The results of the present study demonstrate that hypoxia induces HIF-1α protein stabilization as early as 10 minutes, with a maximum at 3 hours. Hypoxic signaling leading to HIF protein stabilization is mediated via the Shc/Ras signaling cascade, as demonstrated by overexpression of dnShc and dnRas in HUVECs. Hypoxia-induced tyrosine phosphorylation of Shc seems to occur as one of the earliest events, peaking at 10 minutes after hypoxic exposure, followed by subsequent Shc-dependent activation of Ras, which showed maximal activity under the influence of hypoxia at 30 minutes.. Previous studies have suggested that hypoxic signaling leading to HIF expression involves activation of tyrosine kinases, because induction of HIF-1 was inhibited by pretreating cells with the tyrosine kinase inhibitor genistein.14. However, a specific tyrosine kinase initiating the signaling events leading to HIF stabilization has not been identified. It has been shown that the transformation of cells with the ...

The Shc adaptor protein, particularly its p52 isoform, has been identified as a primary signaling partner for the tyrosine(s)-phosphorylated cytoplasmic tails of activated β3 integrins. Inspired by our recent structure of the Shc PTB domain in complex with a bi-phosphorylated peptide derived from β3 cytoplasmic tail, we have initiated the investigation of Shc interaction with phospholipids of the membrane. We are particularly focused on PtdIns and their effects on Shc mediated integrin signaling in vitro. Here we present thermodynamic profiles and molecular details of the interactions between Shc, integrin, and PtdIns, all of which have been studied by ITC and solution NMR methods. A model of p52 Shc interaction with phosphorylated β3 integrin cytoplasmic tail at the cytosolic face of the plasma membrane is proposed based on these data.

This gene encodes three main isoforms that differ in activities and subcellular location. While all three are adapter proteins in signal transduction pathways, the longest (p66Shc) may be involved in regulating life span and the effects of reactive oxygen species. The other two isoforms, p52Shc and p46Shc, link activated receptor tyrosine kinases to the Ras pathway by recruitment of the GRB2/SOS complex. p66Shc is not involved in Ras activation. Unlike the other two isoforms, p46Shc is targeted to the mitochondrial matrix. Several transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Feb 2011] ...

One possible mechanism to explain the activation of MAPK would be through nongenomic effects of the ER acting at the level of the cell membrane (12) . We postulated that membrane-associated ER might use a classical growth factor pathway to transduce its effects in LTED cells. The adaptor protein Shc represents a key modulator of tyrosine kinase-activated peptide hormone receptors (13, 14) . As an upstream regulator of MAPK, Shc transduces mitogenic and differentiation signals from a variety of tyrosine kinase receptors such as those for epidermal growth factor (EGF), nerve growth factor (NGF), platelet-derived growth factor (PDGF), and insulin-like growth factor (IGF), to downstream kinase cascades (15) . On receptor activation and autophosphorylation, Shc binds to the adaptor proteins Grb2 and Sos, which results in activation of Ras, Raf, Mek, and MAPK (15) .. We postulated that estrogen deprivation might trigger activation of a nongenomic, estrogen-regulated, MAPK pathway that uses Shc. We ...

A mammalian adaptor protein with conserved Src homology 2 and phosphotyrosine-binding domains is related to Shc and is specifically expressed in the brain Academic Article ...

Reactome is pathway database which provides intuitive bioinformatics tools for the visualisation, interpretation and analysis of pathway knowledge.

Reactome is pathway database which provides intuitive bioinformatics tools for the visualisation, interpretation and analysis of pathway knowledge.

May play a role in signaling pathways governing cellular proliferation, cell growth and differentiation. May be a component of a novel signaling pathway downstream of Shc. Acts as a positive regulator of FGF signaling in neural progenitor cells ...

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Hepatocellular carcinoma (HCC) is one of the most common cancers with an insidious onset, strong invasiveness, insensitivity to chemotherapy, and poor prognosis, thus makes clinical treatment challenging. The mechanisms require further elucidation for developing novel therapies and targeting drug resistance. Here, we observed high Shc3 expression in patients with chemoresistant and recurrent HCCs. Shc3 overexpression induced a significant increase in MDR1/P-glycoprotein expression, whereas Shc3 knockdown impaired this expression. Further, Shc3 inhibition significantly restored HCC cell sensitivity to doxorubicin and sorafenib. Mechanistically, Shc3 interacted with β-catenin, inhibited destruction complex stability, promoted β-catenin release, and dampened β-catenin ubiquitination. Shc3 bound β-catenin and facilitated its nuclear translocation, prompting the β-catenin/TCF pathway to elevate MDR1 transcription. β-catenin blockage abolished the discrepancy in drug resistance between Shc3-depleted HCC

Thank you for your interest in spreading the word on Circulation Research.. NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address. ...

