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Chicken Monoclonal TPM1 Primary Antibody für ICC, IF - ABIN151405
Gao, Steffen, Ramos: Osteopontin regulates α-smooth muscle actin and calponin in vascular smooth muscle cells. in Cell biology international 2012
Show all 2 Pubmed References
Human Polyclonal TPM1 Primary Antibody für ICC, IF - ABIN4362648
Ek, Andréasson, Hober, Kampf, Pontén, Uhlén, Merz, Borrebaeck: From gene expression analysis to tissue microarrays: a rational approach to identify therapeutic and diagnostic targets in lymphoid malignancies. in Molecular & cellular proteomics : MCP 2006
The tendency of smooth muscle tropomyosin to form semi-rigid polymers with continuous and undampened rigidity may compensate for the lack of troponin-based structural support in smooth muscles.
Deletion of regions 2-3 in tropomyosin (zeige TPM2 Antikörper) alpha resulted in an 60 % decrease in both isometric tension and stiffness of tropomyosin (zeige TPM2 Antikörper)-reconstituted myocardium.
Tropomyosin (zeige TPM2 Antikörper) is primarily responsible for the change in the kinetic constants of the elementary steps of the cross bridge cycle.
Tm affects the conformation of actin so as to increase the area of hydrophobic interaction between actin and myosin molecules
Stress fibre formation and up-regulation of alpha-smooth muscle actin (zeige ACTG2 Antikörper) (alphaSMA (zeige ACTA2 Antikörper)) induced by TGFbeta2 could be reversed by Tpm1/2 knock-down by siRNA.
The cMyBP-C hypertrophic cardiomyopathy variant L348P enhances thin filament activation through an increased shift in tropomyosin (zeige TPM2 Antikörper) position.
three-dimensional structure of F-actin at a resolution of 3.7 A in complex with tropomyosin (zeige TPM2 Antikörper) at a resolution of 6.5 A, determined by electron cryomicroscopy
data also identify a novel alphaTM1/Tmod1 (zeige TMOD1 Antikörper)-based pathway stabilizing F-actin at cell-cell junctions, which may be required for maintenance of cell shapes during embryonic cardiac morphogenesis (zeige XIRP1 Antikörper).
This is the first study to demonstrate that decreasing phosphorylation of tropomyosin (zeige TPM2 Antikörper) can rescue a hypertrophic cardiomyopathic phenotype.
Tropomyosin (zeige TPM2 Antikörper) dephosphorylation results in myocyte hypertrophy with increases in SERCA2a (zeige ATP2A2 Antikörper) expression.
The results identify a novel mode of myofilament desensitization to Ca(2 (zeige CA2 Antikörper)+) associated with a DCM linked switch in TPM1-kappa.
signaling by alpha-tropomyosin may have a role in familial hypertrophic cardiomyopathy
A point mutation in alpha-TM causes a disease similar to familial hypertophic cardiomyopahy.
PTB (zeige PTBP1 Antikörper) interacting protein raver1 (zeige RAVER1 Antikörper) regulates alpha-tropomyosin alternative splicing.
This study demonstrated that sarcomeric TPM1 plays vital roles in cardiogenesis and is a suitable candidate gene for screening individuals with isolated congenital heart defects .
Tpm (zeige TPMT Antikörper) isoforms 1.8/9 are enriched in the lamellipodium of fibroblasts as detected with a novel isoform-specific monoclonal antibody. RNAi-mediated silencing of Tpm1.8/9 led to an increase of Arp2 (zeige ACTR2 Antikörper)/3 accumulation at the cell periphery and a decrease in the persistence of lamellipodia and cell motility.
TPM1-AS regulates the alternative splicing of TPM1 through an interaction with RBM4 (zeige RBM4 Antikörper) and involves in TPM1-mediated filopodium formation and migration of cancer cells
The impact of tropomyosins on actin filament assembly is isoform specific.
TPM1 is the second gene linked to EA with LVNC in humans, implicating overlap in the molecular basis of structural and myopathic heart disease.
data demonstrate that the K15N mutation alters pointed end dynamics by affecting molecular interactions between Tpm1.1, Lmod2 (zeige LMOD2 Antikörper) and Tmod1 (zeige TMOD1 Antikörper).
