Goat Anti-mouse IgG-HRP #abs20001

abs20001-100ul

In Stock

64

abs20001-500ul

In Stock

251

abs20001-1ml

In Stock

377

The Goat anti-Mouse IgG (H+L) antibody, conjugated with HRP, has the ability to recognize both the heavy chain and the light chains of mouse IgG, as well as the light chains of other antibody classes.

Source

Goat

Specificity

IgG h+l

Species Reactivity

Mouse

Application

ELISA: 0.1 - 0.01 ug/ml
IHC: 5.0 - 1.0 ug/ml
WB: 0.5 - 0.05ug/ml

Properties

Form

liquid

Concentration

1mg/ml

Purification

Antigen Affinity Purified

Clonality

Polyclonal Antibody

Isotype

IgG

Stability & Storage

Store at 4℃ for one year.

Storage buffer

HEPES-Saline with stabilizer at a concentration of 50mM and including 0.002% Thimerosal is a well-known solution. It is widely used in various scientific experiments and research studies. The HEPES-Saline solution provides a stable pH environment for biochemical reactions, while the stabilizer helps to maintain the integrity and functionality of the biological samples. Thimerosal, on the other hand, acts as a preservative, safeguarding the solution against microbial contamination. Together, these components offer a reliable and effective solution for various biological and chemical applications.

Conjugate

HRP

References

References

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The study titled "In ovo leptin administration affects hepatic lipid metabolism and microRNA expression in newly hatched broiler chickens" was published in the Journal of Animal Science and Biotechnology in 2012. The research focused on the effects of administering leptin, a hormone involved in regulating appetite and metabolism, on hepatic lipid metabolism and microRNA expression in newly hatched broiler chickens.
The researchers investigated the impact of in ovo administration of leptin on the liver's lipid metabolism and the expression of microRNAs, which are small non-coding RNA molecules involved in regulating gene expression. The study aimed to understand the molecular mechanisms by which leptin influences lipid metabolism in chickens.
To conduct the study, newly hatched broiler chickens were divided into two groups: a control group and a group that received in ovo leptin administration. The researchers analyzed the liver tissues of the chickens and examined changes in lipid metabolism and microRNA expression.
The findings of the study suggested that in ovo leptin administration had a significant impact on hepatic lipid metabolism in the newly hatched broiler chickens. The administration of leptin influenced the expression of key genes involved in lipid metabolism, leading to alterations in lipid synthesis, transport, and accumulation in the liver.
Furthermore, the researchers observed changes in the expression levels of specific microRNAs in the liver tissue of chickens that received in ovo leptin administration. These microRNAs are known to be associated with lipid metabolism and may play a role in mediating the effects of leptin on hepatic lipid metabolism.
Overall, the study provides insights into the molecular mechanisms underlying the effects of leptin on hepatic lipid metabolism in newly hatched broiler chickens. The findings contribute to our understanding of the role of leptin in regulating lipid metabolism and highlight potential targets for improving lipid metabolism and overall health in poultry.
Apelin-13 induces cell proliferation and autophagy in lung adenocarcinoma cells through the mediation of ERK1/2. The research team, including Li Yang, Tao Su, Deguan Lv, Feng Xie, Wei Liu, Jiangang Cao, Irshad Ali Sheikh, Xuping Qin, Lanfang Li, and Linxi Chen, explored the signaling pathway involved in these cellular processes.
The study focused on the role of ERK1/2, a key protein involved in cell growth and survival. The researchers found that apelin-13, a bioactive peptide, stimulated cell proliferation in lung adenocarcinoma cells. Furthermore, it induced autophagy, a cellular process that helps in the degradation of damaged proteins and organelles.
By using specific inhibitors and siRNAs, the team elucidated that apelin-13 triggered these effects through the activation of ERK1/2 pathway. Inhibition of ERK1/2 signaling significantly reduced apelin-13-induced cell proliferation and autophagy, suggesting its crucial role in these processes.
Understanding the underlying mechanisms of lung adenocarcinoma progression is essential to develop targeted therapies. This research sheds light on the involvement of apelin-13 and the ERK1/2 pathway in promoting cell proliferation and autophagy in lung adenocarcinoma. Further studies are needed to explore the potential of targeting this signaling pathway for therapeutic intervention in lung adenocarcinoma.