Редактирование: TFRC

Transferrin receptor protein 1 (TR) (TfR) (TfR1) (Trfr) (T9) (p90) (CD71 antigen) [Contains: Transferrin receptor protein 1, serum form (sTfR)]

==Publications==

{{medline-entry
|title=Identification of reference genes for RT-qPCR data normalisation in aging studies.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31562345
|abstract=Aging is associated with changes in gene expression levels that affect cellular functions and predispose to age-related diseases. The use of candidate genes whose expression remains stable during aging is required to correctly address the age-associated variations in expression levels. Reverse transcription quantitative-polymerase chain reaction (RT-qPCR) has become a powerful approach for sensitive gene expression analysis. Reliable RT-qPCR assays rely on the normalisation of the results to stable reference genes. Taken these data together, here we evaluated the expression stability of eight frequently used reference genes in three aging models: oncogene-induced senescence (OIS), in vitro and in vivo aging. Using NormFinder and geNorm algorithms, we identified that the most stable reference gene pairs were [[PUM1]] and [[TBP]] in OIS, [[GUSB]] and [[PUM1]] for in vitro aging and [[GUSB]] and [[OAZ1]] for in vivo aging. To validate these candidates, we used them to normalise the expression data of [[CDKN1A]], [[APOD]] and [[TFRC]] genes, whose expression is known to be affected during OIS, in vitro and in vivo aging. This study demonstrates that accurate normalisation of RT-qPCR data is crucial in aging research and provides a specific subset of stable reference genes for future aging studies.
|mesh-terms=* Aging
* Algorithms
* Gene Expression Profiling
* Genes, Essential
* Humans
* Real-Time Polymerase Chain Reaction
* Software

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6764958
}}
{{medline-entry
|title=[[SQSTM1]]/p62 and [[PPARGC1A]]/PGC-1alpha at the interface of autophagy and vascular senescence.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31441382
|abstract=Defective macroautophagy/autophagy and mitochondrial dysfunction are known to stimulate senescence. The mitochondrial regulator [[PPARGC1A]] (peroxisome proliferator activated receptor gamma, coactivator 1 alpha) regulates mitochondrial biogenesis, reducing senescence of vascular smooth muscle cells (VSMCs); however, it is unknown whether autophagy mediates [[PPARGC1A]]-protective effects on senescence. Using [i]ppargc1a [/i] VSMCs, we identified the autophagy receptor [[SQSTM1]]/p62 (sequestosome 1) as a major regulator of autophagy and senescence of VSMCs. Abnormal autophagosomes were observed in VSMCs in aortas of [i]ppargc1a [/i] mice. [i]ppargc1a [/i] VSMCs in culture presented reductions in LC3-II levels; in autophagosome number; and in the expression of [[SQSTM1]] (protein and mRNA), [[LAMP2]] (lysosomal-associated membrane protein 2), [[CTSD]] (cathepsin D), and [[TFRC]] (transferrin receptor). Reduced [[SQSTM1]] protein expression was also observed in aortas of [i]ppargc1a [/i] mice and was upregulated by [[PPARGC1A]] overexpression, suggesting that [[SQSTM1]] is a direct target of [[PPARGC1A]]. Inhibition of autophagy by 3-MA (3 methyladenine), spautin-1 or [i]Atg5[/i] (autophagy related 5) siRNA stimulated senescence. Rapamycin rescued the effect of [i]Atg5[/i] siRNA in [i]Ppargc1a [/i] , but not in [i]ppargc1a [/i] VSMCs, suggesting that other targets of [[MTOR]] (mechanistic target of rapamycin kinase), in addition to autophagy, also contribute to senescence. [i]Sqstm1[/i] siRNA increased senescence basally and in response to [[AGT]] II (angiotensin II) and zinc overload, two known inducers of senescence. Furthermore, [i]Sqstm1 [/i]gene deficiency mimicked the phenotype of [i]Ppargc1a[/i] depletion by presenting reduced autophagy and increased senescence [i]in vitro[/i] and [i]in vivo[/i]. Thus, [[PPARGC1A]] upregulates autophagy reducing senescence by a [[SQSTM1]]-dependent mechanism. We propose [[SQSTM1]] as a novel target in therapeutic interventions reducing senescence. 3-MA: 3 methyladenine; ACTA2/SM-actin: actin, alpha 2, smooth muscle, aorta; ACTB/β-actin: actin beta; [[AGT]] II: angiotensin II; ATG5: autophagy related 5; BECN1: beclin 1; CAT: catalase; CDKN1A: cyclin-dependent kinase inhibitor 1A (P21); Chl: chloroquine; [[CTSD]]: cathepsin D; CYCS: cytochrome C, somatic; DHE: dihydroethidium; DPBS: Dulbecco's phosphate-buffered saline; EL: elastic lamina; EM: extracellular matrix; FDG: fluorescein-di-β-D-galactopyranoside; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; γH2AFX: phosphorylated H2A histone family, member X, H DCFDA: 2',7'-dichlorodihydrofluorescein diacetate; [[LAMP2]]: lysosomal-associated membrane protein 2; MASMs: mouse vascular smooth muscle cells; MEF: mouse embryonic fibroblast; [[NBR1]]: [[NBR1]], autophagy cargo receptor; NFKB/NF-κB: nuclear factor of kappa light polypeptide gene enhancer in B cells; [[MTOR]]: mechanistic target of rapamycin kinase; NFE2L2: nuclear factor, erythroid derived 2, like 2; NOX1: NADPH oxidase 1; OPTN: optineurin; PFA: paraformaldehyde; PFU: plaque-forming units; [[PPARGC1A]]/PGC-1α: peroxisome proliferator activated receptor, gamma, coactivator 1 alpha; Ptdln3K: phosphatidylinositol 3-kinase; RASMs: rat vascular smooth muscle cells; ROS: reactive oxygen species; SA-GLB1/β-gal: senescence-associated galactosidase, beta 1; SASP: senescence-associated secretory phenotype; SIRT1: sirtuin 1; Spautin 1: specific and potent autophagy inhibitor 1; [[SQSTM1]]/p62: sequestosome 1; SOD: superoxide dismutase; TEM: transmission electron microscopy; TFEB: transcription factor EB; [[TFRC]]: transferrin receptor; TRP53/p53: transformation related protein 53; TUBG1: tubulin gamma 1; VSMCs: vascular smooth muscle cells; WT: wild type.

|keywords=* Aging
* SQSTM1
* autophagy
* oxidative stress
* senescence
* vascular biology
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7469683
}}