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Rare-earth iron garnets (REIGs) are the benchmark systems for magnonics, including the longitudinal spin Seebeck effect (LSSE). While most research has focused on single-crystalline REIGs on complimentary garnet substrates, moving to more, cost-effective complementary metal-oxide semiconductor (CMOS)-compatible substrates is important to integrate REIG thin films with existing technology. In this regard, we grow a 130 nm-thick polycrystalline gadolinium iron garnet (GdIG) film on the Si/SiO2 substrate and investigate the temperature-dependent LSSE. Interestingly, the polycrystalline GdIG film exhibits perpendicular magnetic anisotropy (PMA) at room temperature which is induced by tensile in-plane (IP)-strain originating from the thermal-expansion mismatch between the GdIG film and the substrate during rapid thermal annealing. Further, a spin-reorientation transition from the out-of-plane IP direction below TS = 180 K is observed. Additionally, the film reveals a magnetic compensation temperature, T Comp , of ≈240 K. The LSSE voltage not only demonstrates a sign-inversion around T Comp , but also shows noticeable changes around T S. As compared to a single-crystalline GdIG film, the lower LSSE voltage for the polycrystalline GdIG is attributed to the higher effective magnetic anisotropy and enhanced magnon scattering at the grain boundaries. Our study not only paves the way for the cost-effective growth of CMOS-compatible REIG-based systems with PMA for magnonic memory and information processing applications, but also highlights the fact that the spincaloritronic and spin-insulatronic properties of the polycrystalline REIGs follow those of their single-crystalline counterparts with reduced spin-to-charge conversion efficiency through LSSE which can be tuned further by controlling the average gran size and interface engineering. [ABSTRACT FROM AUTHOR]

The magnon propagation length (MPL) is one of the crucial factors to govern spin transport in a magnetic material. Here, we determine MPL ($\xi$) in compensated ferrimagnetic Gd3Fe5O12 (GdIG) thin films at room temperature by investigating longitudinal spin Seebeck effect (LSSE) in Gd3Ga5O12 (GGG)/GdIG($t$)/Pt (5 nm) heterostructures with different thicknesses ($t$) of the GdIG film. All films possess in-plane (IP) magnetic easy axis, and the compensation temperature shifts down to lower temperature with decreasing GdIG thickness. At room temperature, the LSSE signal is rather constant with thickness between $t = 221$ and 89 nm, but drops significantly below $t = 50$ nm. By fitting the thickness dependence of the LSSE voltage to a modified atomistic spin model considering the influence of saturation magnetization, we obtain $\xi $ = 45 nm ± 8 nm for GdIG thin films at room temperature. The MPL of GdIG is much shorter than that of Y3Fe5O12 films ($\xi $ ~90–140 nm), but higher than that of Fe3O4 films ($\xi $ ~20 nm). The obtained value of $\xi $ explains the drop in the LSSE voltage in GdIG films when the film thickness is reduced below 50 nm, knowledge of which is also essential to the design of spincaloritronic devices based on GdIG films. [ABSTRACT FROM AUTHOR]

The authors report on a systematic investigation of the longitudinal spin Seebeck effect (LSSE) in a GGG(Gd3Ga5O12)/GdIG(Gd3Fe5O12)/Pt film series exhibiting an in‐plane magnetic easy axis with a compensation temperature (TComp) that decreases from 270 to 220 K when decreasing GdIG film thickness from 272 to 31 nm, respectively. For all the films, the LSSE signal flips its sign below TComp. The authors demonstrate a universal scaling behavior of the temperature dependence of LSSE signal for the GdIG films around their respective TComp. Additionally, the authors demonstrate LSSE in a 31 nm GdIG film grown on a lattice‐mismatched GSGG (Gd3Sc2Ga3O12) substrate that exhibits an out‐of‐plane magnetic easy axis at room temperature. However, this sample reveals a spin reorientation transition where the magnetic easy axis changes its orientation to in‐plane at low temperatures. A clear distinction is observed in the LSSE signal for the GSGG/GdIG(31 nm)/Pt heterostructure, relative to GGG/GdIG(31 nm)/Pt showing an in‐plane magnetic easy axis. The findings underscore a strong correlation between the LSSE signal and the orientation of magnetic easy axis in compensated ferrimagnets and opens the possibility to tune LSSE through effective anisotropy. [ABSTRACT FROM AUTHOR]

