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Merck
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ABC471

Sigma-Aldrich

Anti-KLF15 Antibody

1.0 mg/mL, from rabbit

Sinónimos:

Krueppel-like factor 15, Kidney-enriched krueppel-like factor, KLF15

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About This Item

Código UNSPSC:
12352203
eCl@ss:
32160702
NACRES:
NA.41

origen biológico

rabbit

forma del anticuerpo

affinity isolated antibody

tipo de anticuerpo

primary antibodies

clon

polyclonal

purificado por

affinity chromatography

reactividad de especies

human

reactividad de especies (predicha por homología)

primate (based on 100% sequence homology), bat (based on 100% sequence homology), baboon (based on 100% sequence homology), chimpanzee (based on 100% sequence homology), monkey (based on 100% sequence homology)

concentración

1.0 mg/mL

técnicas

immunohistochemistry: suitable
western blot: suitable

Nº de acceso NCBI

Nº de acceso UniProt

Condiciones de envío

wet ice

modificación del objetivo postraduccional

unmodified

Información sobre el gen

human ... KLF15(28999)

Descripción general

KLF15, also known as Krueppel-like factor 15, Kidney-enriched krueppel-like factor, and encoded by the gene KLF15/KKLF, is a transcriptional regulator that affects expression in a wide variety of developmental and cellular systems. These include glial cell differentiation, cardiac circadian expression regulation, podocyte differentiation, glomerular visceral epithelial cell differentiation, glucose transport, and negative regulation of Peptidyl-lysine acetylation. KLF15 is highly expressed in liver, skeletal muscle, cardiomyocytes and kidney cells. KLF15 is a biomarker in patients with non-ischemic cardiomyopathy, glomerular disease, and aortic aneurysm. In such patients KLF15 expression is severely down regulated. KLF15 deficiency affects the cardiac rhythm and may play a role in ventricular arrhythmias and pathological conditions of the heart.

Inmunógeno

Epitope: Unknown
KLH-conjugated linear peptide corresponding to human KLF15.

Aplicación

Anti-KLF15 Antibody detects level of KLF15 & has been published & validated for use in KLF15.
Immunohistochemistry Analysis: A 1:50 dilution from a representative lot detected KLF15 in human liver tissue.
Research Category
Apoptosis & Cancer
Research Sub Category
Apoptosis - Additional

Calidad

Evaluated by Western Blotting in human skeletal muscle tissue lysate.

Western Blotting Analysis: 0.5 µg/mL of this antibody detected KLF15 in 10 µg of human skeletal muscle tissue lysate.

Descripción de destino

~46 kDa observed

Forma física

Affinity purified
Purified rabbit polyclonal in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.

Almacenamiento y estabilidad

Stable for 1 year at 2-8°C from date of receipt.

Cláusula de descargo de responsabilidad

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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Código de clase de almacenamiento

12 - Non Combustible Liquids

Clase de riesgo para el agua (WGK)

WGK 1

Punto de inflamabilidad (°F)

Not applicable

Punto de inflamabilidad (°C)

Not applicable


Certificados de análisis (COA)

Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»

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Yue-Tong Guo et al.
Journal of the American Heart Association, 10(16), e020554-e020554 (2021-08-06)
Background Adventitial remodeling is a pathological hallmark of hypertension that results in target organ damage. Activated adventitial fibroblasts have emerged as critical regulators in this process, but the precise mechanism remains unclear. Methods and Results Interleukin 11 (IL-11) knockout and
Xiangchen Gu et al.
Kidney international, 92(5), 1178-1193 (2017-06-28)
Large epidemiological studies clearly demonstrate that multiple episodes of acute kidney injury contribute to the development and progression of kidney fibrosis. Although our understanding of kidney fibrosis has improved in the past two decades, we have limited therapeutic strategies to
Yiqing Guo et al.
Journal of the American Society of Nephrology : JASN, 29(10), 2529-2545 (2018-08-26)
Podocyte injury is the hallmark of proteinuric kidney diseases, such as FSGS and minimal change disease, and destabilization of the podocyte's actin cytoskeleton contributes to podocyte dysfunction in many of these conditions. Although agents, such as glucocorticoids and cyclosporin, stabilize

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