TY - JOUR. T1 - Erbin suppresses the MAP kinase pathway. AU - Huang, Yang Z.. AU - Zang, Mengwei. AU - Xiong, Wen C.. AU - Luo, Zhijun. AU - Mei, Lin. PY - 2003/1/10. Y1 - 2003/1/10. N2 - We present evidence here that Erbin is a negative regulator of the Ras-Raf-Erk signaling pathway. Expression of Erbin decreases transcription of the AChR ε-subunit gene, an event that is mediated by Erk activation. Although it interacts with the ErbB2 C terminus through the PDZ domain, Erbin has no effect on ErbB2 tyrosine phosphorylation or binding to the adaptor proteins Shc and Grb2. In contrast, expression of Erbin greatly impairs activation of Erk, but not Akt, by ligands that activate receptor tyrosine kinases. Moreover, Erbin inhibits the Erk activation by active Ras, while it fails to do so in the presence of active Raf-1. Erbin associates with active Ras, but not inactive Ras nor Raf. Consistently, Erbin interferes with the interaction between Ras and Raf both in vivo and in vitro. Finally, ...

Expression of SHC1 (p66, SHC, ShcA) in kidney tissue. Antibody staining with HPA001844, CAB005374 and CAB016305 in immunohistochemistry.

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This study reports the molecular mechanisms responsible for the previously observed atherogenic properties of the adaptor protein p66Shc. In particular, it provides mechanistic evidence on how p66Shc mediates the deleterious effects of oxLDL uptake in the endothelium, eventually leading to vascular dysfunction and plaque formation. In primary HAECs, oxLDL induces phosphorylation of p66Shc at the Ser36 residue through activation of PKCβ2 and JNK, respectively. Further, we demonstrated that serial activation of PKCβ2 and JNK, eventually leading to p66Shc phosphorylation, is the main mechanism responsible for increased O2−· generation following exposure of HAECs to oxLDL.. p66Shc is the only isoform of the Shc adaptor protein family that acts as a redox enzyme. p66Shc appears to be equally involved in mediating acute and chronic oxidative stress, and it represents an important final common molecular pathway in aging and chronic cardiovascular disease.26 The latter effect of p66Shc may be of ...

Like soloing rock climbers, adherent cells need a good handhold to survive. Ma et al. now identify an adaptor protein that monitors the cells grip and signals death if the grip fails.. Death following detachment, known as anoikis, is a form of programmed cell death that ensures the disposal of displaced adherent cells. Lack of anoikis is thought to give cells metastatic potential.. A number of survival factors have been identified that are activated by integrin attachment to the extracellular matrix. Binding to soluble matrix fragments, rather than to a fixed matrix, does not prevent anoikis. This difference suggests that mechanical tension is also being measured.. Inside the cell, integrins associate with signaling adaptor proteins of the Shc family. One family member, p66Shc, has been suggested to promote apoptosis. The team now shows that an epithelial cell line that resists anoikis does not express p66Shc. Giving these cells back some p66Shc reestablished detachment-induced death. Normal ...

Cell migration is a complex process that can be regulated by multiple mechanisms, including by the newly discovered tumor suppressor protein PTEN (Tamura et al. 1998, Tamura et al. 1999a). This phosphatase has both phosphoinositol lipid and phosphoprotein substrates (Maehama and Dixon 1998; Myers et al. 1998; Tamura et al. 1998). In this study, we have explored the integration of the regulation of cell migration by PTEN, Shc, and FAK pathways. We examined the intriguing possibility that the effects of PTEN on Shc phosphorylation levels and on cell migration might be causally related, e.g., through a previously undescribed Shc-initiated pathway for regulation of the speed or directionality components of cell migration.. Using transfection reconstitution, dominant negative, and biochemical approaches, we have found the following. (a) We have established a mechanism for our previous observation that PTEN transfection reduces the tyrosine phosphorylation of Shc and inhibits MAP kinase activation by ...

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Expression of SHC1 (p66, SHC, ShcA) in bronchus tissue. Antibody staining with HPA001844, CAB005374 and CAB016305 in immunohistochemistry.

Three components that have each been associated separately with the aging process in worm or rodent model systems have now been linked together by Nemoto and Finkel in a mammalian signaling pathway that may regulate longevity. An increase in intracellular oxidants decreased the activity of a forkhead transcription factor, whose inhibition has been implicated in aging. This effect required expression of the intracellular protein p66shc. Preservation of forkhead activity resulted in higher oxidant scavenging and a decrease on overall cellular oxidant levels. The use of reactive oxygen species as signaling agents may have important therapeautic implications.. S. Nemoto, T. Finkel, Redox regulation of forkhead proteins through a p66shc-dependent signaling pathway. Science 295: 2450-2452 (2002). [Abstract] [Full Text]. ...

