DCLK2 ELISA Kit

Name: DCLK2 ELISA Kit
SKU: DEIA-XYA536
Rating: 5 (1 reviews)

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

COA

SDS

Datasheet

Summary

Sample

cultured cells

Species Reactivity

Human; Mouse

Detection Method

Indirect ELISA

Intended Use

The DCLK2 Cell-Based ELISA Kit is a convenient, lysate-free, high throughput and sensitive assay kit that can monitor DCLK2 protein expression profile in cells. The kit can be used for measuring the relative amounts of DCLK2 in cultured cells as well as screening for the effects that various treatments, inhibitors (ie. siRNA or chemicals), or activators have on DCLK2.

Contents of Kit

1. 96-Well Cell Culture Clear-Bottom Microplate: 1 plate
2. 10x TBS: 24 mL (10x), Clear
3. Quenching Buffer: 24 mL (1x), Clear
4. Blocking Buffer: 50 mL (1x), Clear
5. 10x Wash Buffer: 50 mL (10x), Clear
6. 100x Anti-DCLK2 Antibody (Rabbit Polyclonal): 60 μL (100x), Purple
7. 100x Anti-GAPDH Antibody (Mouse Monoclonal): 60 μL (100x), Green
8. HRP-Conjugated Anti-Rabbit IgG Antibody: 6 mL (1x), Glass
9. HRP-Conjugated Anti-Mouse IgG Antibody: 6 mL (1x), Glass
10. Primary Antibody Diluent: 12 mL (1x), Clear
11. Ready-to-Use Substrate: 12 mL (1x), Brown
12. Stop Solution: 12 mL (1x), Clear
13. Crystal Violet Solution: 6 mL (1x), Glass
14. SDS Solution: 24 mL (1x), Clear
15. Adhesive Plate Seals: 4 seals

Storage

4°C/6 Months

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Doublecortin-Like Kinases Promote Neuronal Survival and Induce Growth Cone Reformation via Distinct Mechanisms

NEURON

Authors: Nawabi, Homaira; Belin, Stephane; Cartoni, Romain; Williams, Philip R.; Wang, Chen; Latremoliere, Alban; Wang, Xuhua; Zhu, Junjie; Taub, Daniel G.; Fu, Xiaoqin; Yu, Bin; Gu, Xiaosong; Woolf, Clifford J.; Liu, Judy S.; Gabel, Christopher V.; Steen, Judith A.; He, Zhigang

Abstract

After axotomy, neuronal survival and growth cone reformation are required for axon regeneration. We discovered that doublecortin-like kinases (DCLKs), members of the doublecortin (DCX) family expressed in adult retinal ganglion cells (RGCs), play critical roles in both processes, through distinct mechanisms. Overexpression of DCLK2 accelerated growth cone re-formation in vitro and enhanced the initiation and elongation of axon re-growth after optic nerve injury. These effects depended on both the microtubule (MT)-binding domain and the serine-proline-rich (S/P-rich) region of DCXs in-cis in the same molecules. While the MT-binding domain is known to stabilize MT structures, we show that the S/P-rich region prevents F-actin destabilization in injured axon stumps. Additionally, while DCXs synergize with mTOR to stimulate axon regeneration, alone they can promote neuronal survival possibly by regulating the retrograde propagation of injury signals. Multifunctional DCXs thus represent potential targets for promoting both survival and regeneration of injured neurons.

Epilepsy associated with autism and attention deficit hyperactivity disorder: Is there a genetic link?

BRAIN & DEVELOPMENT

Authors: Lo-Castro, Adriana; Curatolo, Paolo

Abstract

Autism Spectrum Disorders (ASDs) and Attention Deficit and Hyperactivity Disorder (ADHD) are the most common comorbid conditions associated with childhood epilepsy. The co-occurrence of an epilepsy/autism phenotype or an epilepsy/ADHD phenotype has a complex and heterogeneous pathogenesis, resulting from several altered neurobiological mechanisms involved in early brain development, and influencing synaptic plasticity, neurotransmission and functional connectivity. Rare clinically relevant chromosomal aberrations, in addition to environmental factors, may confer an increased risk for ASDs/ADHD comorbid with epilepsy. The majority of the candidate genes are involved in synaptic formation/remodeling/maintenance (NRX1, CNTN4, DCLK2, CNT-NAP2, TRIM32, ASTN2, CTNTN5, SYN1), neurotransmission (SYNGAP1, GABRG1, CHRNA7), or DNA methylation/chromatin remodeling (MBD5). Two genetic disorders, such as Tuberous sclerosis and Fragile X syndrome may serve as models for understanding the common pathogenic pathways leading to ASDs and ADHD comorbidities in children with epilepsy, offering the potential for new biologically focused treatment options. (C) 2013 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved.