SCIENCE

APOPTOSIS

Apoptosis (from Ancient Greek ἀπόπτωσις “falling off”) is a form of programmed cell death that occurs in multicellular organisms.[2] Biochemical events lead to characteristic cell changes (morphology) and death. These changes include blebbing, cell shrinkage, nuclear fragmentation, chromatin condensation, chromosomal DNA fragmentation, and global[vague] mRNA decay. The average adult human loses between 50 and 70 billion cells each day due to apoptosis.[3][a] For an average human child between the ages of 8 to […]

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KETOGENIC DIET

The ketogenic diet is a high-fat, adequate-protein, low-carbohydrate diet that in medicine is used primarily to treat difficult-to-control (refractory) epilepsy in children. The diet forces the body to burn fats rather than carbohydrates. Normally, the carbohydrates contained in food are converted into glucose, which is then transported around the body and is particularly important in fueling brain function. However, if little carbohydrate remains in

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MATRIX METALLOPROTEINASES (MMPs)

The role of matrix metalloproteinases in aging “Proteases are a set of enzymes that have been involved in multiple biological processes throughout evolution. Among them, extracellular matrix (ECM) remodeling has emerged as one of the most relevant functions exerted by these proteins, being essential in the regulation of critical events such as embryonic development or tissue homeostasis. Hence, it is not

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SENESCENT CELLS, SASP & SENOLYTICS

SHIPPING APRIL 15TH!!! ZOMBIE CELL KILLER   News Articles:  Both Senolytic Molecules Are Inhibitors Of Particular Members Of The Bcl-2 Family Of Apoptosis Regulatory Proteins And Have Distinct Pharmacokinetic Profiles. ‘One Of The Most Important Aging Discoveries Ever’ 100 Is The New 60: The Transformation Of Healthcare 12 Innovations That Could Make Reverse Aging A

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JNK PREVENTS PREMATURE SENESCENCE

Prevention of premature senescence requires JNK activation Premature senescence is considered as a cellular defense mechanism to prevent tumorigenesis. Although recent evidences show that c-Jun N-terminal kinase (JNK) is involved in the senescence process, the mechanism for this regulation is not fully understood. Here, we examined the role of JNK in premature senescence of tumor

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MDM2

MDM2 antagonists attenuate the senescence-associated secretory phenotype Processes that have been linked to aging and cancer include an inflammatory milieu driven by senescent cells. Senescent cells lose the ability to divide, essentially irreversibly, and secrete numerous proteases, cytokines and growth factors, termed the senescence-associated secretory phenotype (SASP). Senescent cells that lack p53 tumor suppressor function

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ONCOGENE ACTIVATION

… : VersicanV1 promotes proliferation and metastasis of hepatocellular carcinoma through the activation of EGFR–PI3K–AKT pathway (oncogene,(2018), 37, 41,(5585 … … and functional interaction between polyoma virus middle T antigen and insulin and IGF-I receptors is required for oncogene activation and tumour initiation … and hormonal aspects of 6 human neoplasias with special emphasis on

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P53

Crucial role of p53-dependent cellular senescence in suppression of Pten-deficient tumorigenesis Human SIR2 deacetylates p53 and antagonizes PML/p53‐induced cellular senescence Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a PML regulates p53 acetylation and premature senescence induced by

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HSP90

Hsp90 (heat shock protein 90) is a chaperone protein that assists other proteins to fold properly, stabilizes proteins against heat stress, and aids in protein degradation. It also stabilizes a number of proteins required for tumor growth, which is why Hsp90 inhibitors are investigated as anti-cancer drugs. Heat shock proteins, as a class, are among the most highly expressed cellular proteins across all species.[3] As their name

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TELOMERE SHORTENING & PREMATURE AGING

A branching process model of telomere shortening A continuous correlation between oxidative stress and telomere shortening in fibroblasts A Critical Role for Pin2/TRF1 in ATM-dependent Regulation INHIBITION OF Pin2/TRF1 FUNCTION COMPLEMENTS telomere shortening, RADIOSENSITIVITY, AND THE G2/M CHECKPOINT DEFECT OF ATAXIA-TELANGIECTASIA CELLS A G-quadruplex-interactive agent, telomestatin (SOT-095), induces telomere shortening with apoptosis and enhances chemosensitivity

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