The insulating nature and the low intrinsic damping of rare earth iron garnets made them the material of choice for spintronic research. While yttrium iron garnet (YIG) thin films are well studied and especially known for their ultralow Gilbert damping parameter, recently other rare earth iron garnet (RIG) thin films with more complex magnetic structures have gained interest. Tunable magnetic properties like the magnetic compensation temperature or perpendicular magnetic anisotropy (PMA) are hereby of great interest for the implementation in spintronic devices. In this regard, calculations predict PMA which can be induced by magnetoelastic anisotropy for the RIGs, depending on the substrate choice and subsequent film strain. We have therefore investigated the influence of lattice mismatch provided by various garnet substrates and film stoichiometry on the structural and magnetic properties of gadolinium iron garnet (GdIG) thin films with thicknesses between 13 and 218 nm. Epitaxial, single-crystalline films exhibiting smooth interfaces were prepared by pulsed laser deposition at elevated temperatures. PMA is obtained for GdIG thin films grown under tensile in-plane strain on Gd3Sc2Ga3O12 (GSGG) substrates. Furthermore, a thickness series reveals a slow structural relaxation and PMA even for 218 nm thick GdIG films. In contrast, slightly off-stoichiometric films show a reduction or even loss in PMA. All GdIG films exhibit a magnetic compensation point in the range between 210–260 K, which is lower than for bulk (286 K). In addition, a temperature dependent spin reorientation transition was observed for GdIG/GSGG samples. Therefore, GdIG films provide tunable magnetic properties controllable by film strain, stoichiometry, and temperature, which will be beneficial for further research in the related fields of magnonics and spintronics. [ABSTRACT FROM AUTHOR]

The magnon propagation length, ⟨ξ⟩, of a ferro-/ferrimagnet (FM) is one of the key factors that controls the generation and propagation of thermally driven magnonic spin current in FM/heavy metal (HM) bilayer based spincaloritronic devices. For the development of a complete physical picture of thermally driven magnon transport in FM/HM bilayers over a wide temperature range, it is of utmost importance to understand the respective roles of temperature-dependent Gilbert damping (α) and effective magnetic anisotropy ( K eff ) in controlling the temperature evolution of ⟨ξ⟩. Here, we report a comprehensive investigation of the temperature-dependent longitudinal spin Seebeck effect (LSSE), radio frequency transverse susceptibility, and broad-band ferromagnetic resonance measurements on Tm 3 Fe 5 O 12 (TmIG)/Pt bilayers grown on different substrates. We observe a significant drop in the LSSE voltage below 200 K independent of TmIG film thickness and substrate choice. This is attributed to the noticeable increases in effective magnetic anisotropy field, H K eff (∝ K eff ) and α that occur within the same temperature range. From the TmIG thickness dependence of the LSSE voltage, we determined the temperature dependence of ⟨ξ⟩ and highlighted its correlation with the temperature-dependent H K eff and α in TmIG/Pt bilayers, which will be beneficial for the development of rare-earth iron garnet based efficient spincaloritronic nanodevices.

Impaired Ca2+ signaling in prostate cancer contributes to several cancer hallmarks, such as enhanced proliferation and migration and a decreased ability to induce apoptosis. Na+ influx via transient receptor potential melastatin 4 channel (TRPM4) can reduce store-operated Ca2+ entry (SOCE) by decreasing the driving force for Ca2+. In patients with prostate cancer, gene expression of TRPM4 is elevated. Recently, TRPM4 was identified as a cancer driver gene in androgen-insensitive prostate cancer.We investigated TRPM4 protein expression in cancer tissue samples from 20 patients with prostate cancer. We found elevated TRPM4 protein levels in prostatic intraepithelial neoplasia (PIN) and prostate cancer tissue compared to healthy tissue. In primary human prostate epithelial cells (hPEC) from healthy tissue and in the androgen-insensitive prostate cancer cell lines DU145 and PC3, TRPM4 mediated large Na+ currents. We demonstrated significantly increased SOCE after siRNA targeting of TRPM4 in hPEC and DU145 cells. In addition, knockdown of TRPM4 reduced migration but not proliferation of DU145 and PC3 cells. Taken together, our data identify TRPM4 as a regulator of SOCE in hPEC and DU145 cells, demonstrate a role for TRPM4 in cancer cell migration and suggest that TRPM4 is a promising potential therapeutic target.

Depletion of internal Ca(2+) stores activates store-operated Ca(2+) channels. The most prominent members of this class of channels are Ca(2+) release-activated Ca(2+) (CRAC) channels, which are present in a variety of cell types including immune cells. CRAC channels are composed of ORAI proteins, which are activated by endoplasmic reticulum-bound STIM proteins on Ca(2+) store depletion. The underlying Ca(2+) current is called ICRAC, which is required for many cellular functions including T-cell activation, mast cell activation, Ca(2+)-dependent gene expression, and refilling of internal Ca(2+) stores. To analyze ICRAC or the Ca(2+) current through heterologously expressed ORAI channels, whole-cell patch clamp is the technique of choice. It allows the direct analysis of ion currents through CRAC/ORAI channels. The patch-clamp technique has been used to determine selectivity, permeability, rectification, inactivation, and several other biophysical and pharmacological properties of the channels, and is the most direct and reliable technique to analyze ICRAC., (© 2014 Cold Spring Harbor Laboratory Press.)

