non-transgenic mice in chaperone-sufficient or deficient backgrounds were examined for representative behavioral paradigms for locomotion and memory network functions: (i) spatial orientation and locomotion was monitored by open field test; (ii) sequential organization and associative learning was monitored by fear conditioning; and (iii) evoked behavioral response was tested by hot plate method. Interestingly, alpha B-crystallin/HspB2 deficient transgenic mice were severely impaired in locomotion compared to each genetic model separately. Our results highlight a synergistic effect of combining chaperone deficiency in a transgenic mouse model for AD underscoring an important role for chaperones in protein misfolding diseases.

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