The properties about p21 phospho-Tyr57 CDKN1 Polyclonal Antibody

Does anybody ever known about p21 phospho-Tyr57 CDKN1 Polyclonal Antibody? i know a little aboout it, and i will tell you to see if you know about it.


Product name:p21 phospho-Tyr57 CDKN1 Polyclonal Antibody

Applications:IHC-P, WB-Ce

Immunogne:Rabbit polyclonal antibody raised against synthetic phosphopeptides of CDKN1A.

Description:This p21 phospho-Tyr57 CDKN1 Polyclonal Antibody encodes a potent cyclin-dependent kinase inhibitor. The encoded protein binds to and inhibits the activity of cyclin-CDK2 or -CDK4 complexes, and thus functions as a regulator of cell cycle progression at G1. The expression of this gene is tightly controlled by the tumor suppressor protein p53, through which this protein mediates the p53-dependent cell cycle G1 phase arrest in response to a variety of stress stimuli. This protein can interact with proliferating cell nuclear antigen (PCNA), a DNA polymerase accessory factor, and plays a regulatory role in S phase DNA replication and DNA damage repair. This protein was reported to be specifically cleaved by CASP3-like caspases, which thus leads to a dramatic activation of CDK2, and may be instrumental in the execution of apoptosis following caspase activation. Two alternatively spliced variants, which encode an identical protein, have been reported.

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What is β–Amyloid (1-42),human Amyloid β-Protein (Human, 1-42)

Products Name: β–Amyloid (1-42),human Amyloid β-Protein (Human, 1-42)
Molecular Formula: C203H311N55O60S
Purity (HPLC):  98%min.
Appearance: White powder

β–Amyloid (1-42),human Amyloid β-Protein (Human, 1-42) is the main component of amyloid plaques (deposits found in the brains of patients with Alzheimer's disease). Similar plaques appear in some variants of Lewy body dementia and in inclusion body myositis (a muscle disease), while β–Amyloid (1-42),human Amyloid β-Protein (Human, 1-42) can also form the aggregates that coat cerebral blood vessels in cerebral amyloid angiopathy. The plaques are composed of a tangle of regularly ordered fibrillar aggregates called amyloid fibers, a protein fold shared by other peptides such as the prions associated with protein misfolding diseases. Recent research suggests that soluble oligomeric forms of the peptide may be causative agents in the development of Alzheimer's disease A number of genetic, cell biology, biochemical and animal studies support the concept that Aβ plays a central role in the development of Alzheimer’s disease pathology.

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Let me introduce you p27/Kip1B phospho-Ser10 CDKN1B Polyclonal Antibody

Do you ever curious about p27/Kip1B phospho-Ser10 CDKN1B Polyclonal Antibody? did you ever want to know about it but no body can tell you? ok, now ,i can tell you about it. 

Product name:p27/Kip1B phospho-Ser10 CDKN1B Polyclonal Antibody

Applications:IHC-P, WB-Ce

Immunogne:Rabbit polyclonal antibody raised against synthetic phosphopeptides of CDKN1B.

Description:p27/Kip1B phospho-Ser10 CDKN1B Polyclonal Antibody encodes a cyclin-dependent kinase inhibitor, which shares a limited similarity with CDK inhibitor CDKN1A/p21. The encoded protein binds to and prevents the activation of cyclin E-CDK2 or cyclin D-CDK4 complexes, and thus controls the cell cycle progression at G1. The degradation of this protein, which is triggered by its CDK dependent phosphorylation and subsequent ubiquitination by SCF complexes, is required for the cellular transition from quiescence to the proliferative state.

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The medical uses about Endothelin 1

Endothelin 1 transcript is constitutively destabilized by its 3'-UTR through two destabilizing elements, DE1 and DE2. DE1 functions through a conserved ARE by the AUF1-proteasome pathway and is regulated by the heat shock pathway. In a healthy individual, a delicate balance between vasoconstriction and vasodilation is maintained by endothelin and other vasoconstrictors on the one hand and nitric oxide, prostacyclin and other vasodilators on the other.

Overproduction of endothelin in the lungs may cause pulmonary hypertension, which can sometimes be treated by the use of an endothelin receptor antagonist, such as bosentan, sitaxentan or ambrisentan. The latter drug selectively blocks endothelin A receptors, decreasing the vasoconstrictive actions and allowing for increased beneficial effects of endothelin B stimulation, such as nitric oxide production. The precise effects of endothelin B receptor activation depends on the type of cells involved.

Because of its powerful vasoconstrictor properties, and its effects on intracellular calcium, ET-1 has been implicated in the pathogenesis of hypertension, coronary vasospasm, and heart failure. In the latter condition, Endothelin 1 is released by the failing myocardium where it can contribute to calcium overload and hypertrophy. Endothelin  receptor antagonists have been shown to decrease mortality and improve hemodynamics in experimental models of heart failure. A number of studies suggest a role for ET-1 in pulmonary hypertension, as well as in systemic hypertension. A non-selective Endothelin 1 receptor antagonist (bosentan) is currently used in the treatment of pulmonary hypertension.

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