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AB53642

Anti-Calbindin antibody, prediluted

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(1 Publication)

Rabbit Polyclonal Calbindin antibody. Suitable for IHC-P and reacts with Human samples. Cited in 1 publication.

View Alternative Names

CAB27, CALB1, Calbindin, Calbindin D28, D-28K

1 Images
Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-Calbindin antibody, prediluted (AB53642)
  • IHC-P

Unknown

Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-Calbindin antibody, prediluted (AB53642)

ab53642 at a ready to use dilution staining human cerebellum; formalin fixed, paraffin embedded.

Key facts

Host species

Rabbit

Clonality

Polyclonal

Isotype

IgG

Carrier free

No

Reacts with

Human

Applications

IHC-P

applications

Immunogen

The exact immunogen used to generate this antibody is proprietary information.

Reactivity data

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Properties and storage information

Form
Liquid
Purification technique
Affinity purification Immunogen
Storage buffer
pH: 7.6 Preservative: 0.1% Sodium azide Constituents: Tris buffered saline, 1% BSA
Shipped at conditions
Blue Ice
Appropriate long-term storage conditions
+4°C

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

Calbindin also known as calbindin-D28k is a calcium-binding protein with a molecular mass of approximately 28 kDa. This target is mainly expressed in the neurons of the brain such as in the cerebellum and hippocampus as well as in the kidneys and intestine. Calbindin plays a mechanical role in binding and buffering intracellular calcium ions which is important for the regulation of calcium-dependent signaling pathways. Researchers often use techniques like Calbindin IHC (immunohistochemistry) and ELISA to study its distribution and presence within tissues.
Biological function summary

Calbindin contributes to cellular homeostasis by managing intracellular calcium levels. It does not appear to be part of a larger protein complex but operates independently. This protein helps to protect neurons from calcium overload potentially safeguarding against excitotoxicity which occurs when neurons die from excessive stimulation. Calbindin's function as a calcium buffer is of particular importance in maintaining neuron function and survival in areas with high neuronal activity.

Pathways

Calbindin has a significant role in the calcium signaling pathway and is also involved in the vitamin D pathway. The calcium signaling pathway is vital for many cellular processes like muscle contraction neurotransmitter release and gene expression. The vitamin D pathway regulates calcium and phosphate homeostasis in the body. Calbindin's relationship with proteins such as calmodulin and parvalbumin both involved in calcium regulation highlights its importance in maintaining cellular functions.

Abnormal Calbindin expression has been observed in conditions like epilepsy and Parkinson's disease. In epilepsy its decreased expression can impact the ability of neurons to regulate calcium properly leading to increased vulnerability to seizures. In Parkinson's disease altered Calbindin levels have been associated with the selective vulnerability of dopamine neurons. These diseases highlight the connection between Calbindin and proteins like alpha-synuclein known for its role in Parkinson's pathology emphasizing the need to understand its contribution to disease mechanisms.

Product protocols

For this product, it's our understanding that no specific protocols are required. You can visit:

Target data

Buffers cytosolic calcium. May stimulate a membrane Ca(2+)-ATPase and a 3',5'-cyclic nucleotide phosphodiesterase.
See full target information CALB1

Publications (1)

Recent publications for all applications. Explore the full list and refine your search

Journal of innate immunity 14:629-642 PubMed35613551

2022

Regulation of TLR10 Expression and Its Role in Chemotaxis of Human Neutrophils.

Applications

Unspecified application

Species

Unspecified reactive species

Yadu Balachandran,Sarah Caldwell,Gurpreet Kaur Aulakh,Baljit Singh
View all publications

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