Metastasis is the leading reason behind morbidity for lung cancers sufferers. instillation of adenovirus expressing Cre-recombinase (Jackson migration assays the Compact disc24 knockdown lines demonstrated markedly much less migration weighed against control shGFP cells (Fig?3C); the shCD24-Low-1 and shCD24-Low-5 lines demonstrated a 3-collapse and 4-collapse reductions in migration respectively (appearance and high degrees of E-cadherin […]. ...

The Center for Sustainable Health Care Quality and Equity (SHC), a division of the National Minority Quality Forum (NMQF), is emphasizing the need for health systems and providers to reevaluate their flu vaccination efforts directed at their underserved patient populations in anticipation of a potentially dangerous flu season that could be complicated by the ongoing COVID-19 pandemic and other circulating respiratory viruses.

J:32205 OBryan JP, et al., A mammalian adaptor protein with conserved Src homology 2 and phosphotyrosine-binding domains is related to Shc and is specifically expressed in the brain. Proc Natl Acad Sci U S A. 1996 Apr 2;93(7):2729-34 ...

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Background. Reduced endothelial progenitor cell (EPC) differentiation is one relevant component of angiogenesis impairment in diabetic patients. A close relationship exists between hyperglycemia, oxidative stress and diabetic complications. In fact, high glucose determines the overproduction of reactive oxygen species (ROS) by the mitochondria. p66Shc gene regulates the apoptotic responses to oxidative stress. Indeed, p66Shc−/ − mice display decreased ROS production and increased resistance to ROS-induced cell death in a variety of patho-physiologic settings. We examined whether EPC differentiation deficit induced by high glucose was rescued in EPC derived from p66Shc−/ − mice.. Methods and results. EPC differentiation was assessed measuring the number of fibronectin-adhering cells that displayed Ac-LDL uptake and expressed Von Willebrand factor, but not Mac3 when cultured either in 50 mM glucose (HG) or mannitol (M), for 7 days. In peripheral-blood EPC, HG significantly decreased the ...

TY - JOUR. T1 - SHCBP1 is required for midbody organization and cytokinesis completion. AU - Asano, Eri. AU - Hasegawa, Hitoki. AU - Hyodo, Toshinori. AU - Ito, Satoko. AU - Maeda, Masao. AU - Chen, Dan. AU - Takahashi, Masahide. AU - Hamaguchi, Michinari. AU - Senga, Takeshi. N1 - Funding Information: This research was funded by a grant from the Ministry of Education, Culture, Sports, Science and Technology of Japan (23107010 to T. Senga).. PY - 2014/9/1. Y1 - 2014/9/1. N2 - The centralspindlin complex, which is composed of MKLP1 and MgcRacGAP, is one of the crucial factors involved in cytokinesis initiation. Centralspindlin is localized at the middle of the central spindle during anaphase and then concentrates at the midbody to control abscission. A number of proteins that associate with centralspindlin have been identified. These associating factors regulate furrowing and abscission in coordination with centralspindlin. A recent study identified a novel centralspindlin partner, called Nessun ...

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A decrease in reactive oxygen species (ROS) production has been associated with extended life span in animal models of longevity. Mice deficient in the p66Shc gene are long-lived, and their cells are both resistant to oxidative stress and produce less ROS. Our microarray analysis of p66Shc(−/−) mouse tissues showed alterations in transcripts involved in heme and superoxide production and insulin signaling. Thus, we carried out analysis of ROS production by NADPH oxidase (PHOX) in macrophages of control and p66Shc knock-out mice. p66Shc(−/−) mice had a 40% reduction in PHOX-dependent superoxide production. To confirm whether the defect in superoxide production was a direct consequence of p66Shc deficiency, p66Shc was knocked down with siRNA in the macrophage cell line RAW264, and a 30% defect in superoxide generation was observed. The pathway of PHOX-dependent superoxide generation was investigated. PHOX protein levels were not decreased in mutant macrophages; however, the rate and extent ...

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S cerevisiae SHC1 protein: a high pH inducible gene required for growth at alkaline pH in S. cerevisiae; Required for proper maturation of the ascospore through its participation in the synthesis of the chitosan layer; amino acid sequence in first source

Sidney Health Center is a not-for-profit community based medical center that has been serving people in the MonDak region for more than 100 years. Our passion for caring is shared by the doctors, nurses, and several hundred employees and volunteers.Sidney Health Center includes an acute care hospital, clinic area, retail pharmacy and a 93-bed extended care facility offering a complete range of services including Assisted Living, Cardiac Rehabilitation, emergency department, hospice, obstetrics, oncology and radiation therapy, radiology, rehabilitation, surgery, and respiratory. SHC Receives Quality Award

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The Student Health and Counseling Center has moved from our old office to the brand new SHCC! We are located across from the Woodcock Education Building, and next to the Winters Math and Nursing Building.. The Student Health and Counseling Center is here to provide support to our students for medical and counseling needs. We also provide health education, events, and prevention services to empower our students in making healthy choices for themselves.. And when you arent feeling great, know that our staff is here for you!. ...

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