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AB9870

Sigma-Aldrich

Anti-STIM1 Antibody

Chemicon®, from rabbit

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Synonym(s):
Stromal interaction molecule 1
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

rabbit

Quality Level

antibody form

purified antibody

antibody product type

primary antibodies

clone

polyclonal

species reactivity

human, mouse

manufacturer/tradename

Chemicon®

technique(s)

western blot: suitable

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

General description

TRP (transient receptor potential)-related ion channels (TRPCs) have been postulated as candidates for forming both receptor-operated (ROCE) and capacitative Ca2+ entry channels across the plasma membrane. ER transmembrane protein STIM1 senses the depletion of Ca2+ from ER stores. Orai proteins, interacting with TRPCs, act as regulatory subunits that confers STIM1-mediated store depletion sensitivity to these channels and regulate Ca2+ influx through the plasma membrane.

Specificity

Catalogue No. AB9870 recognizes the C-Terminus of STIM1.

Immunogen

Synthetic Linear Peptide

Application

Anti-STIM1 Antibody is an antibody against STIM1 for use in WB.
Optimal working dilutions must be determined by the end user.
Research Category
Neuroscience
Research Sub Category
Ion Channels & Transporters

Quality

Routinely evaluated in western blotting using Jurkat lysate.

Target description

80 kDa

Physical form

Format: Purified
Protein A purified
Purified in PBS with 0.05% NaN3

Storage and Stability

Maintain at 2-8°C in undiluted aliquots for up to 1 year after date of receipt.

Analysis Note

Control
Jurkat lysate.

Legal Information

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

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

WGK 2

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

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Roberto Silva-Rojas et al.
Human molecular genetics, 28(10), 1579-1593 (2018-12-24)
Strict regulation of Ca2+ homeostasis is essential for normal cellular physiology. Store-operated Ca2+ entry (SOCE) is a major mechanism controlling basal Ca2+ levels and intracellular Ca2+ store refilling, and abnormal SOCE severely impacts on human health. Overactive SOCE results in
Julie Perroud et al.
Journal of cell science, 130(18), 3083-3093 (2017-08-02)
Ca2+ signaling plays a key role during human myoblast differentiation. Among Ca2+-sensitive pathways, calcineurin is essential for myoblast differentiation and muscle regeneration. Nuclear factor of activated T-cell (NFAT) transcription factors are the major calcineurin targets. We investigated the expression and
Mathilde Chivet et al.
The Journal of general physiology, 155(1) (2022-11-22)
The expression of the Huntingtin protein, well known for its involvement in the neurodegenerative Huntington's disease, has been confirmed in skeletal muscle. The impact of HTT deficiency was studied in human skeletal muscle cell lines and in a mouse model
Paula Nunes-Hasler et al.
Nature communications, 8(1), 1852-1852 (2017-11-28)
Antigen cross-presentation by dendritic cells (DC) stimulates cytotoxic T cell activation to promote immunity to intracellular pathogens, viruses and cancer. Phagocytosed antigens generate potent T cell responses, but the signalling and trafficking pathways regulating their cross-presentation are unclear. Here, we
Georges Arielle Peche et al.
Neuropathology : official journal of the Japanese Society of Neuropathology, 40(6), 559-569 (2020-10-20)
Tubular aggregate myopathy (TAM) is a progressive disorder characterized by muscle weakness, cramps, and myalgia. TAM clinically overlaps with Stormorken syndrome (STRMK), combining TAM with miosis, thrombocytopenia, hyposplenism, ichthyosis, short stature, and dyslexia. TAM and STRMK arise from gain-of-function mutations

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