Results 51 to 60 of about 52,713 (325)

Sorting nexin 6 enhances lamin a synthesis and incorporation into the nuclear envelope. [PDF]

open access: yesPLoS ONE, 2014
Nuclear lamins are important structural and functional proteins in mammalian cells, but little is known about the mechanisms and cofactors that regulate their traffic into the nucleus.
Jose M González-Granado   +6 more
doaj   +1 more source

Heterozygous lamin B1 and lamin B2 variants cause primary microcephaly and define a novel laminopathy

open access: yesGenetics in Medicine, 2020
Lamins are the major component of nuclear lamina, maintaining structural integrity of the nucleus. Lamin A/C variants are well established to cause a spectrum of disorders ranging from myopathies to progeria, termed laminopathies.
D. Parry   +97 more
semanticscholar   +1 more source

Persistence of laminations [PDF]

open access: yesBulletin of the Brazilian Mathematical Society, New Series, 2010
We present a modern proof of some extensions of the celebrated Hirsch-Pugh-Shub theorem on persistence of normally hyperbolic compact laminations. Our extensions consist of allowing the dynamics to be an endomorphism, of considering the complex analytic case and of allowing the laminations to be non compact.
openaire   +3 more sources

Baculovirus infection induces disruption of the nuclear lamina

open access: yesScientific Reports, 2017
Baculovirus nucleocapsids egress from the nucleus primarily via budding at the nuclear membrane. The nuclear lamina underlying the nuclear membrane represents a substantial barrier to nuclear egress. Whether the nuclear lamina undergoes disruption during
Xiaomei Zhang   +5 more
doaj   +1 more source

Overexpression and cytoplasmic localization of caspase-6 is associated with lamin A degradation in set of ovarian cancers

open access: yesBiomarker Research, 2018
Background In most women with ovarian cancer, the diagnosis occurs after dissemination of tumor cells beyond ovaries. Several molecular perturbations occur ahead of tumor initiation including loss of lamin A/C. Our hypothesis was that the loss of nuclear
Callinice D Capo-chichi   +2 more
doaj   +1 more source

Native lamin A/C proteomes and novel partners from heart and skeletal muscle in a mouse chronic inflammation model of human frailty

open access: yesFrontiers in Cell and Developmental Biology, 2023
Clinical frailty affects ∼10% of people over age 65 and is studied in a chronically inflamed (Interleukin-10 knockout; “IL10-KO”) mouse model. Frailty phenotypes overlap the spectrum of diseases (“laminopathies”) caused by mutations in LMNA. LMNA encodes
Fatima D. Elzamzami   +9 more
doaj   +1 more source

Structural basis for lamin assembly at the molecular level

open access: yesNature Communications, 2019
Nuclear structure and function are governed by lamins, which are intermediate filaments that mostly consist of α-helices. Different lamin assembly models have been proposed based on low resolution and fragmented structures.
Jinsook Ahn   +8 more
semanticscholar   +1 more source

Altered protein dynamics of disease-associated lamin A mutants

open access: yesBMC Cell Biology, 2004
Background Recent interest in the function of the nuclear lamina has been provoked by the discovery of lamin A/C mutations in the laminopathy diseases. However, it is not understood why mutations in lamin A give such a range of tissue-specific phenotypes.
Worman Howard J   +5 more
doaj   +1 more source

Macrophage‐derived MLKL in alcohol‐associated liver disease: Regulation of phagocytosis

open access: yesHepatology, EarlyView., 2022
EtOH causes leaky gut allowing bacteria and PAMPs into the liver, resulting in hepatic inflammation and injury. We demonstrate that LPS induces STAT1‐mediated expression and phosphorylation of MLKL in macrophages and identify a novel function that myeloid MLKL translocates to phagosomes and lysosomes and regulates phagocytosis, which contributes to the
Xiaoqin Wu   +16 more
wiley   +1 more source

Escape from TGF‐β‐induced senescence promotes aggressive hallmarks in epithelial hepatocellular carcinoma cells

open access: yesMolecular Oncology, EarlyView.
Chronic TGF‐β exposure drives epithelial HCC cells from a senescent state to a TGF‐β resistant mesenchymal phenotype. This transition is characterized by the loss of Smad3‐mediated signaling, escape from senescence, enhanced invasiveness and metastatic potential, and upregulation of key resistance modulators such as MARK1 and GRM8, ultimately promoting
Minenur Kalyoncu   +11 more
wiley   +1 more source

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