Results report evidence for the existence of variants in LHFPL2 (zeige LHFPL2 Antikörper) and TPM1 with low allele frequencies and large effects on age-at-onset of familial Parkinson's disease.
In diabetes, expression of high molecular weight (HMW) isoforms from tropomyosin 1 (TPM1) were markedly decreased but HMW isoforms from tropomyosin 4 (TPM4 (zeige TPM4 Antikörper)) were not significantly different.
results suggest that TPM1 can suppress tumors in oral squamous cell carcinoma, and the TPM1 expression level is related to oral squamous cell carcinoma patient prognosis
We show that the phosphorylation of cTnI and alphaTm vary in the different chambers of the heart, whereas the phosphorylation of MLC2 and cTnT does not.
The results indicate that cross-linking significantly affects properties of Tpm (zeige TPMT Antikörper) and actin-myosin interaction and can explain, at least partly, the role of the interchain disulfide cross-linking of cardiac Tpm (zeige TPMT Antikörper) in human heart diseases.
altered TM-actin contacts destabilized the thin filament and affected the actin-myosin interactions
analysis of the thin filament associated with the R167H and K168E substitutions in tropomyosin (zeige TPM2 Antikörper) Tpm1.1
We propose that TR100 acts to compromise the integrity of Tpm cables rather than prevent overlap complex formation. Our data suggests that TR100 is incorporated into the growing actin-Tpm co-polymer given that its effects cannot be observed on pre-formed Tpm3.1/actin filaments
Maximal Ca(2 (zeige CA2 Antikörper)+) activated force was the same in alphaalphaTm versus betabetaTm myofibrils, but betabetaTm myofibrils showed a marked slowing of relaxation and an impairment of regulation under resting conditions
Tmod1 (zeige TMOD1 Antikörper) and Tmod3 (zeige TMOD3 Antikörper) showed somewhat different tropomyosin (zeige TPM2 Antikörper)-binding site utilization.
Thermal denaturation of rabbit cardiac alpha,alpha-tropomyosin is monitored at neutral pH and compared to shark tropomyosin (zeige TPM2 Antikörper), showing that amino acid substitutions predicted to be unfavorable in one temperature regime are desirable in another.
The rotational motion of a spin label covalently bound to the side chain of a cysteine genetically incorporated into rabbit skeletal muscle tropomyosin (zeige TPM2 Antikörper), was measured.
a computational search assessing electrostatic interactions for multiple azimuthal locations, z-positions, and pseudo-rotations of tropomyosin on F-actin was performed.
This gene is a member of the tropomyosin family of highly conserved, widely distributed actin-binding proteins involved in the contractile system of striated and smooth muscles and the cytoskeleton of non-muscle cells. Tropomyosin is composed of two alpha-helical chains arranged as a coiled-coil. It is polymerized end to end along the two grooves of actin filaments and provides stability to the filaments. The encoded protein is one type of alpha helical chain that forms the predominant tropomyosin of striated muscle, where it also functions in association with the troponin complex to regulate the calcium-dependent interaction of actin and myosin during muscle contraction. In smooth muscle and non-muscle cells, alternatively spliced transcript variants encoding a range of isoforms have been described. Mutations in this gene are associated with type 3 familial hypertrophic cardiomyopathy.
, alpha-tropomyosin 2
, alpha-tropomyosin of skeletal fast muscle
, tropomyosin (CTm4)
, tropomyosin (CTm7)
, tropomyosin alpha-1 chain
, tropomyosin 1 alpha chain
, alpha tropomyosin
, hepatoma alpha tropomyosin
, smooth muscle alpha-tropomyosin
, striated muscle alpha-tropomyosin
, tropomyosin 3 alpha
, alpha-skeletal tropomyosin
, cardiomyopathy, hypertrophic 3
, sarcomeric tropomyosin kappa
, tropomyosin 1 (alpha) isoform 1
, tropomyosin 1 (alpha) isoform 2
, tropomyosin 1 (alpha) isoform 3
, tropomyosin 1 (alpha) isoform 4
, tropomyosin 1 (alpha) isoform 5
, tropomyosin 1 (alpha) isoform 6
, tropomyosin 1 (alpha) isoform 7
, tropomyosin 1-1
, tropomyosin 1 (alpha)