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C1728

Sigma-Aldrich

Anti-Calcium Channel (α1D Subunit) (L-type of Voltage-gated Ca2+ Channel) antibody produced in rabbit

affinity isolated antibody, lyophilized powder

Synonym(s):

Anti-CACH3, Anti-CACN4, Anti-CACNL1A2, Anti-CCHL1A2, Anti-Cav1.3, Anti-PASNA, Anti-SANDD

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About This Item

MDL number:
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

lyophilized powder

species reactivity

mouse, rat

technique(s)

immunocytochemistry: 1:30-1:150
immunoprecipitation (IP): suitable
western blot (chemiluminescent): 1:100-1:200

UniProt accession no.

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

Immunogen

synthetic peptide corresponding to amino acids 859-875 of rat α1D (Accession P27732). This epitope is highly conserved in human and hamster.

Application

Anti-Calcium Channel (α1D Subunit) (L-type of Voltage-gated Ca2+ Channel) antibody produced in rabbit is suitable for the following applications:
  • immunocytochemistry at a dilution of 1:30-1:150
  • immunoprecipitation
  • western blot (chemiluminescent) at a dilution of 1:100-1:200

Biochem/physiol Actions

Cav1.3 also known as the calcium channel, voltage-dependent, L type, α1D subunit (CACNA1D), is a human gene. It responds more sensitively to depolarization than those of Cav1.2 or Cav3.1. Cav1.3 is required for proper hearing as well as sinoatrial node and brain function. It undergoes extensive alternative splicing. Alternative splicing in the C terminus and drastically modifies gating properties of the channel. The L-type calcium channel Cav1.3 is important in human glucose-induced insulin secretion and common variants in CACNA1D may contribute to type 2 diabetes.

Physical form

Lyophilized from phosphate buffered saline, pH 7.4, containing 1% BSA and 0.05% sodium azide

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Hua Huang et al.
Molecular pharmacology, 84(4), 643-653 (2013-08-09)
The transcripts of L-type voltage-gated calcium channels (CaV) 1.3 undergo extensive alternative splicing. Alternative splicing, particularly in the C terminus, drastically modifies gating properties of the channel. However, little is known about whether alternative splicing could modulate the pharmacologic properties
T M Reinbothe et al.
Diabetologia, 56(2), 340-349 (2012-12-12)
Voltage-gated calcium channels of the L-type have been shown to be essential for rodent pancreatic beta cell function, but data about their presence and regulation in humans are incomplete. We therefore sought to elucidate which L-type channel isoform is functionally
Jan Salomonsen et al.
Proceedings of the National Academy of Sciences of the United States of America, 102(24), 8668-8673 (2005-06-09)
CD1 molecules play an important role in the immune system, presenting lipid-containing antigens to T and NKT cells. CD1 genes have long been thought to be as ancient as MHC class I and II genes, based on various arguments, but
Andreas Lieb et al.
Biophysical journal, 106(7), 1467-1475 (2014-04-08)
Activity of voltage-gated Cav1.3 L-type Ca(2+) channels is required for proper hearing as well as sinoatrial node and brain function. This critically depends on their negative activation voltage range, which is further fine-tuned by alternative splicing. Shorter variants miss a
Allison Sargoy et al.
PloS one, 9(1), e84507-e84507 (2014-01-15)
Aberrant calcium regulation has been implicated as a causative factor in the degeneration of retinal ganglion cells (RGCs) in numerous injury models of optic neuropathy. Since calcium has dual roles in maintaining homeostasis and triggering apoptotic pathways in healthy and

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