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anti-Human Lamin B1 Antibodies:
anti-Mouse (Murine) Lamin B1 Antibodies:
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Human Polyclonal Lamin B1 Primary Antibody for ICC, IHC (fro) - ABIN3043687
Zhu, Liu, Li, Liu, Wang, Sun, Xiong, Jiang, Zheng, Hu: Protein tyrosine phosphatase receptor U (PTPRU) is required for glioma growth and motility. in Carcinogenesis 2014
Show all 18 Pubmed References
Human Polyclonal Lamin B1 Primary Antibody for IHC (p), WB - ABIN3042505
Liu, Ma, Wu, Li, Zhang, Han, Wang, Reindl, Wu, Ma: Arginine deiminase augments the chemosensitivity of argininosuccinate synthetase-deficient pancreatic cancer cells to gemcitabine via inhibition of NF-?B signaling. in BMC cancer 2014
Show all 15 Pubmed References
Cow (Bovine) Monoclonal Lamin B1 Primary Antibody for DB, ELISA - ABIN108542
Weaver, Carson, Walker, Chaly, Lach, Raymond, Brown, Sikorska: Degradation of nuclear matrix and DNA cleavage in apoptotic thymocytes. in Journal of cell science 1996
Show all 12 Pubmed References
Human Monoclonal Lamin B1 Primary Antibody for ICC, FACS - ABIN335391
Broers, Bronnenberg, Kuijpers, Schutte, Hutchison, Ramaekers: Partial cleavage of A-type lamins concurs with their total disintegration from the nuclear lamina during apoptosis. in European journal of cell biology 2003
Show all 9 Pubmed References
Human Polyclonal Lamin B1 Primary Antibody for IHC, WB - ABIN6713284
Wen, Liu, Bi, Hu, Chen, Huang, Liang, Li, Lin, Chen: Adiponectin inhibits KISS1 gene transcription through AMPK and specificity protein-1 in the hypothalamic GT1-7 neurons. in The Journal of endocrinology 2012
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Human Polyclonal Lamin B1 Primary Antibody for WB - ABIN2668811
Yang, Fan, Camp, van Buren, Liu, Somcio, Gray, Cheng, Hoff, Ellis: Chronic oxaliplatin resistance induces epithelial-to-mesenchymal transition in colorectal cancer cell lines. in Clinical cancer research : an official journal of the American Association for Cancer Research 2006
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Human Polyclonal Lamin B1 Primary Antibody for IHC, WB - ABIN6669793
Cheng, Wei, Xie, Peng, Yan, Qin, Liu, Xu, Li, Zhang: Alleviation of Toxicity Caused by Overactivation of Pparα through Pparα-Inducible miR-181a2. in Molecular therapy. Nucleic acids 2017
Show all 2 Pubmed References
Human Polyclonal Lamin B1 Primary Antibody for IHC, WB - ABIN3015698
Ma, Fang, Luo, Yang, Wang, Zhang, Wang, Chen, Chan, Liu: The C-ETS2-TFEB Axis Promotes Neuron Survival under Oxidative Stress by Regulating Lysosome Activity. in Oxidative medicine and cellular longevity 2017
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Monoclonal Lamin B1 Primary Antibody for IF, WB - ABIN534184
Krohne, Benavente: The nuclear lamins. A multigene family of proteins in evolution and differentiation. in Experimental cell research 1986
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Polyclonal Lamin B1 Primary Antibody for IHC (fro), IF - ABIN540564
Pollard, Chan, Grant, Sullivan, Tan, Glass: In vitro posttranslational modification of lamin B cloned from a human T-cell line. in Molecular and cellular biology 1990
Show all 2 Pubmed References
Lamin B counteracts the kinesin Eg5 to restrain spindle pole separation during spindle assembly.
TPR contributes to the organization of the nuclear lamina and in cooperation with lamin B1 and lamin A-C guards the interphase assembly of nuclear pore complexes.
E3 ubiquitin ligase RNF123 targets LMNB1, Rb protein and LAP2alpha for proteasomal degradation.
We observed reduced detection of lamin B1 in the ectopic endometrium raising the possibility that the presence of senescent cells might be contributing to the maintenance and progression of endometriosis by apoptosis resistance and peritoneal stress inherent of the disease.
Results show that HECW2 interacts with lamin B1 mediating its ubiquitination and proteasomal degradation.
down-regulation of Lamin B1 and up-regulation of Nephroblastoma overexpressed (NOV) are at least partially responsible for the inhibitory effect of Huaier on the proliferative and invasive capacity of SKHEP-1 cells
The aim of the present study was to elucidate the influence of LMNB1 upregulation on colon cancer cell line after treatment with 5-FU. The results indicate, that overexpression of LMNB1 induced dose-dependent cell death mainly by mitotic catastrophe pathway.
In this report we show that increased self-association propensity of mutant LA modulates the LA-LB1 interaction and precludes the formation of an otherwise uniform laminar network. Our results might highlight the role of homotypic and heterotypic interactions of LA in the pathogenesis of DCM and hence laminopathies in the broader sense.
These results suggest that the nuclear lamins and progerin have marginal roles in the activation of the antioxidant Nrf2 response to arsenic and cadmium.
