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SAB4200106

Sigma-Aldrich

Anti-ULK1 antibody produced in rabbit

enhanced validation

~1.0 mg/mL, affinity isolated antibody

Synonyme(s) :

Anti-ATG1 autophagy related 1 homolog, Anti-UNC51, Anti-Unc51.1, Anti-unc-51-like kinase 1

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About This Item

Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41

Source biologique

rabbit

Niveau de qualité

Conjugué

unconjugated

Forme d'anticorps

affinity isolated antibody

Type de produit anticorps

primary antibodies

Clone

polyclonal

Forme

buffered aqueous solution

Poids mol.

antigen ~150 kDa

Espèces réactives

human

Validation améliorée

recombinant expression
Learn more about Antibody Enhanced Validation

Concentration

~1.0 mg/mL

Technique(s)

western blot: 1-2 μg/mL using whole extracts of HEK-293T cells overexpressing human ULK1.

Numéro d'accès UniProt

Conditions d'expédition

dry ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... ULK1(8408)

Description générale

Uncoordinated 51-like kinase 1 (ULK1) is expressed in skeletal muscle, heart, pancreas, brain, placenta, liver, kidney and lung. This gene is located on human chromosome 2q24.3. ULK1 localizes to cytoplasmic structures. ULK1 and ULK2 is a homolog of autophagy related 1 (Atg1) gene.

Spécificité

Anti-ULK1 recognizes human ULK1.

Application

Anti-ULK1 has been used in immunoblotting.

Actions biochimiques/physiologiques

Uncoordinated 51-like kinase 1 (ULK1) is involved in modulating Atg9 subcellular dynamics. Knockdown of ULK1, but not ULK2, inhibits the autophagic response. Overexpression of ULK1 also inhibits autophagy, suggesting that ULK1 may have multiple mechanisms for regulating autophagy. Knockdown of Ulk1 shRNA can prevent gastric cancer cell survival.

Forme physique

Solution in 0.01 M phos­phate buffered saline, pH 7.4, containing 15 mM sodium azide.

Stockage et stabilité

Store at –20 °C. For continuous use, the product may be stored at 2–8 °C for up to one month. For extended storage, freeze in working aliquots at –20 °C. Repeated freezing and thawing, or storage in “frost-free” freezers, is not recommended. If slight turbidity occurs upon prolonged storage, clarify the solution by centrifugation before use. Working dilutions should be discarded if not used within 12 hours.

Clause de non-responsabilité

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.

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Code de la classe de stockage

10 - Combustible liquids

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Retrouvez la documentation relative aux produits que vous avez récemment achetés dans la Bibliothèque de documents.

Consulter la Bibliothèque de documents

Gemcitabine induces poly (ADP-ribose) polymerase-1 (PARP-1) degradation through autophagy in pancreatic cancer
Wang Y, et al.
PLoS ONE, 9(10), e109076-e109076 (2014)
siRNA screening of the kinome identifies ULK1 as a multidomain modulator of autophagy
Chan EYW, et al.
The Journal of Biological Chemistry, 282(35), 25464-25474 (2007)
Ulk1 over-expression in human gastric cancer is correlated with patients' T classification and cancer relapse
Chen MB, et al.
Testing, 8(20), 33704-33704 (2017)
Human ULK1, a Novel Serine/Threonine Kinase Related to UNC-51 Kinase ofCaenorhabditis elegans: cDNA Cloning, Expression, and Chromosomal Assignment
Kuroyanagi H, et al.
Genomics, 51(1), 76-85 (1998)
Xin Yu et al.
Journal of molecular neuroscience : MN, 50(3), 586-599 (2013-04-18)
Spinocerebellar ataxia type 7 (SCA7) is one of nine neurodegenerative disorders caused by expanded polyglutamine domains. These so-called polyglutamine (polyQ) diseases are all characterized by aggregation. Reducing the level of aggregating polyQ proteins via pharmacological activation of autophagy has been

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