| These results provide the evidence of a direct regulatory role of Snapin on Cav1.3 channels in atrial myocytes. | Physical and functional interaction of Snapin with Cav1.3 calcium channel impacts channel protein trafficking in atrial myocytes.
Sun XL, Yuan JF, Jin T, Cheng XQ, Wang Q, Guo J, Zhang W, Zhang Y, Lu L, Zhang Z. | 12/2/2017 |
| Study used structure modeling and MD simulations to predict omega-currents in CaV1.1 and CaV1.3 channel VSDs when one of the first three S4 gating charges harbors a disease-causing mutation. Using site-directed mutagenesis and electrophysiology, experimentally confirmed that the mutation of R3 charge to His in VSD III of CaV1.3 channels results in an omega-current at hyperpolarizing potentials. | Mechanisms Responsible for ω-Pore Currents in Ca(v) Calcium Channel Voltage-Sensing Domains.
Monteleone S, Lieb A, Pinggera A, Negro G, Fuchs JE, Hofer F, Striessnig J, Tuluc P, Liedl KR., Free PMC Article | 12/2/2017 |
| CACNA1D mutations predominate in small zona glomerulosa (ZG)-like Aldosterone-producing Adenomas. | NEFM (Neurofilament Medium) Polypeptide, a Marker for Zona Glomerulosa Cells in Human Adrenal, Inhibits D1R (Dopamine D1 Receptor)-Mediated Secretion of Aldosterone.
Maniero C, Garg S, Zhao W, Johnson TI, Zhou J, Gurnell M, Brown MJ. | 09/2/2017 |
| The CACNA1C-L762F mutation is associated with development of long QT syndrome through slower channel inactivation and increased sustained and window current. Timothy syndrome -associated mutations localize to specific areas of CACNA1C and are associated with a younger age at presentation, higher QTc, and 2:1 AV block than isolated LQTS-associated mutations. | Novel long QT syndrome-associated missense mutation, L762F, in CACNA1C-encoded L-type calcium channel imparts a slower inactivation tau and increased sustained and window current.
Landstrom AP, Boczek NJ, Ye D, Miyake CY, De la Uz CM, Allen HD, Ackerman MJ, Kim JJ., Free PMC Article | 09/2/2017 |
| Mutations in CACNA1D cause the excessive autonomous aldosterone secretion of Aldosterone-producing Adenomas. | Aldosterone-Producing Adenomas: Histopathology-Genotype Correlation and Identification of a Novel CACNA1D Mutation.
Tan GC, Negro G, Pinggera A, Tizen Laim NMS, Mohamed Rose I, Ceral J, Ryska A, Chin LK, Kamaruddin NA, Mohd Mokhtar N, A Jamal AR, Sukor N, Solar M, Striessnig J, Brown MJ, Azizan EA. | 08/26/2017 |
| While the relative contribution of Cav1.3 to intestinal Ca(2+) absorption and its value as a therapeutic target remain to be established, we postulate that Cav1.3 downregulation in IBD may contribute to the negative systemic Ca(2+) balance, to increased bone resorption, and to reduced bone mineral density in IBD patients. | Expression of Cav1.3 calcium channel in the human and mouse colon: posttranscriptional inhibition by IFNγ.
Radhakrishnan VM, Gilpatrick MM, Parsa NA, Kiela PR, Ghishan FK., Free PMC Article | 07/1/2017 |
| E2 upregulated the expression of Cav1.3 for Ca2+ influx to promote the expression of p-ERK1/2 for cell proliferation in breast cancer cells | Ultrasound-targeted microbubble destruction of calcium channel subunit α 1D siRNA inhibits breast cancer via G protein-coupled receptor 30.
Ji Y, Han Z, Shao L, Zhao Y., Free PMC Article | 03/18/2017 |
| LRP1B, BRD2 and CACNA1D are new candidate genes in fetal metabolic programming of newborns exposed to maternal hyperglycemia. | LRP1B, BRD2 and CACNA1D: new candidate genes in fetal metabolic programming of newborns exposed to maternal hyperglycemia.
