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AV37192

Sigma-Aldrich

Anti-SP1 (AB1) antibody produced in rabbit

IgG fraction of antiserum

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UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

conjugate

unconjugated

antibody form

IgG fraction of antiserum

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

51 kDa

species reactivity

human, mouse, rat

concentration

0.5 mg - 1 mg/mL

technique(s)

western blot: suitable

NCBI accession no.

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

mouse ... SP1(20683)

Immunogen

Synthetic peptide directed towards the middle region of human SP1

Biochem/physiol Actions

SP1 is a transcription factor binds to GC box

Sequence

Synthetic peptide located within the following region: GSSGTSSQGQTPQRVGGLQGSDSLNIQQNQTSGGSLQGSQQKEGEQSQQT

Physical form

Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.

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 1

flash_point_f

Not applicable

flash_point_c

Not applicable


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Hemanth N Banavath et al.
Journal of the American Heart Association, 8(24), e012919-e012919 (2019-12-06)
Background Translocation of miR-181c into cardiac mitochondria downregulates the mitochondrial gene, mt-COX1. miR-181c/d-/- hearts experience less oxidative stress during ischemia/reperfusion (I/R) and are protected against I/R injury. Additionally, miR-181c overexpression can increase mitochondrial matrix Ca2+ ([Ca2+]m), but the mechanism by
Barbara Roman et al.
Journal of molecular and cellular cardiology, 144, 87-96 (2020-05-23)
In cardiomyocytes, there is microRNA (miR) in the mitochondria that originates from the nuclear genome and matures in the cytoplasm before translocating into the mitochondria. Overexpression of one such miR, miR-181c, can lead to heart failure by stimulating reactive oxygen

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