Endogenous calcium release-activated channel (CRAC) currents are usually quite small and not always easy to measure using the patch-clamp technique. While we have, for instance, successfully recorded very small CRAC currents in primary human effector T cells, we have not yet managed to record CRAC in naïve primary human T cells. Many groups, including ours, therefore use Ca(2+) imaging technologies to analyze CRAC-dependent Ca(2+) influx. However, Ca(2+) signals are quite complex and depend on many different transporter activities; thus, it is not trivial to make quantitative statements about one single transporter, in this case CRAC channels. Therefore, a detailed patch-clamp analysis of ICRAC is always preferred. Since many laboratories use Ca(2+) imaging for ICRAC analysis, we detail here the minimal requirements for reliable measurements. Ca(2+) signals not only depend on the net Ca(2+) influx through CRAC channels but also depend on other Ca(2+) influx mechanisms, K(+) channels or Cl(-) channels (which determine the membrane potential), Ca(2+) export mechanisms like plasma membrane Ca(2+) ATPase (PMCA), sarco/endoplasmic reticulum Ca(2+) ATPase (SERCA) or Na(+)-Ca(2+) exchangers, and (local) Ca(2+) buffering often by mitochondria. In this protocol, we summarize a set of experiments that allow (quantitative) statements about CRAC channel activity using Ca(2+) imaging experiments, including the ability to rule out Ca(2+) signals from other sources., (© 2014 Cold Spring Harbor Laboratory Press.)

Although ICRAC and other store-operated currents are often analyzed by Ca(2+) imaging, whole-cell patch clamp, described here, is the preferred technique to analyze ICRAC whenever possible. The whole-cell patch-clamp protocol can even be used to record endogenous ICRAC in primary cells. The small endogenous current size of ICRAC requires some precautions: First, it is important to inhibit potential interferences from other channels in the cell by carefully choosing the combination of pipette and bath solutions. Second, the noise should be <150 fA root mean square (RMS) when the pipette holder (with its wire) with or without a patch pipette is adjusted over (but not in!) the solution using a high amplification gain (50 mV/pA or higher) of the patch-clamp amplifier. In addition, this protocol draws attention to measures that should be considered when recording ICRAC currents from an overexpression system. This protocol also suggests sets of solutions that can be used for distinguishing ICRAC from potentially interfering currents. In addition to the solutions, the identity of ICRAC can be confirmed by the characteristic inward rectification, its high Ca(2+) selectivity, and the reversal potential of more than +50 mV. A few (mostly nonspecific) CRAC channel blockers are known, which can also be applied for characterization purposes., (© 2014 Cold Spring Harbor Laboratory Press.)

Labelled 5α-dihydrotestosterone (DHT) binding experiments have shown that expression levels of (yet unidentified) membrane androgen receptors (mAR) are elevated in prostate cancer and correlate with a negative prognosis. However, activation of these receptors which mediate a rapid androgen response can counteract several cancer hallmark functions such as unlimited proliferation, enhanced migration, adhesion and invasion and the inability to induce apoptosis. Here, we investigate the downstream signaling pathways of mAR and identify rapid DHT induced activation of store-operated Ca2+ entry (SOCE) in primary cultures of human prostate epithelial cells (hPEC) from non-tumorous tissue. Consequently, down-regulation of Orai1, the main molecular component of Ca2+ release-activated Ca2+ (CRAC) channels results in an almost complete loss of DHT induced SOCE. We demonstrate that this DHT induced Ca2+ influx via Orai1 is important for rapid androgen triggered prostate specific antigen (PSA) release. We furthermore identified alterations of the molecular components of CRAC channels in prostate cancer. Three lines of evidence indicate that prostate cancer cells down-regulate expression of the Orai1 homolog Orai3: First, Orai3 mRNA expression levels are significantly reduced in tumorous tissue when compared to non-tumorous tissue from prostate cancer patients. Second, mRNA expression levels of Orai3 are decreased in prostate cancer cell lines LNCaP and DU145 when compared to hPEC from healthy tissue. Third, the pharmacological profile of CRAC channels in prostate cancer cell lines and hPEC differ and siRNA based knock-down experiments indicate changed Orai3 levels are underlying the altered pharmacological profile. The cancer-specific composition and pharmacology of CRAC channels identifies CRAC channels as putative targets in prostate cancer therapy.