Houde AA, Ruchat SM, Allard C, Baillargeon JP, St-Pierre J, Perron P, Gaudet D, Brisson D, Hivert MF, Bouchard L. | 09/24/2016 |
| CACNA1D might not be a risk gene for SCZ in Han Chinese population, which add to the current state of knowledge regarding the susceptibility of CACNA1D to schizophrenia. | Evaluation of genetic susceptibility of common variants in CACNA1D with schizophrenia in Han Chinese.
Guan F, Li L, Qiao C, Chen G, Yan T, Li T, Zhang T, Liu X., Free PMC Article | 07/30/2016 |
| patients with CACNA1D mutations displayed characteristics similar to wild-type aldosterone-producing adenomas | Clinical and Steroidogenic Characteristics of Aldosterone-Producing Adenomas With ATPase or CACNA1D Gene Mutations.
Kitamoto T, Suematsu S, Yamazaki Y, Nakamura Y, Sasano H, Matsuzawa Y, Saito J, Omura M, Nishikawa T. | 07/16/2016 |
| Studies indicate a role for L-type calcium channel Cav1.3 and Cav1.4 in cochlear inner hair cells (IHCs) and retinal photoreceptors (PRs). | Voltage-Gated Cav1 Channels in Disorders of Vision and Hearing.
Joiner ML, Lee A., Free PMC Article | 07/16/2016 |
| Studies indicate the function of L-type calcium channels Cav1.3 in chromaffin cells. | Cav1.3 Channels as Key Regulators of Neuron-Like Firings and Catecholamine Release in Chromaffin Cells.
Vandael DH, Marcantoni A, Carbone E., Free PMC Article | 07/16/2016 |
| Mutations in CACNA1D gene is associated with aldosterone-producing adenomas. | Novel somatic mutations and distinct molecular signature in aldosterone-producing adenomas.
Åkerström T, Willenberg HS, Cupisti K, Ip J, Backman S, Moser A, Maharjan R, Robinson B, Iwen KA, Dralle H, D Volpe C, Bäckdahl M, Botling J, Stålberg P, Westin G, Walz MK, Lehnert H, Sidhu S, Zedenius J, Björklund P, Hellman P. | 05/28/2016 |
| Different mutations (KCNJ5, ATP1A1, ATP2B3, and CACNA1D) are found in different aldosterone-producing nodules from the same adrenal, suggesting that somatic mutations are independent events triggered by mechanisms that remain to be identified. | Different Somatic Mutations in Multinodular Adrenals With Aldosterone-Producing Adenoma.
Fernandes-Rosa FL, Giscos-Douriez I, Amar L, Gomez-Sanchez CE, Meatchi T, Boulkroun S, Zennaro MC., Free PMC Article | 02/13/2016 |
| Study found that two de novo CACNA1D missense mutations affect evolutionary highly conserved regions in the channel's activation gate and disrupt normal channel activity by inducing a pronounced gain of channel function | CACNA1D de novo mutations in autism spectrum disorders activate Cav1.3 L-type calcium channels.
Pinggera A, Lieb A, Benedetti B, Lampert M, Monteleone S, Liedl KR, Tuluc P, Striessnig J., Free PMC Article | 01/2/2016 |
| In overall, we provide evidence that Cav1.2 and Cav1.3 isoforms are capable of potentially functioning as zinc permeation routes, through which zinc entry can be differentially augmented by mild acidifications. | Differential zinc permeation and blockade of L-type Ca2+ channel isoforms Cav1.2 and Cav1.3.
Park SJ, Min SH, Kang HW, Lee JH. | 12/19/2015 |
| Cp8 is a new of Cav1.2 and Cav1.3 channel activators. | Pyrimidine-2,4,6-triones are a new class of voltage-gated L-type Ca2+ channel activators.
Ortner NJ, Bock G, Vandael DH, Mauersberger R, Draheim HJ, Gust R, Carbone E, Tuluc P, Striessnig J., Free PMC Article | 11/21/2015 |
| Cav1.3 was overexpressed in atypical hyperplasia and endometrial carcinoma, and the estrogen-induced phosphorylation of downstream molecular ERK1/2 and CREB is the result of activation of the GPER pathway. | Ca2+ channel subunit α 1D promotes proliferation and migration of endometrial cancer cells mediated by 17β-estradiol via the G protein-coupled estrogen receptor.
