MABE453
Anti-Monoubiquityl-Histon-H2B-(Lys119-)Antikörper, Klon 7B4
clone 7B4, from mouse
Synonym(e):
H2BUb1, Histone H2B type 1-C/E/F/G/I, Histone H2B.1 A, Histone H2B.a, H2B/a, Histone H2B.g, H2B/g, Histone H2B.h, H2B/h, Histone H2B.k, H2B/k, Histone H2B.l, H2B/l, H2BUbK119, H2BK119Ub
Größe auswählen
| Packungsgröße | SKU | Verfügbarkeit | Preis |
|---|---|---|---|
| 100 μg | Warenkorb auf Verfügbarkeit prüfen | € 401,00 |
Über diesen Artikel
biological source
mouse
Quality Level
conjugate
unconjugated
antibody form
purified immunoglobulin
antibody product type
primary antibodies
clone
7B4, monoclonal
species reactivity
human
technique(s)
immunohistochemistry: suitable, western blot: suitable
isotype
IgG2aκ
NCBI accession no.
UniProt accession no.
shipped in
wet ice
target post-translational modification
unmodified
Gene Information
human ... HIST1H2BC(8347)
General description
Immunogen
Application
Epigenetik & Zellkernfunktion
Histone
Western-Blot-Analyse: Eine repräsentative Charge wies Monoubiquityl-Histon-H2B (Lys119) in differenzierten hMSCs nach, die bei der Kontrolle verkürzt wurden, und zeigte einen Signalverlust in differenzierten hMSCs, die mit RNF50-siRNA transfiziert wurden (Karpiuk, O., et al. (2012). Molecular Cell. 46:705-713).
Immunhistochemische Analyse: Eine repräsentative Charge wies Monoubiquityl-Histon-H2B (Lys119) in bösartigen, metastasierten Brusttumoren und normalen angrenzenden Geweben nach (Prenzel, T., et al. (2011). AACR. OF1-OF15).
Physical form
Preparation Note
Analysis Note
Western-Blot-Analyse: 0,5 µg/ml dieses Antikörpers wiesen Monoubiquityl-Histon-H2B (Lys119) in HeLa-Zelllysaten nach, die mit und ohne Nocodazol behandelt wurden.
Other Notes
Disclaimer
1 of 1
Dieser Artikel | |||
|---|---|---|---|
| species reactivity human | species reactivity yeast, human | species reactivity rat, human, mouse | species reactivity mouse, human |
| Gene Information human ... HIST1H2BC(8347) | Gene Information Saccharomyces cerevisiae ... Htb2(852284) | Gene Information human ... Histone H2B(8349) | Gene Information human ... HIST1H2BC(8347) |
| biological source mouse | biological source mouse | biological source rabbit | biological source rabbit |
| conjugate unconjugated | conjugate unconjugated | conjugate - | conjugate - |
| antibody form purified immunoglobulin | antibody form purified immunoglobulin | antibody form affinity isolated antibody | antibody form affinity isolated antibody |
| clone 7B4, monoclonal | clone 1B3F12/A9, monoclonal | clone polyclonal | clone polyclonal |
Still not finding the right product?
Probieren Sie unser Produkt-Auswahlhilfe, um Ihre Auswahl einzugrenzen
Lagerklasse
12 - Non Combustible Liquids
wgk
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
Analysenzertifikate (COA)
Suchen Sie nach Analysenzertifikate (COA), indem Sie die Lot-/Chargennummer des Produkts eingeben. Lot- und Chargennummern sind auf dem Produktetikett hinter den Wörtern ‘Lot’ oder ‘Batch’ (Lot oder Charge) zu finden.
Besitzen Sie dieses Produkt bereits?
In der Dokumentenbibliothek finden Sie die Dokumentation zu den Produkten, die Sie kürzlich erworben haben.
Verwandter Inhalt
"Apoptosis & Autophagy in Cancer: Cell Survival by Eluding Cell Death The ability of tumor cells to elude programmed cell death, also known as apoptosis, is a hallmark of most types of cancer. Similary, autophagy is a highly regulated, homeostatic degradative process where cells destroy their own components via the lysosomal machinery and recycle them for prolonged cell survival. Via extensive crosstalk with pro-apoptotic signaling pathways, autophagy can also contribute to cell death and greatly influence general cell health. Elucidating the correlation between autophagy and apoptotic cell death has become the focus of a great deal of research, particularly in tumor biology. On one hand, autophagy may induce cell death by degrading essential components; on the other hand, it may facilitate survival of cancer cells under unfavorable metabolic conditions."
Cancer is a complex disease manifestation. At its core, it remains a disease of abnormal cellular proliferation and inappropriate gene expression. In the early days, carcinogenesis was viewed simply as resulting from a collection of genetic mutations that altered the gene expression of key oncogenic genes or tumor suppressor genes leading to uncontrolled growth and disease (Virani, S et al 2012). Today, however, research is showing that carcinogenesis results from the successive accumulation of heritable genetic and epigenetic changes. Moreover, the success in how we predict, treat and overcome cancer will likely involve not only understanding the consequences of direct genetic changes that can cause cancer, but also how the epigenetic and environmental changes cause cancer (Johnson C et al 2015; Waldmann T et al 2013). Epigenetics is the study of heritable gene expression as it relates to changes in DNA structure that are not tied to changes in DNA sequence but, instead, are tied to how the nucleic acid material is read or processed via the myriad of protein-protein, protein-nucleic acid, and nucleic acid-nucleic acid interactions that ultimately manifest themselves into a specific expression phenotype (Ngai SC et al 2012, Johnson C et al 2015). This review will discuss some of the principal aspects of epigenetic research and how they relate to our current understanding of carcinogenesis. Because epigenetics affects phenotype and changes in epigenetics are thought to be key to environmental adaptability and thus may in fact be reversed or manipulated, understanding the integration of experimental and epidemiologic science surrounding cancer and its many manifestations should lead to more effective cancer prognostics as well as treatments (Virani S et al 2012).
Global Trade Item Number
| SKU | GTIN |
|---|---|
| MABE453 | 04053252935961 |