We show that epithelial cells failing to undergo proliferation arrest during TGF-beta-induced EMT sustain mitotic abnormalities due to failed cytokinesis, resulting in aneuploidy. This genomic instability is associated with the suppression of multiple nuclear envelope proteins implicated in mitotic regulation and is phenocopied by modulating the expression of LaminB1.
The primary response of cells to various stresses leading to senescence consists of the down-regulation of LBR and LB1 to attain reversal of the chromatin architecture.
Data show that lamins A and B are differently processed in staurosporine and beta-Amyloid peptide fragments Abeta42-treated cells.
The tail domain of lamin B1 is more strongly modulated by divalent cations than lamin A.
An upstream mutation alters LMNB1 gene expression in autosomal dominant adult-onset demyelinating leukodystrophy.
Deregulation of LMNB1 expression induces modified splicing of several genes, likely driven by raver-2 overexpression, and suggest that an alteration of mRNA processing could be a pathogenic mechanism in adult-onset autosomal dominant leukodystrophy.
Lamin B1 levels are increased in oligodendrocytes, the cell type that produces myelin in the central nervous system.
Nuclear envelope remodelling during human spermiogenesis involves somatic B-type lamins and a spermatid-specific B3 lamin isoform.
LMNB1-related autosomal-dominant leukodystrophy is a slowly progressive neurological disease with survival lasting more than two decades after clinical onset.
Lamin B1 overexpression increases nuclear rigidity in autosomal dominant leukodystrophy fibroblasts.
Data indicate that lamin B1 promotes DNA double-strand breaks (DSBs) repair and cell survival.
maintenance of lamin B1 levels is required for DNA replication and repair through regulation of the expression of key factors involved in these essential nuclear functions
The results indicate that finely tuned levels of Lmnb1 are required for neural stem cells differentiation into neurons, proper expression of the astrocytic marker GFAP and corticogenesis.
By using targeted knockout in olfactory epithelial stem cells in adult mice, we show that lamin B1 deficient neurons exhibit attenuated response to odour stimulation. This deficit can be explained by decreased expression of genes involved in mature neuron function, along with increased expression of genes atypical of the olfactory lineage.
The parts of chromatin interact with nuclear lamina proteins like Lamin B1 and, therefore, can be identified in a given cell type by chromatin profiling of these proteins.
While the distribution patterns of both lamins closely paralleled the respective stages of mitosis, Nup160 localization in metaphase oocytes corresponded to that in mitotic prometaphase rather than metaphase.
Here we report that in primary mouse cortical neurons, LMNB1 overexpression reduces axonal outgrowth, whereas deficiency of endogenous Lmnb1 results in aberrant dendritic development.
Analysis of lamin B1 expression in different regions of the brain in wild-type animals showed that the level of Lmnb1 transcript decreased significantly in an age-dependent manner.
Data show that lamins B1 and B2 have unique functions and that increased production of one B-type lamin cannot compensate for the loss of the other.
lamins B1 and B2 have unique roles in the developing brain and increased production of one B-type lamin does not fully complement loss of the other.
Lamin-B1 is required for organization of lamin-A/C and lamin-B2 in mouse embryonic stem cells and Lamin-B1 is required for organization of lamin-A/C and lamin-B2 in differentiated cells
farnesylation of lamin B1--but not lamin B2--is crucial for brain development and for retaining chromatin within the bounds of the nuclear lamina during neuronal migration.
lamin B1 overexpression mediates oligodendrocyte cell-autonomous neuropathology in adult-onset autosomal-dominant leukodystrophy.
We conclude that lamin B1 is a modifier gene of major effect for Neural tube defects resulting from loss of Grhl3 function
Lamin B1 is lost from primary human and murine cell strains when they are induced to senesce.
Lamin B1 is essential for brain development and is required for the integrity of the nuclear lamina.
study found that embryonic stem cells do not need any lamins for self-renewal and pluripotency; however, B-type lamins are required for proper organogenesis
Absence of both Lmnb1 and Lmnb2 in keratinocytes has no effect on cell proliferation or the development of skin and hair.
lamin B1 mutant mice provide evidence for a broad and nonredundant function of lamin B1 in mammalian development.
Post-translationally processed lamin B1 has some control of gene expression as well as chromosome position.
lamin B1 serves a fundamental role within the nuclear envelope: anchoring the nucleus to the cytoskeleton.
lamin A/C, lamin B1, and viral US3 kinase have roles in viral infectivity, virion egress, and the targeting of herpes simplex virus U(L)34-encoded protein to the inner nuclear membrane
The nuclear lamina consists of a two-dimensional matrix of proteins located next to the inner nuclear membrane. The lamin family of proteins make up the matrix and are highly conserved in evolution. During mitosis, the lamina matrix is reversibly disassembled as the lamin proteins are phosphorylated. Lamin proteins are thought to be involved in nuclear stability, chromatin structure and gene expression. Vertebrate lamins consist of two types, A and B. This gene encodes one of the two B type proteins, B1. Alternative splicing results in transcript variants and a duplication of this gene is associated with autosomal dominant adult-onset leukodystrophy (ADLD).