Hao J, Bao X, Jin B, Wang X, Mao Z, Li X, Wei L, Shen D, Wang JL. | 09/26/2015 |
| A meta-analysis of genome-wide association studies of blood pressure and hypertension in Chinese identified three new loci (CACNA1D, CYP21A2, and MED13L) and a newly discovered variant near SLC4A7. | Genome-wide association study in Chinese identifies novel loci for blood pressure and hypertension.
Lu X, Wang L, Lin X, Huang J, Charles Gu C, He M, Shen H, He J, Zhu J, Li H, Hixson JE, Wu T, Dai J, Lu L, Shen C, Chen S, He L, Mo Z, Hao Y, Mo X, Yang X, Li J, Cao J, Chen J, Fan Z, Li Y, Zhao L, Li H, Lu F, Yao C, Yu L, Xu L, Mu J, Wu X, Deng Y, Hu D, Zhang W, Ji X, Guo D, Guo Z, Zhou Z, Yang Z, Wang R, Yang J, Zhou X, Yan W, Sun N, Gao P, Gu D., Free PMC Article | 07/25/2015 |
| ablation of Cav1.3 results in a decrease in the protein expression of myosin light chain 2, which interacts and increases the membrane localization of SK2 channels. | Regulation of gene transcription by voltage-gated L-type calcium channel, Cav1.3.
Lu L, Sirish P, Zhang Z, Woltz RL, Li N, Timofeyev V, Knowlton AA, Zhang XD, Yamoah EN, Chiamvimonvat N., Free PMC Article | 05/9/2015 |
| Article summarises the latest findings and specify the roles of Cav1.2 and Cav1.3 in neurological and psychiatric diseases.Individually, CACNA1C polymorphisms and CACNA1D variants have been linked to a variety of psychiatric diseases and to congenital deafness, respectively. [Review] | The role of L-type voltage-gated calcium channels Cav1.2 and Cav1.3 in normal and pathological brain function.
Berger SM, Bartsch D. | 04/4/2015 |
| CACNA1D gene overexpression is associated with prostate cancer progression and might play an important role in Ca(2+) influx, AR activation, and cell growth in prostate cancer cells | Cav1.3 channel α1D protein is overexpressed and modulates androgen receptor transactivation in prostate cancers.
Chen R, Zeng X, Zhang R, Huang J, Kuang X, Yang J, Liu J, Tawfik O, Thrasher JB, Li B. | 02/28/2015 |
| RNA editing of CaV1.3 channels(CDI) acts to modulate CDI in ways that substantiate a recently emerging mechanism where apoCaM begins preassociated with the IQ domain and other channel elements. | Continuously tunable Ca(2+) regulation of RNA-edited CaV1.3 channels.
Bazzazi H, Ben Johny M, Adams PJ, Soong TW, Yue DT., Free PMC Article | 01/10/2015 |
| in patients with aldosterone-producing adenomas, CACNA1D mutations were associated with smaller adenomas. | Genetic spectrum and clinical correlates of somatic mutations in aldosterone-producing adenoma.
Fernandes-Rosa FL, Williams TA, Riester A, Steichen O, Beuschlein F, Boulkroun S, Strom TM, Monticone S, Amar L, Meatchi T, Mantero F, Cicala MV, Quinkler M, Fallo F, Allolio B, Bernini G, Maccario M, Giacchetti G, Jeunemaitre X, Mulatero P, Reincke M, Zennaro MC. | 10/18/2014 |
| Results illustrate that the voltage sensors of Cav1.3 channels respond more sensitively to depolarization than those of Cav1.2 or Cav3.1 | C-terminal modulatory domain controls coupling of voltage-sensing to pore opening in Cav1.3 L-type Ca(2+) channels.
Lieb A, Ortner N, Striessnig J., Free PMC Article | 09/6/2014 |